Latest News on Tumour Necrosis: Feb 2021

Tumour necrosis factor and cancer

Tumour necrosis factor (TNF) is a major inflammatory cytokine that was first identified for its ability to induce rapid haemorrhagic necrosis of experimental cancers. When efforts to harness this anti-tumour activity in cancer treatments were underway, a paradoxical tumour-promoting role of TNF became apparent. Now that links between inflammation and cancer are appreciated, is TNF a target or a therapeutic in malignant disease — or both? [1]

Macrophage-induced angiogenesis is mediated by tumour necrosis factor-α

Macrophages are important in the induction of new blood vessel growth during wound repair, inflammation and tumour growth1–4. We show here that tumour necrosis factor-α (TNF-α), a secretory product of activated macrophages that is believed to mediate tumour cytotoxicity5–9, is a potent inducer of new blood vessel growth (angiogenesis). In vivo, TNF-α induces capillary blood vessel formation in the rat cornea and the developing chick chorioallantoic membrane at very low doses. In vitro, TNF-α stimulates chemotaxis of bovine adrenal capillary endothelial cells and induces cultures of these cells grown on type-1 collagen gels to form capillary-tube-like structures. The angiogenic activity produced by activated murine peritoneal macrophages is completely neutralized by a polyclonal antibody to TNF-α, suggesting immunological features are common to TNF-α and the protein responsible for macrophage-derived angiogenic activity. In inflammation and wound repair, TNF-α could augment repair by stimulating new blood vessel growth; in tumours, TNF-α might both stimulate tumour development by promoting vessel growth and participate in tumour destruction by direct cytotoxicity10–12. [2]

Tumour necrosis factor-α as a tumour promoter

It is becoming more evident that many aspects of tumour promotion arise from persistent and unresolving inflammation. One of the key molecules mediating the inflammatory processes in tumour promotion is the cytokine, tumour necrosis factor-α (TNF-α). Clinically, elevated serum concentrations and increased expression of TNF-α are present in various pre-neoplastic and malignant diseases, compared with serum and tissue from healthy individuals. Although over the last few decades high-dose administration of TNF-α has been used as a cytotoxic agent, recent pre-clinical cancer models have provided critical evidence to support the link between chronic, low level TNF-α exposure and the acquisition of pro-malignant phenotype (i.e., increased growth, invasion and metastasis). Furthermore, sophisticated cellular systems are being utilised to dissect the crucial role TNF-α plays in the communication of stromal/inflammatory cells and tumour cells. Understanding the intricate roles of TNF-α in the process of tumour promotion will assist in the development of novel cancer therapeutics. [3]

The Safety and Effectiveness of Single and Repeat Dosing of Intra-Articular Anti-Tumour Necrosis Factor Treatment after Failure of Intra-Articular Steroids

Objectives: To determine if intra-articular (ia) anti-tumour necrosis factor (TNF) yielded benefit in patients failing ia steroid injections and determine the safety and durability of single and repeated ia anti-TNF treatment in inflammatory arthritis.
Methods: Patients with inflammatory arthritis having one or two active joints, and having failed previous ia steroids were injected with ia adalimumab or ia etanercept mixed with triamcinolone and lidocaine via a retrospective chart audit.
Results: Twenty-six patients were followed: 18 received ia adalimumab, 12 received ia etanercept and 4 received both. Twenty-five knees, 17 ankles, 1 wrist and 1 PIP were injected of whom 6 had repeated injections to a joint. Nine were on concomitant systemic anti-TNF therapy. Fifteen had RA, 4 had a seronegativearthropathy, 3 had psoriatic arthritis, and 4 had other arthritis. When determining a response to ia anti-TNF for > 2 months in patients with sufficient follow up 13 of 18 receiving iaadalimumab and 6/7 with ia etanercept had benefit. There were no serious adverse events (SAEs) and only one AE in a wrist post ia adalimumab, with rebound inflammation after 6 weeks of marked relief. Two were able to cancel or postpone joint surgery(knee and ankle)and one cancelled an yttrium injection.
Conclusions: There were no SAEs and prolonged benefit was found with ia anti-TNF and steroids and lidocaine compared to previous ia steroids with lidocaine in the majority (20/27). Although not approved for ia administration, ia anti-TNFs may be cost effective in persistent synovitis of one or two joints recalcitrant to ia steroids. [4]

Changes in Lipid Peroxidation, Free Radical Scavengers and Tumour Necrosis Factor-alpha in Serum of Wistar Rats with Induced Thyroid Dysfunction

Aim: To assess the changes in lipid peroxidation, free radical scavengers and tumour necrosis factor-alpha in serum of Wistar rats with induced thyroid dysfunction.

Study Design: An experimental animal study was conducted in which Wistar rats with induced thyroid dysfunction were studied.

Place and Duration of Study: Animal House, Faculty of Pharmaceutical Sciences, Usmanu Danfodiyo University, Sokoto and Department of Chemical Pathology, Faculty of Medical Laboratory Sciences, Usmanu Danfodiyo University, Sokoto, between June, 2016 and December, 2016.

Methodology: Twenty-one (21) male Wistar rats weighing 140 – 180 grams were randomly divided into three groups. Therefore, each group consists of 7 rats. Euthyroid (control): untreated receiving daily intraperitoneal injection of 0.9% normal saline solution; hypothyroid:  treated with daily oral administration of 6-propyl-2-thiouracil (5 mg/100 g) and hyperthyroid: treated with daily intraperitoneal injection of L-thyroxine (0.1 µg/g). At the end of the 30 days treatment,  rats were fasted for 12 hours and blood samples were collected under chloroform anaesthesia for the estimation of serum total triidothyronine (tT3), total tetraiodothyronine (tT4), thyroid stimulating hormone (TSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), malondialdehyde (MDA) and tumour necrosis-alpha (TNF-α) using standard techniques. The rats were then scarified by cervical decapitation and slices of liver tissue were made for histological examination.

Results: The result indicated that final body weight, and serum tT3, tT4, SOD, CAT and GPX were significantly (P<0.05; P< 0.001) lower in hypothyroid and hyperthyroid rats while, serum MDA and TNF-α were significantly (P<0.05; P< 0.001) higher in hypothyroid and hyperthyroid compared with euthyroid rats. Serum TSH was significantly (P< 0.001) higher in hypothyroid compared with euthyroid and hyperthyroid rats. Histological examination of the hepatocellular tissue of euthyroid rat revealed normochromic and normocytic cellular architecture. There was polymorphocytic infiltration with mild inflammation and hypochromatic liver in hypothyroid rats while, conspicuous infiltrations of polymorphs in all fields were observed in hyperthyroid rats.

Conclusion: In this study, serum MDA and TNF-α were significantly higher, and SOD, CAT and GPX activities were lower in experimental hypothyroid and hyperthyroid rats. The result therefore suggests that a decreased antioxidant capacity coupled with increased oxidative stress and TNF-α may play an important role in the pathogenesis of hepatic injury due to thyroid dysfunction and underscores the role of antioxidants in reducing oxidative stress associated with thyroid dysfunction. [5]

Reference

[1] Balkwill, F., 2009. Tumour necrosis factor and cancer. Nature reviews cancer9(5), pp.361-371.

[2] Leibovich, S.J., Polverini, P.J., Shepard, H.M., Wiseman, D.M., Shively, V. and Nuseir, N., 1987. Macrophage-induced angiogenesis is mediated by tumour necrosis factor-α. Nature329(6140), pp.630-632.

[3] Szlosarek, P., Charles, K.A. and Balkwill, F.R., 2006. Tumour necrosis factor-α as a tumour promoter. European journal of cancer42(6), pp.745-750.

[4] Chia, J. and Pope, J. (2011) “The Safety and Effectiveness of Single and Repeat Dosing of Intra-Articular Anti-Tumour Necrosis Factor Treatment after Failure of Intra-Articular Steroids”, Journal of Advances in Medicine and Medical Research, 2(1), pp. 39-53. doi: 10.9734/BJMMR/2012/805.

[5] Yeldu, M.H. and Ishaq, S., 2017. Changes in Lipid Peroxidation, Free Radical Scavengers and Tumour Necrosis Factor-alpha in Serum of Wistar Rats with Induced Thyroid Dysfunction. Annual Research & Review in Biology, pp.1-14.

Latest News on Tumour Progression: Feb 2021

Tumour-educated macrophages promote tumour progression and metastasis

Evidence from clinical and experimental studies indicates that macrophages promote solid-tumour progression and metastasis. Macrophages are educated by the tumour microenvironment, so that they adopt a trophic role that facilitates angiogenesis, matrix breakdown and tumour-cell motility — all of which are elements of the metastatic process. During an inflammatory response, macrophages also produce many compounds — ranging from mutagenic oxygen and nitrogen radicals to angiogenic factors — that can contribute to cancer initiation and promotion. Macrophages therefore represent an important drug target for cancer prevention and cure. [1]

Epithelial–mesenchymal transitions in tumour progression

Without epithelial–mesenchymal transitions, in which polarized epithelial cells are converted into motile cells, multicellular organisms would be incapable of getting past the blastula stage of embryonic development. However, this important developmental programme has a more sinister role in tumour progression. Epithelial–mesenchymal transition provides a new basis for understanding the progression of carcinoma towards dedifferentiated and more malignant states. [2]

