Regulation of cancer cell metabolism
Interest within the topic of neoplasm metabolism has waxed and waned over the past century of cancer analysis. the first observations of Warburg and his contemporaries established that there area unit elementary variations within the central metabolic pathways in operation in malignant tissue. However, the initial hypotheses that were supported these observations well-tried inadequate to clarify tumorigenesis, and also the factor revolution pushed neoplasm metabolism to the margins of cancer analysis. In recent years, interest has been revived because it has become clear that several of the signalling pathways that area unit littered with genetic mutations and also the neoplasm microenvironment have a profound impact on core metabolism, creating this subject once more one among the foremost intense areas of analysis in cancer biology. 
Tumor suppressors and cell metabolism: a recipe for cancer growth
Growing tumors face 2 major metabolic challenges—how to satisfy the bioenergetic and synthesis demands of enlarged cell proliferation, and the way to survive environmental fluctuations in external nutrient and O accessibility once tumour growth outpaces the delivery capabilities of the prevailing vasculature. Cancer cells show dramatically altered metabolic electronic equipment that seems to directly result from the oncogenic mutations hand-picked throughout the tumorigenic method. associate rising theme in cancer biology is that a lot of of the genes that may initiate tumorigenesis are elaborately connected to metabolic regulation. In turn, it seems that variety of well-established tumour suppressors play important roles in suppressing growth and/or proliferation once intracellular provides of essential metabolites become reduced. during this review, we have a tendency to think about the potential role of tumour suppressors as metabolic regulators. 
Cancer Cell Metabolism: One Hallmark, Many Faces
Cancer cells should wire cellular metabolism to satisfy the stress of growth and proliferation. though several of the metabolic alterations area unit for the most part almost like those in traditional proliferating cells, they’re aberrantly driven in cancer by a mix of genetic lesions and nongenetic factors like the neoplasm microenvironment. However, one model of altered neoplasm metabolism doesn’t describe the total of metabolic changes which will support cell growth. Instead, the range of such changes among the metabolic program of a neoplastic cell will dictate by what suggests that proliferative rewiring is driven, and may additionally impart heterogeneousness within the metabolic dependencies of the cell. an improved understanding of this heterogeneousness could alter the event and optimisation of therapeutic ways that focus on neoplasm metabolism. 
Immunometabolism and natural killer cell responses
Natural killer (NK) cells are lymphocytes with vital roles in innate and adaptive immune responses to tumours and virus infection. However, in sure chronic diseases, as well as fat and cancer, NK cell practical responses are impaired. Recently, analysis has highlighted the importance of NK cell metabolism in facilitating strong NK cell effector functions. This Review describes our current understanding of mouse and human NK cell metabolism and also the key signalling pathways that mediate metabolic responses in NK cells. what is more, it explores however defects in metabolism will contribute to the generation of dysfunctional NK cells in chronic sickness. Finally, the potential for brand spanking new therapeutic methods targeting cellular metabolism is mentioned. 
Comparison of Various Solutions for Temporary Storage of Umbilical Cord Derived Mesenchymal Stem Cells
Aims: to see whether or not physical saline, phosphate buffered saline (PBS) and high aldohexose Dulbecco’s changed Eagle’s Medium (DMEM-HG) were appropriate as temporary storage resolution.
Study Design: In vitro experimental analytical study.
Place and period of Study: vegetative cell Medical Technology Integrated Service Unit, RSCM/Faculty of drugs Universitas state, Jakarta, Indonesia, from August through Gregorian calendar month 2016.
Methodology: we have a tendency to did viability assessments at varied time points, particularly when zero, 3, 6, 24, 48, 72, 96, and 168 hours within the 3 storage solutions. For population doubling time (PDT) assessments the cells were re-cultured when varied time points within the tested solutions. All viability and PDT assessments were wiped out four replications. moreover, for all storage solutions, variations between the assorted time points in terms of viability and PDT were compared and checked by ANOVA or Kruskal-Wallis test.
Results: Viability was >70% up to seventy two hours in PBS and physical saline, and up to ninety six hours in DMEM-HG. Decrease in viability began to be vital compared to initial viability when half dozen, 24, and seventy two hours in PBS, physical saline, and DMEM-HG severally. Increase in PDT began to be vital compared to initial PDT when three, 6, and twenty four hours in PBS, physical saline, and DMEM-HG severally.
Conclusion: For our UC-MSCs, DMEM-HG is that the best temporary storage resolution, and storage mustn’t exceed twenty four hours. 
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 Jones, R.G. and Thompson, C.B., 2009. Tumor suppressors and cell metabolism: a recipe for cancer growth. Genes & development, 23(5), pp.537-548. (Web Link)
 Cantor, J.R. and Sabatini, D.M., 2012. Cancer cell metabolism: one hallmark, many faces. Cancer discovery, 2(10), pp.881-898. (Web Link)
 Immunometabolism and natural killer cell responses
Katie L. O’Brien & David K. Finlay
Nature Reviews Immunologyvolume 19, pages282–290 (2019). (Web Link)
 Krishnanda, S., Agarwal, R., Yausep, O., Rizkita, M., Angraeni, R. and Pawitan, J. (2017) “Comparison of Various Solutions for Temporary Storage of Umbilical Cord Derived Mesenchymal Stem Cells”, Annual Research & Review in Biology, 21(2), pp. 1-8. doi: 10.9734/ARRB/2017/38233. (Web Link)