Tumour progression and the nature of cancer

The nature of neoplasia and its sometime end result, cancer, has been studied by exposition and explanation of the sequential lesions of tumour progression. Neoplastic lesions were divided into four classes on the basis of growth characteristics and whether lesional growth is confined to one or more tissue compartments. Class IA, the initial lesion, an orderly, probably clonal growth, usually differentiates and disappears. Class IB: Failure to differentiate accompanied by disorderly growth. Class IC: Randomly dispersed atypical cells, constituting a precursor state. Class II, intermediate lesions, apparently arising from the atypical cells, show temporally unrestricted growth within the tissue compartment of origin. Class III lesions, primary invasive cancers, show temporally unrestricted growth in two or more tissue compartments and metastasise along different paths, a property associated with extracellular matrix interaction. The metastatic pathways may result from different subsets of cells in the primary cancer. Class IV lesions are the metastases. It was concluded that, all neoplasms develop in the same way, have the same general behavioural characteristics, and, when malignant, all interact with the extracellular matrix of the primary and the secondary sites. The origins and development of cancer are considered to be pluralistic and not due to a discrete change in a cell, whose progeny, as a result of that discrete change, carries all of the information required to explain the almost limitless events of a neoplastic system. [3]

Dissecting Biology of Solid Tumour: The Microenvironment and Cancer Progression

Focus on cancer therapy is experiencing a major paradigm shift from ways of attacking tumor cells to a strategy for specifically targeting the tumor microenvironment (TME). This approach requires a comprehensive understanding of roles of each component of the tumor environment. A description of the tumor microenvironment and its impact on tumor progression is presented here. Available studies indicate that both tumor/epithelial and stroma characteristics play important roles in cancer progression. Details of this work show that different components of the tumor microenvironment contribute towards cancer progression and clearly suggest a role for use of combination therapies for tight tumor control. [4]

KRAS Mutation is a Local Tumour Event and Not a Field Change in Pancreatobiliary Tumours

Background: KRAS mutation (KRM) is the earliest, most common mutation in pancreatic cancer. Accurate assessment of tumour KRM status in pancreatobiiary tumours is relevant in an era of targeted molecular therapies.

Aim: To assess KRM in tumour and non-tumourous margin tissue in patients undergoing a pancreatic resection.

Study Design: Original research, retrospective review of prospectively collected specimens.

Place and Duration of Study: Patients who had undergone pancreaticoduodenectomy and distal pancreatic resection at the Royal Adelaide Hospital from 2011-2012 were consented for the study.

Methods: Patient demographics, background history and tumour details were collated. Tumour tissue and margin areas were macrodissected from FFPE tissue sections following identification by a pathologist. DNA was prepared from the tissue using the QIAamp FFPE Tissue kit (Qiagen GmbH, Hilden Germany). KRM at codons 12 and 13 was assessed using SNaPShot TM (Applied Biosystems, Warrington UK) in tumour tissue and non-tumourous margin tissue.

Fourteen patients were included in the study. The median age of the patients in the study was 68 (range 57-86) years. The M : F ratio was 8 : 6.

Results: Twelve patients had adenocarcinomas (5 pancreatic; 4 ampullary, 3 biliary) and two had benign mucinous tumours. Six patients with adenocarcinomas had KRM (5@codon 12 and 1@codon 13). Margin tissue was negative for KRM in all the tested patients (p<0.016 Fisher) particularly, in those with tumour KRM.

Tumours with KRM were associated with larger tumours 30(22-65) mm vs 20(15-35) mm [median(range)](p = .045 – MW-U). Nodal disease occurred in 6/6 with KRM vs 2/6 without KRM (p = .61 – Fisher).

Conclusions: KRM is a local tumour event and not a field change. This suggests that testing for KRM should be reliant on tumour tissue and not surrounding normal margin tissue. KRM was associated with larger malignant tumours and a trend towards nodal disease. [5]

Reference

[1] Pollard, J.W., 2004. Tumour-educated macrophages promote tumour progression and metastasis. Nature Reviews Cancer, 4(1), pp.71-78.

[2] Thiery, J.P., 2002. Epithelial–mesenchymal transitions in tumour progression. Nature reviews cancer, 2(6), pp.442-454.

[3] Clark, W.H., 1991. Tumour progression and the nature of cancer. British journal of cancer, 64(4), pp.631-644.

[4] Omabe, M. and Onyekachi, O.B., 2013. Dissecting Biology of Solid Tumour: The Microenvironment and Cancer Progression. Journal of Advances in Medicine and Medical Research, pp.1786-1797.

[5] Chandrasegaram, M.D., Chen, D.Y., Tan, C.P., Neo, E.L., Dolan, P.M., Chen, J.W., Brooke-Smith, M.E., Cheetham, G., Ruszkiewicz, A. and Worthley, C.S., 2013. KRAS mutation is a local tumour event and not a field change in pancreatobiliary tumours. Journal of Advances in Medicine and Medical Research, pp.2069-2075.

Latest News on Cancer Screening: Dec 2020

Colorectal cancer screening: Clinical guidelines and rationale

Evidence exists that reductions in colorectal cancer (CRC) mortality can be achieved through detection and treatment of early-stage CRCs and the identification and removal of adenomatous polyps, the precursor to these cancers. An expert, multidisciplinary panel was convened to review this evidence and to produce recommendations to guide clinicians and the public in making decisions regarding CRC screening and surveillance. As part of its review, the panel also commissioned a simulation model that estimates and compares the clinical consequences (benefits and major complications) of each screening approach. This guideline report presents the panel’s recommendations with respect to screening and surveillance in people at average risk for CRC and those at increased risk because of a family history of CRC or genetic syndromes or a personal history of adenomatous polyps, inflammatory bowel disease, or curative-intent resection of CRC. The cost- effectiveness of potential screening strategies was taken into account when preparing the recommendations. A summary of the evidence on each screening test’s performance, effectiveness, frequency, complications, ‘and patient acceptance is included. Also provided are suggestions for ways to increase compliance with the recommendations, questions for which additional research is needed, and the results of the simulation model on screening consequences. [1]

Enthusiasm for Cancer Screening in the United States

Context Public health officials, physicians, and disease advocacy groups have worked hard to educate individuals living in the United States about the importance of cancer screening.

Objective To determine the public’s enthusiasm for early cancer detection.

Design, Setting, and Participants Survey using a national telephone interview of adults selected by random digit dialing, conducted from December 2001 through July 2002. Five hundred individuals participated (women aged ≥40 years and men aged ≥50 years; without a history of cancer).

Main Outcome Measures Responses to a survey with 5 modules: a general screening module (eg, value of early detection, total-body computed tomography); and 4 screening test modules: Papanicolaou test; mammography; prostate-specific antigen (PSA) test; and sigmoidoscopy or colonoscopy.

Results Most adults (87%) believe routine cancer screening is almost always a good idea and that finding cancer early saves lives (74% said most or all the time). Less than one third believe that there will be a time when they will stop undergoing routine screening. A substantial proportion believe that an 80-year-old who chose not to be tested was irresponsible: ranging from 41% with regard to mammography to 32% for colonoscopy. Thirty-eight percent of respondents had experienced at least 1 false-positive screening test; more than 40% of these individuals characterized that experience as “very scary” or the “scariest time of my life.” Yet, looking back, 98% were glad they had had the initial screening test. Most had a strong desire to know about the presence of cancer regardless of its implications: two thirds said they would want to be tested for cancer even if nothing could be done; and 56% said they would want to be tested for what is sometimes termed pseudodisease (cancers growing so slowly that they would never cause problems during the persons lifetime even if untreated). Seventy-three percent of respondents would prefer to receive a total-body computed tomographic scan instead of receiving $1000 in cash.

Conclusions The public is enthusiastic about cancer screening. This commitment is not dampened by false-positive test results or the possibility that testing could lead to unnecessary treatment. This enthusiasm creates an environment ripe for the premature diffusion of technologies such as total-body computed tomographic scanning, placing the public at risk of overtesting and overtreatment. [2]

American Cancer Society Guidelines for Breast Cancer Screening: Update 2003

In 2003, the American Cancer Society updated its guidelines for early detection of breast cancer based on recommendations from a formal review of evidence and a recent workshop. The new screening recommendations address screening mammography, physical examination, screening older women and women with comorbid conditions, screening women at high risk, and new screening technologies. [3]

Breast Cancer Screening Awareness and Practice among Women in Sagamu Local Government Area, South-Western Nigeria: A Community Based Study

Introduction: Breast cancer is the leading female malignancy in the world and the second principal cause of cancer deaths in women worldwide. It has a poorer outcome among African-American women compared with the whites due to more advanced stage at presentation. This study therefore examines the factors influencing breast cancer screening awareness and practices among women in Ogun State, Western Nigeria.

Methods: This analytical cross-sectional study was conducted between April 22nd and13th May, 2013. A multi stage cluster sampling technique was used to select the participants into the study. One participant per each household was selected into the study. A semi- structured questionnaire was used to collect relevant information.

Results: A total of 495 women were interviewed in this study, the mean age of the respondents was 36.45 years ranging from 19 to 63 years. Only 48.5% of respondents knew the commonest age group at risk of breast cancer and 59.4% knew breast cancer can be detected early. Majority [81.0%] were not aware of mammography and none of the respondents knew the age when regular screening should commence. One hundred percent of our respondents have never had mammography done for any reason whatsoever. Majority of respondents [85.0%] have never asked anyone about mammography. Predictors of awareness of mammography were marital status [O.R= 1.61, C.I=1.35-3.05], tertiary education [OR= 2.14 C.I=1.13-6.08] and Nuclear family structure [OR=1.83, C.I=1.13-3.74].

Conclusion: This study revealed a low level of awareness of mammography and mammographic screening. None of the respondents had ever undergone mammography. Public education and awareness programs should be developed to promote early detection and diagnosis in the prevention of breast cancer in women in Nigeria and other developing countries. [4]

Genotyping Human Papillomavirus in Women Attending Cervical Cancer Screening Clinic in Harare, Zimbabwe

Aim: To determine the prevalence of human papillomavirus genotypes in women attending a cervical cancer screening VIAC (visual inspection with acetic acid) clinic.

Study Design: Cross-sectional study.

Place and Duration of Study: VIAC clinic at Parirenyatwa Referral Hospital in Harare in Zimbabwe between February and April 2015.

Methodology: Sexually active women were recruited and they provided their socio-demographic data and self-collected vaginal swabs. HIV status of the participants was determined. DNA was extracted from the swabs using the standard phenol-chloroform method. HPV DNA was detected using the standard consensus MY09/11-GP5+/GP6+ nested polymerase chain reaction. Amplicons were sequenced and sequences analyzed using bioinformatics tools to identify the HPV genotypes.

Results: Sixty women were recruited. Their age ranged from 21-83 years, with a mean of 40.1 years. Most of the women were married and resided in the urban areas. Of the 60 participants, 50% (30/60) were HIV-positive. The prevalence of HPV genotypes in the study subjects was 56.7% (34/60). HPVs were most prevalent in women aged 30 years and below, and became less prevalent as the age increased. The predominant genotypes detected were HPV-16, -58, -52, -45, -18, -33, -51, -6, -81, -11, -70, -62, -32 and -40.

Conclusion: A number of HPV genotypes were detected in half of women tested. There was no significance association between risk-factors (parity, level of education, residence, history of STI, contraceptive use and sexual debut) and HPV infection. The findings of this study showed that consensus nested PCR and DNA sequencing could be used to detect HPV genotypes in women in cervical cancer screening programs. Although this method is sensitive, it is inefficient at detecting multiple HPV infections. [5]

Reference

[1] Winawer, S.J., Fletcher, R.H., Miller, L., Godlee, F., Stolar, M.H., Mulrow, C.D., Woolf, S.H., Glick, S.N., Ganiats, T.G., Bond, J.H. and Rosen, L., 1997. Colorectal cancer screening: clinical guidelines and rationale. Gastroenterology, 112(2), pp.594-642.

[2] Schwartz, L.M., Woloshin, S., Fowler Jr, F.J. and Welch, H.G., 2004. Enthusiasm for cancer screening in the United States. Jama, 291(1), pp.71-78.

[3] Smith, R.A., Saslow, D., Sawyer, K.A., Burke, W., Costanza, M.E., Evans III, W.P., Foster Jr, R.S., Hendrick, E., Eyre, H.J. and Sener, S., 2003. American Cancer Society guidelines for breast cancer screening: update 2003. CA: a cancer journal for clinicians, 53(3), pp.141-169.

[4] Amoran, O. E., Toyobo, T. O. and Fatugase, O. K. (2014) “Breast Cancer Screening Awareness and Practice among Women in Sagamu Local Government Area, South-Western Nigeria: A Community Based Study”, Current Journal of Applied Science and Technology, 4(16), pp. 2320-2332. doi: 10.9734/BJAST/2014/9050.

[5] Matuvhunye, T., Mandishora, R. S., Chin’ombe, N., Chakafana, G., Mbanga, J., Zumbika, E. and Pedersen, B.- (2016) “Genotyping Human Papillomavirus in Women Attending Cervical Cancer Screening Clinic in Harare, Zimbabwe”, Microbiology Research Journal International, 16(6), pp. 1-9. doi: 10.9734/BMRJ/2016/28481.

Latest News on Ovarian Cancer: Dec 2020

The biology of ovarian cancer

The biology of ovarian cancer broadly defined covers essentially all aspects of the disease from how it arises to how it responds to chemotherapy, often becomes refractory to treatment, and ultimately kills the patient. In this article, we take the liberty of discussing many of these issues to some degree in context of the “natural/clinical” history/biology of the disease. We focus on concepts of how the disease develops, efforts to identify histologic changes that may precede the development of overt ovarian cancer, efforts to define how the growth and function of the normal ovarian surface epithelium are regulated to gain insights into how aberrant function of these pathways may contribute to the initiation of the disease, molecular biological studies on clinical ovarian cancer specimens, efforts to experimentally induce the malignant transformation of ovarian surface epithelial cells, and efforts to understand why ovarian cancer is often initially responsive to chemotherapy but ultimately becomes refractory. [1]

Epidemiology of Ovarian Cancer

Ovarian cancer represents the sixth most commonly diagnosed cancer among women in the world, and causes more deaths per year than any other cancer of the female reproductive system. Despite the high incidence and mortality rates, the etiology of this disease is poorly understood. Established risk factors for ovarian cancer include age and having a family history of the disease, while protective factors include increasing parity, oral contraceptive use, and oophorectomy. Lactation, incomplete pregnancies, and surgeries such as hysterectomy and tubal ligation may confer a weak protective effect against ovarian cancer. Infertility may contribute to ovarian cancer risk among nulliparous women. Other possible risk factors for ovarian cancer include postmenopausal hormone-replacement therapy and lifestyle factors such as cigarette smoking and alcohol consumption. Many of the causes of ovarian cancer are yet to be identified. Additional research is needed to better understand the etiology of this deadly disease. [2]

Rethinking ovarian cancer: recommendations for improving outcomes

There have been major advances in our understanding of the cellular and molecular biology of the human malignancies that are collectively referred to as ovarian cancer. At a recent Helene Harris Memorial Trust meeting, an international group of researchers considered actions that should be taken to improve the outcome for women with ovarian cancer. Nine major recommendations are outlined in this Opinion article. [3]

Ovarian Cancer Symptom Awareness and Its Response among Female Health Workers

Objectives: To determine the level of awareness of ovarian cancer symptoms and help-seeking responses of female health workers.

Methods: Four hundred and fifty seven female health workers were randomly selected and made to complete a structured proforma adapted from the Ovarian Cancer Awareness Measure (Ovarian CAM), which is a site-specific version of the generic Cancer Awareness Measure. Questions were asked on level of awareness of ovarian cancer early symptoms, anticipated time and the barriers to help-seeking responses.

Results: Out of 457 clients, 211 (46.2%) were able to recall at least one warning symptom of ovarian cancer while 20 (4.4%) were able to recall more than 3 warning symptoms. On the other end, when presented with a list of warning symptoms of ovarian cancer, identification ranged from 33.7-72.0% for the symptoms. As high as 28.0% could not identify any of the listed warning symptoms though some of them are also well known symptoms of late stage of ovarian cancer as well. A range of 11.7 – 27.3% of those who have ever seen a cancer patient before will seek for immediate medical help for various ovarian cancer symptoms. Also, having experienced a form of cancer before showed no relationship with the identification of all the warning signs of ovarian cancer outlined (P value ranged from .15 to .93).

Conclusion: The level of awareness of ovarian cancer warning symptomsis very low among the female health workers, and there is a poor medical help seeking habit even among those that could identify those symptoms. Efforts at improving these factors are therefore recommended. [4]

Cytotoxic and Apoptotic Effects of the Bark of Two Common Mango (Mangifera indica) Varieties from Sri Lanka on Breast and Ovarian Cancer Cells

Aims: The present study was planned to evaluate cytotoxic and apoptotic properties of the bark of two common mango varieties (Mangifera indica L.) grown in Sri Lanka [Rata Amba (RA) and Karthakolomban (KA)] in MCF-7 (ER positive breast cancer), MDA-MB-231 (triple negative breast cancer), SKOV-3 (ovarian epithelial cancer) cancer cell lines and normal mammary epithelial cells (MCF-10A).

Place and Duration of the Study: At the Institute of Biochemistry, Molecular Biology and Biotechnology, University of Colombo between 1st of February 2015 to April 2015.

Methodology: Cancer cells and normal cells were treated with organic extracts (hexane, chloroform, ethyl acetate and methanol) of RA and KA bark and cytotoxic effects were evaluated by SRB assay. Free radical scavenging ability on 1,1-diphenyl-2-picrylhydrazyl (DPPH) was also tested for active extracts. Furthermore, apoptotic effects of cytotoxic extracts were analysed by caspase 3 and 7 activation, DNA fragmentation, acridine orange/ethidium bromide (AO/EB) and Hoechst staining.

Results: Of the four solvent extracts used, only the methanol extract showed anti-proliferative effects against all three cancer cell lines in a dose-dependent manner. Cytotoxicity of the methanol extract of RA was higher (MCF-7 IC50- 81.1 µg/mL, MDA-MB-231 IC50- 91. 5 µg/mL and SKOV-3 IC50- 71.5 µg/mL) compared to that of the methanol extract of KA (MCF-7 IC50- 123.9 µg/mL, MDA-MB-231 IC50- 111.2 µg/mL and SKOV-3 IC50- 137.2 µg/mL). Both the methanol extracts showed less cytotoxicity to normal mammary epithelial cells [IC50- 255.6 µg/mL (RA) and IC50- 615.6 µg/mL (KA)]. Methanol extracts also exhibited strong free radical scavenging ability on 1,1-diphenyl-2-picrylhydrazyl (DPPH). Furthermore, methanol extract showed apoptotic effect against all tested cancer cell lines.

Conclusion: Overall findings of this study suggest that methanol extracts of the bark of two common mango varieties tested exhibit cytotoxicity through induction of apoptosis through caspase dependent mechanisms. [5]

Reference

[1] Auersperg, N., Edelson, M.I., Mok, S.C., Johnson, S.W. and Hamilton, T.C., 1998, June. The biology of ovarian cancer. In Seminars in oncology (Vol. 25, No. 3, p. 281).

[2] Permuth-Wey, J. and Sellers, T.A., 2009. Epidemiology of ovarian cancer. In Cancer epidemiology (pp. 413-437). Humana Press.

[3] Vaughan, S., Coward, J.I., Bast, R.C., Berchuck, A., Berek, J.S., Brenton, J.D., Coukos, G., Crum, C.C., Drapkin, R., Etemadmoghadam, D. and Friedlander, M., 2011. Rethinking ovarian cancer: recommendations for improving outcomes. Nature Reviews Cancer, 11(10), pp.719-725.

[4] Adeyemi, A. S., Afolabi, A. F. and Adedeji, O. A. (2014) “Ovarian Cancer Symptom Awareness and Its Response among Female Health Workers”, Journal of Advances in Medicine and Medical Research, 5(8), pp. 978-986. doi: 10.9734/BJMMR/2015/13354.

[5] Ediriweera, M., Tennekoon, K., Samarakoon, S., Thabrew, I. and de Silva, E. D. (2016) “Cytotoxic and Apoptotic Effects of the Bark of Two Common Mango (Mangifera indica) Varieties from Sri Lanka on Breast and Ovarian Cancer Cells”, Journal of Pharmaceutical Research International, 10(2), pp. 1-7. doi: 10.9734/BJPR/2016/24004.

Latest News on Medulloblastoma: Dec 2020

Medulloblastoma Comprises Four Distinct Molecular Variants

Purpose

Recent genomic approaches have suggested the existence of multiple distinct subtypes of medulloblastoma. We studied a large cohort of medulloblastomas to determine how many subgroups of the disease exist, how they differ, and the extent of overlap between subgroups.

Methods

We determined gene expression profiles and DNA copy number aberrations for 103 primary medulloblastomas. Bioinformatic tools were used for class discovery of medulloblastoma subgroups based on the most informative genes in the data set. Immunohistochemistry for subgroup-specific signature genes was used to determine subgroup affiliation for 294 nonoverlapping medulloblastomas on two independent tissue microarrays.

Results

Multiple unsupervised analyses of transcriptional profiles identified the following four distinct, nonoverlapping molecular variants: WNT, SHH, group C, and group D. Supervised analysis of these four subgroups revealed significant subgroup-specific demographics, histology, metastatic status, and DNA copy number aberrations. Immunohistochemistry for DKK1 (WNT), SFRP1 (SHH), NPR3 (group C), and KCNA1 (group D) could reliably and uniquely classify formalin-fixed medulloblastomas in approximately 98% of patients. Group C patients (NPR3-positive tumors) exhibited a significantly diminished progression-free and overall survival irrespective of their metastatic status.

Conclusion

Our integrative genomics approach to a large cohort of medulloblastomas has identified four disparate subgroups with distinct demographics, clinical presentation, transcriptional profiles, genetic abnormalities, and clinical outcome. Medulloblastomas can be reliably assigned to subgroups through immunohistochemistry, thereby making medulloblastoma subclassification widely available. Future research on medulloblastoma and the development of clinical trials should take into consideration these four distinct types of medulloblastoma. [1]

Intertumoral Heterogeneity within Medulloblastoma Subgroups

While molecular subgrouping has revolutionized medulloblastoma classification, the extent of heterogeneity within subgroups is unknown. Similarity network fusion (SNF) applied to genome-wide DNA methylation and gene expression data across 763 primary samples identifies very homogeneous clusters of patients, supporting the presence of medulloblastoma subtypes. After integration of somatic copy-number alterations, and clinical features specific to each cluster, we identify 12 different subtypes of medulloblastoma. Integrative analysis using SNF further delineates group 3 from group 4 medulloblastoma, which is not as readily apparent through analyses of individual data types. Two clear subtypes of infants with Sonic Hedgehog medulloblastoma with disparate outcomes and biology are identified. Medulloblastoma subtypes identified through integrative clustering have important implications for stratification of future clinical trials. [2]

Medulloblastoma: Clinical and biologic aspects

Medulloblastoma is the most common childhood primary CNS tumor, and treatment approaches have evolved over the past three decades. The biologic under-pinnings of medulloblastoma are not fully characterized, but recent work has identified new, important directions for research. Stratification of patients with medulloblastoma into risk groups is the backbone of most ongoing therapeutic studies. Patients are usually characterized as being either average risk or poor risk, although an intermediate risk group may exist. Standard treatment for older children with medulloblastoma consists of radiation and, for most, chemotherapy. Children with nondisseminated disease at the time of diagnosis have been reported to have as high as an 80% five-year disease-free survival rate after treatment with reduced dose (2340 cGy) craniospinal irradiation, local boost radiation therapy (5500 cGy), and chemotherapy, given during and after radiation therapy. Preradiation chemotherapy has yet to be shown to be of benefit for children with medulloblastoma. Children with disseminated disease are a highly problematic subgroup of patients to treat. A variety of new approaches are being studied, most of which are intensifying chemotherapy either prior to or after radiation. Long-term survivors of medulloblastoma are at significant risk for permanent endocrinologic, cognitive, and psychological sequelae. Infants and very young children with medulloblastoma remain a difficult therapeutic challenge because they have the most virulent form of the disease and are at highest risk for treatment-related sequelae. [3]

Desmoplastic Medulloblastoma Patients Survival after Multimodality Treatment

Aims: This is to investigate the results of the multimodality regimen including surgery, postoperative craniospinal irradiation and clarify the role of chemotherapy as well as the influence of multiple variables on desmoplastic medulloblastoma patient’s survival.

Study Design: Original research papers.

Place and Duration of Study: It took place in the period between January 2001 and Sept 2015 at Neurosurgery and Clinical Oncology & Nuclear Remedies Departments of Mansoura university Hospital.

Methodology: We reviewed data of (28) patients histological confirmed as desmoplastic medulloblastoma (17 male beside 11 female) including clinical history, examination, investigation and management.

Results: The median age was 17.8 years, (range 3-41) with male to female ratio was (1.5:1). The most dominating symptoms were vomiting (82%) and throbbing headache (71.4%). The positioning of tumor was lateral in 64.3% and midline in 35.7%. The total resection of the tumor was achieved in 17 (60.7%) patients. All patients received craniospinal irradiation. The median dosage to the posterior fossa was 54 Gy (range 49- 56 Gy). 71.4% of the patients received adjuvant chemotherapy. The median follow-up was 52.3 months (range 25 -120). Five years’ overall survival rates were 71.4% and 67.8% respectively.8 patients developed relapse. Posterior fossa was the commonest site for relapse (21.4%). Brain stem infiltration was bad prognostic factor (p= 0.006). The extent of surgical resection can be considered a good prognostic factor (p=0.004). Age, sex and tumor location did not significantly affect the results of survival. One of the most reported side effect was substantially, sensory neuropathy, nausea, vomiting, fever and neutropenia.

Conclusion: Patients with desmoplastic medulloblastoma being given chemotherapy adjuvant to surgical resection and radiotherapy (Multimodality approach) remain alive longer than patients who had management of surgery and radiotherapy only although brain stem infiltration, large post-operative residual are often associated with poor prognosis. [4]

Outcome and Predictive Factors of Radiation Therapy for Medulloblastoma: Mansoura Experience

Background: Medulloblastomas are the most common infratentorial malignant brain tumors with an incidence rate of 0.5 in 100.000 typically arising in childhood at age 5-9 years.

Aim of Work: Exploring the epidemiological characteristics, treatment outcome and prognostic factors of medulloblastoma patients whom were referred to Mansoura Clinical Oncology &Nuclear Medicine Department for adjuvant treatment through the period from Jan. 1997 to Dec. 2011 inclusive.

Patients and Methods: Sixty-Two patients records were in harmony with the eligibility criteria . Males were slightly larger in number [33 cases (53%)]. The majority of the cases were of pediatric age (42 patient representing 68%). Complete resection was possible in only 31 cases (50%).The classic type was the commonest [36 cases (58%)]. The majority were of the of M0 stage [52 cases (84%)] and of high risk category [37 cases (60%)]. Median dose to posterior fossa was 52.5 Gray (range, 43-56 Gray). The Chemotherapy was administrated in forty-seven patients (75.8%). The toxicity of treatment were graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events (version 3.0).

Results: Adjuvant Radiotherapy was generally well tolerated. The median overall survival time and median progression – free survival were 90 & 72 months respectively. Relapse was reported in 28 patients (45.16%).M staging, extensiveness of resection, hydrocephalus at presentation and time elapsed till radiotherapy all affected significantly the prognosis.

Conclusion: In conclusion, this study highlights the effect of stage, completeness of surgery, and early initiation of adjuvant radiotherapy on the outcome. [5]

Reference

[1] Northcott, P.A., Korshunov, A., Witt, H., Hielscher, T., Eberhart, C.G., Mack, S., Bouffet, E., Clifford, S.C., Hawkins, C.E., French, P. and Rutka, J.T., 2011. Medulloblastoma comprises four distinct molecular variants. Journal of clinical oncology, 29(11), p.1408.

[2] Cavalli, F.M., Remke, M., Rampasek, L., Peacock, J., Shih, D.J., Luu, B., Garzia, L., Torchia, J., Nor, C., Morrissy, A.S. and Agnihotri, S., 2017. Intertumoral heterogeneity within medulloblastoma subgroups. Cancer cell, 31(6), pp.737-754.

[3] Packer, R.J., Cogen, P., Vezina, G. and Rorke, L.B., 1999. Medulloblastoma: clinical and biologic aspects. Neuro-oncology, 1(3), pp.232-250.

[4] El-Badry, A., Abdel Bari Mattar, M., A. Toson, E. and Abdelkhalek, A. (2016) “Desmoplastic Medulloblastoma Patients Survival after Multimodality Treatment”, International Neuropsychiatric Disease Journal, 8(2), pp. 1-8. doi: 10.9734/INDJ/2016/25411.

[5] Abd El-Ghaffar, D., Farouk Akl, M., Halim, A. and Eita, M. (2017) “Outcome and Predictive Factors of Radiation Therapy for Medulloblastoma: Mansoura Experience”, Journal of Cancer and Tumor International, 5(3), pp. 1-11. doi: 10.9734/JCTI/2017/33525.

Latest News on Neck Cancer : Dec 2020

Head and neck cancer

Most head and neck cancers are squamous cell carcinomas that develop in the upper aerodigestive epithelium after exposure to carcinogens such as tobacco and alcohol. Human papillomavirus has also been strongly implicated as a causative agent in a subset of these cancers. The complex anatomy and vital physiological role of the tumour-involved structures dictate that the goals of treatment are not only to improve survival outcomes but also to preserve organ function. Major improvements have been accomplished in surgical techniques and radiotherapy delivery. Moreover, systemic therapy including chemotherapy and molecularly targeted agents—namely, the epidermal growth factor receptor inhibitors—has been successfully integrated into potentially curative treatment of locally advanced squamous-cell carcinoma of the head and neck. In deciding which treatment strategy would be suitable for an individual patient, important considerations include expected functional outcomes, ability to tolerate treatment, and comorbid illnesses. The collaboration of many specialties is the key for optimum assessment and decision making. We review the epidemiology, molecular pathogenesis, diagnosis and staging, and the latest multimodal management of squamous cell carcinoma of the head and neck. [1]

The molecular biology of head and neck cancer

Head and neck squamous cell carcinomas (HNSCCs) are caused by tobacco and alcohol consumption and by infection with high-risk types of human papillomavirus (HPV). Tumours often develop within preneoplastic fields of genetically altered cells. The persistence of these fields after treatment presents a major challenge, because it might lead to local recurrences and second primary tumours that are responsible for a large proportion of deaths. Aberrant signalling pathways have been identified in HNSCCs and inhibition of epidermal growth factor receptor (EGFR) has proved a successful therapeutic strategy. In this Review, we discuss the recent literature on tumour heterogeneity, field cancerization, molecular pathogenesis and the underlying causative cancer genes that can be exploited for novel and personalized treatments of patients with HNSCC. [2]

Head and Neck Cancer: Changing Epidemiology, Diagnosis, and Treatment

Head and neck cancers account for less than 5% of all cancers and for less than 3% of all cancer deaths in the United States. The populations at risk for head and neck cancers are those who have a long-standing history of smoking and alcohol use. More recently, the incidence of oropharyngeal cancer in younger populations has been increasing and is associated with exposure to the human papillomavirus. This subset of patients appears to have a better overall prognosis and to respond better to treatment. This review is limited to head and neck cancers of squamous cell histology, which constitute more than 90% of head and neck cancers. Because treatment of head and neck cancers is complex and involves multiple modalities, a multidisciplinary approach is needed. This review focuses on the goal of organ preservation and postoperative treatment of high-risk patients with the concurrent use of chemotherapy and radiation therapy. This review also highlights recent advances in treatment using molecularly targeted therapies, specifically the role of inhibitors of the epidermal growth factor receptor in locally advanced and recurrent/metastatic squamous cell cancer of the head and neck. Studies in the English language were identified by searching the MEDLINE, EMBASE database (1980-2007) using the search terms head and neck, squamous cell, carcinoma, chemotherapy, radiation, human papillomavirus, epidermal growth factor receptor, and targeted therapy. [3]

The Relationship between Single Nucleotide Polymorphisms of Gene XRCC1 and Toxicity Induced Radiation in Patients with Head and Neck Cancer

Aims: The head and neck cancer is one of the most common types and their treatment brings complications such as dermatitis, mucositis and dysphagia. Studies of genetic variations of patients are those that enable the identification of prognostic factors for treatment, generally based on greater risk of injury to healthy tissue.

Study Design: This study examined the association between single nucleotide polymorphisms (SNPs) of XRCC1 gene in patients with head and neck cancer with adverse reactions presented in normal tissues as result of radiotherapy.

Place and Duration of Study: The study was conduct at Pontifícia Universidade Católica de Goiás, and the patients were recruited at Hospital Araújo Jorge, Associação de Combate ao Câncer em Goiás, Radiotherapy Service.

Methodology: We evaluated 54 patients, through a retrospective study, based on data contained in records and teletherapy records of patients with this cancer who underwent radiotherapy for at least 5 years.

Results: The mean age of patients was 58.43±13.79 years and the mean dose was applied 64,02Gy. Regarding the acute and late toxicities, patients analyzed showed a higher frequency of low-grade morbidities when compared to high grade. For acute toxicity, patients presenting polymorphism rs1799782 had an increased risk for developing mucositis, but the other polymorphisms were not statistically significant for the development of these changes (dermatitis, xerostomia and mucositis) acute. Patients who have studied polymorphisms have no increased risk of developing chronic changes of the larynx and esophagus (P>.05). In relation to the suspension of radiotherapy, patients with polymorphism rs25487 had reduced risk to have treatment discontinued, while patients with polymorphism rs25489 have an increased risk. Conclusion: Studies of genetic variants XRCC1 gene family should continue, to develop mechanisms to determine the degree of radiosensitivity in risk organs in patients with head and neck tumor. Thus, the personalized treatment with ionizing radiation can be prescribed for patients decreasing complications and improving the effectiveness of treatment and quality of life of patients. [4]

Epidemiology of Head and Neck Cancers in Maiduguri-Northeastern Nigeria

Head and neck cancers is one of the common health problems in our environment affecting relatively the youth. The paucity of literature on community based studies in Nigeria to determine the incidence of the disease obscure its burden, pattern and magnitude. This study presents epidemiological characteristics of head and neck cancers in Maiduguri as seen during the period of insurgency.

A 5 year retrospective review of patients seen from January, 2010 to December, 2014 with histologically diagnosed head and neck cancers. Data extracted from the records of histopathology department of University of Maiduguri Teaching Hospital was analyzed using SPSS version 16.0.

Of the 7655 patients, 1312 (17.14%) were cancers and 217 (16.54%) of this was head and neck malignancies. Average age was 35.5years with SD±20.07. About 69% of cases were epithelial in origin and 60.83% of patients were less than 41 years of age. The age group worse affected by carcinoma is older than those with sarcoma and lymphoma.

Head and neck is not uncommon in Maiduguri even in the face of insurgency, it is also among one of the common health problems of the relatively young. This therefore call for in-depth research on aetiological factors. Relevant authorities shall also establish oncology centers which will promote education, screening programmes, early detection, prevention and control of head and neck cancers. [5]

Reference

[1] Argiris, A., Karamouzis, M.V., Raben, D. and Ferris, R.L., 2008. Head and neck cancer. The Lancet, 371(9625), pp.1695-1709.

[2] Leemans, C.R., Braakhuis, B.J. and Brakenhoff, R.H., 2011. The molecular biology of head and neck cancer. Nature reviews cancer, 11(1), pp.9-22.

[3] Marur, S. and Forastiere, A.A., 2008, April. Head and neck cancer: changing epidemiology, diagnosis, and treatment. In Mayo Clinic Proceedings (Vol. 83, No. 4, pp. 489-501). Elsevier.

[4] Augusto de Oliveira Neto, O., Lázaro de Carvalho Vasconcelos, G., de Abreu Mendonça, Y., Castro Dourado Pinezi, J. and de Bastos Ascenço Soares, R. (2016) “The Relationship between Single Nucleotide Polymorphisms of Gene XRCC1 and Toxicity Induced Radiation in Patients with Head and Neck Cancer”, Journal of Cancer and Tumor International, 4(1), pp. 1-17. doi: 10.9734/JCTI/2016/27419.

[5] Kodiya, A. M., Adamu, A. I., Nggada, H. A., Garandawa, H. I., Ngamdu, Y. B., Sandabe, M. B. and Isa, A. (2015) “Epidemiology of Head and Neck Cancers in Maiduguri-Northeastern Nigeria”, Journal of Advances in Medicine and Medical Research, 11(5), pp. 1-7. doi: 10.9734/BJMMR/2016/20344.

Latest News on Cancer Surgery : Nov 2020


Impaired immunologic reactivity and recurrence following cancer surgery

One hundred patients were tested for their ability to react to 7 commonly encountered skin test antigens and to develop delayed cutaneous hypersensitivity to 2, 4‐dinitrochlorobenzene (DNCB). Following sensitization, more than 95% of normal patients, but only 60% of patients with potentially resectable neoplasms, exhibited delayed cutaneous hypersensitivity to DNCB. A correlation is suggested between the inability to react to DNCB and the incidence of either inoperability, local recurrence, or distant metastases within 6 months post‐operatively. Ninety‐three percent (27/29) of patients who failed to react to DNCB were inoperable or developed early recurrence, whereas 92% (50/54) of patients who reacted to DNCB were free of disease for 6 months; but many of these patients were nonreactive to all of the common skin test antigens. These studies suggest that there is a significant correlation between cell mediated immunologic reactivity as measured by delayed cutaneous hypersensitivity to DNCB and the course of malignant disease following definitive cancer surgery. [1]

Guidelines 2000 for Colon and Rectal Cancer Surgery

Background: Oncologic resection techniques affect outcome for colon cancer and rectal cancer, but standardized guidelines have not been adopted. The National Cancer Institute sponsored a panel of experts to systematically review current literature and to draft guidelines that provide uniform definitions, principles, and practices. Methods: Methods were similar to those described by the American Society of Clinical Oncology in developing practice guidelines. Experts representing oncology and surgery met to review current literature on oncologic resection techniques for level of evidence (I–V, where I is the best evidence and V is the least compelling) and grade of recommendation (A–D, where A is based on the best evidence and D is based on the weakest evidence). Initial guidelines were drafted, reviewed, and accepted by consensus. Results: For the following seven factors, the level of evidence was II, III, or IV, and the findings were generally consistent (grade B): anatomic definition of colon versus rectum, tumor–node–metastasis staging, radial margins, adjuvant R0 stage, inadvertent rectal perforation, distal and proximal rectal margins, and en bloc resection of adherent tumors. For another seven factors, the level of evidence was II, III, or IV, but findings were inconsistent (grade C): laparoscopic colectomy; colon lymphadenectomy; level of proximal vessel ligation, mesorectal excision, and extended lateral pelvic lymph node dissection (all three for rectal cancer); no-touch technique; and bowel washout. For the other four factors, there was little or no systematic empirical evidence (grade D): abdominal exploration, oophorectomy, extent of colon resection, and total length of rectum resected. Conclusions: The panel reports surgical guidelines and definitions based on the best available evidence. The availability of more standardized information in the future should allow for more grade A recommendations. [2]

Impact of Hospital Volume on Operative Mortality for Major Cancer Surgery

Context.— Hospitals that treat a relatively high volume of patients for selected surgical oncology procedures report lower surgical in-hospital mortality rates than hospitals with a low volume of the procedures, but the reports do not take into account length of stay or adjust for case mix.

Objective.— To determine whether hospital volume was inversely associated with 30-day operative mortality, after adjusting for case mix.

Design and Setting.— Retrospective cohort study using the Surveillance, Epidemiology, and End Results (SEER)–Medicare linked database in which the hypothesis was prospectively specified. Surgeons determined in advance the surgical oncology procedures for which the experience of treating a larger volume of patients was most likely to lead to the knowledge or technical expertise that might offset surgical fatalities.

Patients.— All 5013 patients in the SEER registry aged 65 years or older at cancer diagnosis who underwent pancreatectomy, esophagectomy, pneumonectomy, liver resection, or pelvic exenteration, using incident cancers of the pancreas, esophagus, lung, colon, and rectum, and various genitourinary cancers diagnosed between 1984 and 1993.

Main Outcome Measure.— Thirty-day mortality in relation to procedure volume, adjusted for comorbidity, patient age, and cancer stage.

Results.— Higher volume was linked with lower mortality for pancreatectomy (P=.004), esophagectomy (P<.001), liver resection (P=.04), and pelvic exenteration (P=.04), but not for pneumonectomy (P=.32). The most striking results were for esophagectomy, for which the operative mortality rose to 17.3% in low-volume hospitals, compared with 3.4% in high-volume hospitals, and for pancreatectomy, for which the corresponding rates were 12.9% vs 5.8%. Adjustments for case mix and other patient factors did not change the finding that low volume was strongly associated with excess mortality.

Conclusions.— These data support the hypothesis that when complex surgical oncologic procedures are provided by surgical teams in hospitals with specialty expertise, mortality rates are lower. [3]

The Impact of Body Mass Index on the Surgical Outcomes in Open Rectal Cancer Surgery

Technical difficulties which affect the outcomes of abdominal operations are common in obese patients, especially in rectal and gastric cancer cases. In several studies, it has been shown that increased body mass index (BMI) is associated with increased morbidity, reduced lymph node retrieval and prolonged hospital stay after colorectal surgery. The aim of this study was to assess the influence of obesity on the surgical outcomes (surgical margin, number of lymph nodes excised) of rectal cancer patients who were operated by open surgery. One hundred rectal cancer patients who underwent open surgery in a single center between January 2011 and August 2014 were included in this study. Patients were divided into two groups according to their BMI values. According to their preoperative BMI values, patients with a BMI of ≥30 kg/m2 (n=29) were defined as ‘obese’. Patients with a BMI of <30 kg/m2 (n=71) were placed in the normal (non-obese) group. Demographic data, surgical margins, the number of lymph nodes retrieved and surveillance of both groups were compared. Obese and normal groups were statistically indifferent in terms of age, sex and stage of the disease. Comparison of the obese and normal groups showed no statistically significant difference in terms of surgical margins and the number of lymph nodes retrieved. This study showed that obesity does not affect the surgical outcomes in rectal cancer. However, prospective studies with larger patient series are needed. [4]

Bronchial Sleeve Resection for Lung Cancer Preoperative Empyema

Surgical management of the cancer with empyema has rarely been reported in the literature because few of such cases are operable. Many patients might be misevaluated because of the incorrect staging associated with an acute or sub-acute infection. Even in the presence of an operable tumor mass; surgeons behave timid to these patients because of the possibility of infective postoperative complications. The balance between expected benefits and possible risk of surgical intervention is also important. If it is indicated, by the time pleural empyema is restored, procedures such as resection and even bronchoplasty should be performed.

59-years old patient with squamous cell carcinoma that completely obstructed left basal segments and caused to empyema. A thoracic catheter was inserted. Multiple pleural irrigations were done and proper antibiotherapy. Pathologic diagnosis of pleural fluid and pleural biopsy were benign. Pleural cultures were negative and amount of empyema fluid volume has decreased within two months. Positron emission tomography (PET) revealed a 2.5 cm sized left infrahilar tumor, right paratracheal, prevascular and subcarinal lymph nodes and non-homogeneous increased pleural activity. Mediastinal lymph nodes were evaluated as reactive with mediastinoscopy. Left lower lobectomy and lingulectomy were performed with bronchial resection and pathologic stage was 2A (T1bN1MO). [5]

Reference

[1] Eilber, F.R. and Morton, D.L., 1970. Impaired immunologic reactivity and recurrence following cancer surgery. Cancer, 25(2), pp.362-367.

[2] Nelson, H., Petrelli, N., Carlin, A., Couture, J., Fleshman, J., Guillem, J., Miedema, B., Ota, D. and Sargent, D., 2001. Guidelines 2000 for colon and rectal cancer surgery. Journal of the National Cancer Institute, 93(8), pp.583-596.

[3] Begg, C.B., Cramer, L.D., Hoskins, W.J. and Brennan, M.F., 1998. Impact of hospital volume on operative mortality for major cancer surgery. Jama, 280(20), pp.1747-1751.

[4] Solmaz, A., Gülçiçek, O., Binboğa, E., Biricik, A., Erçetin, C., Yiğitbaş, H., Yavuz, E., Çelik, A. and Çelebi, F. (2016) “The Impact of Body Mass Index on the Surgical Outcomes in Open Rectal Cancer Surgery”, Journal of Advances in Medicine and Medical Research, 14(10), pp. 1-5. doi: 10.9734/BJMMR/2016/25148.

[5] Kuman, N., Çokpınar, S. and Yaman, E. (2015) “Bronchial Sleeve Resection for Lung Cancer Preoperative Empyema”, Journal of Advances in Medicine and Medical Research, 7(1), pp. 82-85. doi: 10.9734/BJMMR/2015/16007.

Latest News on Cancer Metastasis : Nov 2020


Involvement of chemokine receptors in breast cancer metastasis

Breast cancer is characterized by a distinct metastatic pattern involving the regional lymph nodes, bone marrow, lung and liver. Tumour cell migration and metastasis share many similarities with leukocyte trafficking, which is critically regulated by chemokines and their receptors. Here we report that the chemokine receptors CXCR4 and CCR7 are highly expressed in human breast cancer cells, malignant breast tumours and metastases. Their respective ligands CXCL12/SDF-1α and CCL21/6Ckine exhibit peak levels of expression in organs representing the first destinations of breast cancer metastasis. In breast cancer cells, signalling through CXCR4 or CCR7 mediates actin polymerization and pseudopodia formation, and subsequently induces chemotactic and invasive responses. In vivo, neutralizing the interactions of CXCL12/CXCR4 significantly impairs metastasis of breast cancer cells to regional lymph nodes and lung. Malignant melanoma, which has a similar metastatic pattern as breast cancer but also a high incidence of skin metastases, shows high expression levels of CCR10 in addition to CXCR4 and CCR7. Our findings indicate that chemokines and their receptors have a critical role in determining the metastatic destination of tumour cells. [1]

Breast cancer metastasis: markers and models

Breast cancer starts as a local disease, but it can metastasize to the lymph nodes and distant organs. At primary diagnosis, prognostic markers are used to assess whether the transition to systemic disease is likely to have occurred. The prevailing model of metastasis reflects this view — it suggests that metastatic capacity is a late, acquired event in tumorigenesis. Others have proposed the idea that breast cancer is intrinsically a systemic disease. New molecular technologies, such as DNA microarrays, support the idea that metastatic capacity might be an inherent feature of breast tumours. These data have important implications for prognosis predicition and our understanding of metastasis. [2]

The pathogenesis of cancer metastasis

Metastases do not result from random survival of cells released from the primary tumour but from the selective growth of specialised subpopulations of highly metastatic cells endowed with specific properties that befit them to complete each step of the metastatic process. [3]

Small Cell Lung Carcinoma with Overt Cutaneous Metastasis; Unusual Case

Small cell lung carcinoma is a rapidly progressive neuroendocrine tumor having a poor prognosis. It is considered as a systemic disease, because it has diffuse involvement, distant organ metastasis, and regional lymphatic involvement at the time of initial diagnosis. While small cell lung carcinomahas a lot of metastasis to bone, liver, surrenal and other hemithorax in the onset of disease, cutaneous metastasis are rarely seen. Skin metastasis are encountered in lower than 0.5% of the patients with metastatic diseases. In this article, we aimed to present a case of small cell lung carcinoma with cutaneous metastasis which is rarely seen in the literature. [4]


Hepatic Metastasis in a Nigerian with Differentiated Thyroid Cancer- An Uncommon Presentation: Case Report

The papillary and follicular histological sub-types of thyroid cancer are referred to as differentiated thyroid cancers. When these tumors metastasize, they rarely do so to the liver. Hepatic metastasis is very uncommon in this group of cancers and has only been reported in a handful of cases. We present one such case in a Nigerian patient and note its unique presentation and with it, we highlight the need for careful attention to be paid to clinical and investigation findings when attempts are being made to arrive at a definitive diagnosis in cases of suspected primary liver cell cancers which are common in this part of the world. [5]

Reference

[1] Müller, A., Homey, B., Soto, H., Ge, N., Catron, D., Buchanan, M.E., McClanahan, T., Murphy, E., Yuan, W., Wagner, S.N. and Barrera, J.L., 2001. Involvement of chemokine receptors in breast cancer metastasis. nature, 410(6824), pp.50-56.
[2] Weigelt, B., Peterse, J.L. and Van’t Veer, L.J., 2005. Breast cancer metastasis: markers and models. Nature reviews cancer, 5(8), pp.591-602.

[3] Poste, G. and Fidler, I.J., 1980. The pathogenesis of cancer metastasis. Nature, 283(5743), pp.139-146.

[4] Yasar, Z., Tekelıoglu, V., Can, G., Yuce, Y., Ozyalvaclı, G. and Uyeturk, U. (2015) “Small Cell Lung Carcinoma with Overt Cutaneous Metastasis; Unusual Case”, Journal of Advances in Medicine and Medical Research, 6(6), pp. 625-629. doi: 10.9734/BJMMR/2015/13754.

[5] Adeleye, O., Oluyemi, A., Habeeb, M., Adeyomoye, A. and AbdulKareem, F. (2015) “Hepatic Metastasis in a Nigerian with Differentiated Thyroid Cancer- An Uncommon Presentation: Case Report”, Journal of Cancer and Tumor International, 2(4), pp. 206-209. doi: 10.9734/JCTI/2015/20790.

Latest Research News on pancreatic cancer : Aug – 2020

Molecular targeting therapy for pancreatic cancer

Pancreatic carcinogenesis is driven by multiple genetic and epigenetic changes. The epidermal growth factor receptor (EGFR) and its downstream signaling pathways, Ras-Raf-MEK-ERK axis, play important roles in pancreatic cancer development. The phosphoinositol 3 kinase (PI3 K)/Akt and the nuclear factor κB (NF-κB) pathways control both proliferation and resistance to apoptosis of pancreatic cancer. The role of cyclooxygenase (COX) and lipoxygenase (LOX) in the development of pancreatic cancer has been made known recently. The elucidation of these molecular events has led to several distinct therapeutic advances, including therapies that target EGFR, the Ras-Raf-MEK-ERK axis, the COX-2 and LOX pathways, and others. Many novel agents have been developed and are undergoing clinical investigation, such as monoclonal antibodies against EGFR, tyrosine kinase inhibitors (TKIs), farnesyl transferase inhibitors (FTIs), Bay43-9006, CI-1040, CCI-779, celecoxib, and LY293111. This review highlights recent advances in the development of these agents. [1]

Borderline Resectable Pancreatic Cancer: Definitions, Management, and Role of Preoperative Therapy

With recent advances in pancreatic imaging and surgical techniques, a distinct subset of pancreatic tumors is emerging that blurs the distinction between resectable and locally advanced disease: tumors of “borderline resectability.” In our practice, patients with borderline-resectable pancreatic cancer include those whose tumors exhibit encasement of a short segment of the hepatic artery, without evidence of tumor extension to the celiac axis, that is amenable to resection and reconstruction; tumor abutment of the superior mesenteric artery involving <180° of the circumference of the artery; or short-segment occlusion of the superior mesenteric vein, portal vein, or their confluence with a suitable option available for vascular reconstruction because the veins are normal above and below the area of tumor involvement. With currently available surgical techniques, patients with borderline-resectable pancreatic head cancer are at high risk for a margin-positive resection. Therefore, our approach to these patients is to use preoperative systemic therapy and local-regional chemoradiation to maximize the potential for an R0 resection and to avoid R2 resections. In our experience, patients with favorable responses to preoperative therapy (radiographical evidence of tumor regression and improvement in serum tumor marker levels) are the subset of patients who have the best chance for an R0 resection and a favorable long-term outcome. [2]

Epidemiology of pancreatic cancer

In the United States the incidence of and mortality from pancreatic cancer have increased over the past several decades but have tended to level off in recent years. The rates are higher in blacks than in whites and higher in males than in females. Mortality rates increase with age but there appears to be a decline in elderly blacks, possibly on an artifactual basis. There is a suggestion that rates are higher in Jews. No consistent differences by socioeconomic status or by geographic location within the United States have been identified. Both genetic and environmental factors may be playing significant roles in this disease. Cigarette smoking may be etiologically related, or at the very least, may help to identify a group of patients at increased risk of pancreatic cancer. However, the relative risk estimated for cigarette smoking is much lower than that found for cancer of the lung. The leveling off in incidence and mortality rates for pancreatic cancer in recent years also differs from the time trends observed for lung cancer. However, this could result from differences in site-specific carcinogens and from the fact that the lung is the first organ to be exposed to cigarette smoke in the highest concentrations and prior to the metabolism of any of its components.

Dietary factors may have an important role in pancreatic cancer, but further research is needed to clarify this relationship. In particular, the possibility that dietary fats may be implicated and that vitamins or fiber may be protective in this disease remains to be explored. Finally, there is suggestive evidence that specific chemical exposures may be carcinogenic for the pancreas. Many of the data are from animal studies, and the findings from human studies are not entirely consistent. [3]

Identification of Candidate Biomarkers and Cancer Genes AHNAK2 and EPPK1 in Pancreatic Cancer

Aims: The lack of specific symptoms at early tumor stages, together with a high biological aggressiveness of the tumor contribute to the high mortality rate for pancreatic cancer (PC). Improved screening for earlier diagnosis, through the detection of diagnostic and prognostic biomarkers provides the best hope of increasing the rate of curatively resectable carcinomas. The aim of this study is to provide new targets for use as biomarkers in PC.

Study Design: In a previous study, we identified novel candidate cancer genes and biomarkers that were significantly upregulated in PC, through a meta-analysis of large number of microarray datasets, using bioinformatics methods.  In this study, we analyzed the expression of these genes in a panel of pancreatic cancer cell lines by quantitative Reverse Transcription-PCR (qRT-PCR).

Place and Duration of Study: Department of Chemistry and Biochemistry and Department of Biology, University of Northern Iowa, USA, between June 2014 and Dec 2015.

Methodology: We analyzed the expression of three genes, AHNAK2, EPPK1 and IGHG3 in a panel of seven standard PC cell lines, AsPC-1, BxPC-3, Capan-2, CFPAC-1, HPAF-II, PANC-1, and SW 1990 by Relative Quantification. qRT-PCR experiments were conducted in triplicate, and each experiment was replicated twice using different passages.

Results: AHNAK2 was significantly upregulated in all PC cell lines tested, with P values < 0.005 except for PANC-1 (P < 0.05). EPPK1 too was significantly upregulated (P < 0.05) in six of seven PC cell lines tested. While IGHG3 was nominally upregulated in all PC cell lines, upregulation was significant (P < 0.05) in only four PC cell lines.

Conclusion: Our results confirm that AHNAK2 and EPPK1 are novel candidates for use as biomarkers in pancreatic cancer. IGHG3 does not appear to be a suitable candidate, due to its low levels of expression in both PC and control cell lines. [4]

Exocrine Pancreatic Cancer: A Clinico-epidemiologic Study

Background: Incidence of pancreatic cancer is relatively low compared to other types of cancer but had the lowest survival rate of all cancers.

Objective: To describe clinical-epidemiological features of pancreatic cancer patients recorded in our region and assessed its different prognostic factors.

Materials and Methods: The medical records of patients with pancreatic cancer attended to Clinical Oncology, and Nuclear Medicine department and Oncology centre between 2005-2014 were reviewed.

Results: This retrospective study included 380 patients with exocrine pancreatic cancer. Median age was 56 years with male predominance (65%). The most predominant histologic type was adenocarcinoma with grade III in 55% of patients. Tumours were located at the head of the pancreas were 75.5%, followed by the body (20.8%). Most patients presented with metastatic disease (57.9%). The pain was the most common presenting symptom (63.9%), while jaundice was found in 47.4% of patients. 23.7% of patients were smokers and 19.7% suffered from diabetes mellitus. 1-year survival rate was 28%. On multivariate analysis; we found significant lower survival rate with male gender (P=0.004), high-grade disease (P=0.002), older age (P=0.001), PC located in tail and body (P=0.006), high level of CA19-9(> 37U/L) (P=0.001), and metastatic cases (P=0.003).

Conclusion: This study is a clinical-epidemiologic survey of pancreatic cancer in our locality. However, because of its relatively small number of patients and retrospective nature; larger prospective studies are needed to study the epidemiologic and genetic basis of pancreatic cancer in our region. [5]

Reference

[1] Xiong, H.Q., 2004. Molecular targeting therapy for pancreatic cancer. Cancer chemotherapy and pharmacology, 54(1), pp.S69-S77.

[2] Varadhachary, G.R., Tamm, E.P., Abbruzzese, J.L., Xiong, H.Q., Crane, C.H., Wang, H., Lee, J.E., Pisters, P.W., Evans, D.B. and Wolff, R.A., 2006. Borderline resectable pancreatic cancer: definitions, management, and role of preoperative therapy. Annals of surgical oncology, 13(8), pp.1035-1046.

[3] Gordis, L. and Gold, E.B., 1984. Epidemiology of pancreatic cancer. World journal of surgery, 8(6), pp.808-821.

[4] Smith, A., Poole, L., Dhanwada, K. and Goonesekere, N. C. W. (2016) “Identification of Candidate Biomarkers and Cancer Genes AHNAK2 and EPPK1 in Pancreatic Cancer”, Journal of Advances in Medicine and Medical Research, 18(8), pp. 1-8. doi: 10.9734/BJMMR/2016/28034.

[5] Ahmed El-Hadaad, H., Ahmed Wahba, H., Abozeed, W., Elnahas, W. and Roshdy, S. (2018) “Exocrine Pancreatic Cancer: A Clinico-epidemiologic Study”, Journal of Cancer and Tumor International, 7(3), pp. 1-7. doi: 10.9734/JCTI/2018/31933.

Latest News on Neck Cancer : Aug – 2020

The chemoradiation paradigm in head and neck cancer

In this article, we use the example of head and neck cancer to show how concurrent chemoradiotherapy is used to treat a cancer where locoregional control is central for treatment success. The advent of concurrent chemoradiation has significantly contributed to the curability of head and neck cancer, including locoregionally advanced disease. Preserving organ function and reducing toxic effects are increasingly the focus of clinical trials. We review the available chemoradiotherapy platforms used for head and neck cancer, with initial discussions focused on single-agent cytotoxic-based regimens. We then assess the literature on multiagent-based regimens and include a discussion of the integration of novel agents, such as EGFR inhibitors, and antiangiogenic drugs into treatment platforms. Although single-agent cisplatin-based chemoradiotherapy is still widely used as a standard therapy, we propose that evidence increasingly shows that multiagent-based chemoradiotherapy, and EGFR-inhibitor-based treatments, offer distinct advantages. We provide guidance for clinicians based on current clinical trial evidence on how to choose appropriate treatment platforms for their patients. [1]

 

Randomized Phase III Trial of Neoadjuvant Chemotherapy in Head and Neck Cancer: 10-Year Follow-Up

In 1986, we initiated a multicenter, randomized trial to compare induction chemotherapy with cisplatin and 5-fluorouracil followed by locoregional treatment (surgery and radiotherapy or radiotherapy alone) with locoregional treatment alone in patients with head and neck squamous cell carcinoma. Here we report the long-term results of the trial. A total of 237 patients with nonmetastatic stage III or IV head and neck carcinoma were randomly assigned to receive four cycles of neoadjuvant chemotherapy followed by locoregional treatment (group A) or locoregional treatment alone (group B). Among all patients, overall survival at 5 and 10 years was 23% (95% confidence interval [CI] = 15.3% to 30.9%) and 19% (95% CI = 11.6% to 26.4%), respectively, for those in group A and 16% (95% CI = 9.6% to 23.4%) and 9% (95% CI = 3.5% to 14.7%), respectively, for those in group B ( P = .13). Among operable patients, we observed no difference between group A and group B in overall survival at 5 and 10 years (group A, 31% [95% CI = 14.9% to 47.3%] and 22.7% [95% CI = 7.1% to 38.3%], respectively; group B, 43.3% [95% CI = 25.6% to 61.0%] and 14.2% [95% CI = 0.1% to 28.3%], respectively; P = .73). Among inoperable patients, overall survival at 5 and 10 years was 21% (95% CI = 12.3% to 30.1%) and 16% (95% CI = 7.7% to 23.9%), respectively, for group A and 8% (95% CI = 1.5% to 12.3%) and 6% (95% CI = 0.1% to 9.1%), respectively, for group B (log-rank P = .04). Four cycles of neoadjuvant chemotherapy is a promising approach for treating patients with inoperable advanced head and neck cancer but not for treating patients with operable disease. [2]

 

Head and neck cancer: a global perspective on epidemiology and prognosis

Head and neck cancers (ICD-9 categories 140-149 and 161) are common in several regions of the world where tobacco use and alcohol consumption is high. The age standardized incidence rate of head and neck cancer (around 1990) in males exceeds 30/100, 000 in regions of France, Hong Kong, the Indian sub-continent, Central and Eastern Europe, Spain, Italy, Brazil, and among US blacks. High rates (> 10/100,000) in females are found in the Indian sub-continent, Hong Kong and Philippines. The highest incidence rate reported in males is 63.58 (France, Bas-Rhin) and in females 15.97 (India, Madras). The variation in incidence of cancers by subsite of head and neck is mostly related to the relative distribution of major risk factors such as tobacco or betel quid chewing, cigarette or bidi smoking, and alcohol consumption. Some degree of misclassification by subsites is a clear possibility in view of the close proximity of the anatomical subsites. While mouth and tongue cancers are more common in the Indian sub-continent, nasopharyngeal cancer is more common in Hong Kong; pharyngeal and/or laryngeal cancers are more common in other populations. While the overall incidence rates show a declining trend in both sexes in India, Hong Kong, Brazil and US whites, an increasing trend is observed in most other populations, particularly in Central and Eastern Europe, Scandinavia, Canada, Japan and Australia. The overall trends are a reflection of underlying trends in cancers of major subsites which seem to be related to the changing prevalence of risk factors. The five year relative survival varies from 20-90% depending upon the subsite of origin and the clinical extent of disease. While primary prevention is the potential strategy for long term disease control, early detection and treatment may have limited potential to improve mortality in the short term. [3]

Epidemiology of Head and Neck Cancers in Maiduguri-Northeastern Nigeria

Head and neck cancers is one of the common health problems in our environment affecting relatively the youth. The paucity of literature on community based studies in Nigeria to determine the incidence of the disease obscure its burden, pattern and magnitude. This study presents epidemiological characteristics of head and neck cancers in Maiduguri as seen during the period of insurgency.

A 5 year retrospective review of patients seen from January, 2010 to December, 2014 with histologically diagnosed head and neck cancers. Data extracted from the records of histopathology department of University of Maiduguri Teaching Hospital was analyzed using SPSS version 16.0.

Of the 7655 patients, 1312 (17.14%) were cancers and 217 (16.54%) of this was head and neck malignancies. Average age was 35.5years with SD±20.07. About 69% of cases were epithelial in origin and 60.83% of patients were less than 41 years of age. The age group worse affected by carcinoma is older than those with sarcoma and lymphoma.

Head and neck is not uncommon in Maiduguri even in the face of insurgency, it is also among one of the common health problems of the relatively young. This therefore call for in-depth research on aetiological factors. Relevant authorities shall also establish oncology centers which will promote education, screening programmes, early detection, prevention and control of head and neck cancers. [4]

The Relationship between Single Nucleotide Polymorphisms of Gene XRCC1 and Toxicity Induced Radiation in Patients with Head and Neck Cancer

Aims: The head and neck cancer is one of the most common types and their treatment brings complications such as dermatitis, mucositis and dysphagia. Studies of genetic variations of patients are those that enable the identification of prognostic factors for treatment, generally based on greater risk of injury to healthy tissue.

Study Design: This study examined the association between single nucleotide polymorphisms (SNPs) of XRCC1 gene in patients with head and neck cancer with adverse reactions presented in normal tissues as result of radiotherapy.

Place and Duration of Study: The study was conduct at Pontifícia Universidade Católica de Goiás, and the patients were recruited at Hospital Araújo Jorge, Associação de Combate ao Câncer em Goiás, Radiotherapy Service.

Methodology: We evaluated 54 patients, through a retrospective study, based on data contained in records and teletherapy records of patients with this cancer who underwent radiotherapy for at least 5 years.

Results: The mean age of patients was 58.43±13.79 years and the mean dose was applied 64,02Gy. Regarding the acute and late toxicities, patients analyzed showed a higher frequency of low-grade morbidities when compared to high grade. For acute toxicity, patients presenting polymorphism rs1799782 had an increased risk for developing mucositis, but the other polymorphisms were not statistically significant for the development of these changes (dermatitis, xerostomia and mucositis) acute. Patients who have studied polymorphisms have no increased risk of developing chronic changes of the larynx and esophagus (P>.05). In relation to the suspension of radiotherapy, patients with polymorphism rs25487 had reduced risk to have treatment discontinued, while patients with polymorphism rs25489 have an increased risk. Conclusion: Studies of genetic variants XRCC1 gene family should continue, to develop mechanisms to determine the degree of radiosensitivity in risk organs in patients with head and neck tumor. Thus, the personalized treatment with ionizing radiation can be prescribed for patients decreasing complications and improving the effectiveness of treatment and quality of life of patients. [5]

 

Reference

[1] Seiwert, T.Y., Salama, J.K. and Vokes, E.E., 2007. The chemoradiation paradigm in head and neck cancer. Nature clinical practice Oncology, 4(3), pp.156-171.

[2] Zorat, P.L., Paccagnella, A., Cavaniglia, G., Loreggian, L., Gava, A., Mione, C.A., Boldrin, F., Marchiori, C., Lunghi, F., Fede, A. and Bordin, A., 2004. Randomized phase III trial of neoadjuvant chemotherapy in head and neck cancer: 10-year follow-up. Journal of the National Cancer Institute, 96(22), pp.1714-1717.

[3] Sankaranarayanan, R., Masuyer, E., Swaminathan, R., Ferlay, J. and Whelan, S., 1998. Head and neck cancer: a global perspective on epidemiology and prognosis. Anticancer research, 18(6B), pp.4779-4786.

[4] Kodiya, A. M., Adamu, A. I., Nggada, H. A., Garandawa, H. I., Ngamdu, Y. B., Sandabe, M. B. and Isa, A. (2015) “Epidemiology of Head and Neck Cancers in Maiduguri-Northeastern Nigeria”, Journal of Advances in Medicine and Medical Research, 11(5), pp. 1-7. doi: 10.9734/BJMMR/2016/20344.

[5] Augusto de Oliveira Neto, O., Lázaro de Carvalho Vasconcelos, G., de Abreu Mendonça, Y., Castro Dourado Pinezi, J. and de Bastos Ascenço Soares, R. (2016) “The Relationship between Single Nucleotide Polymorphisms of Gene XRCC1 and Toxicity Induced Radiation in Patients with Head and Neck Cancer”, Journal of Cancer and Tumor International, 4(1), pp. 1-17. doi: 10.9734/JCTI/2016/27419.