NURS 5301 Advanced Pathophysiology First Exam Review

Advanced Pathophysiology First Exam Review Review how cancer cells work Chapter 12 – Cancer Biology p. 346 (a) Several of the hallmarks/enablers are mostly genomic alterations that initiate and maintain development of cancer. These hallmarks include sustained proliferative signaling, evading growth suppression, genomic instability, and replicative immortality. (b) Cancerous cells characteristically express mutated or overexpressed proto-oncogenes, referred to as oncogenes, which are independent of normal regulatory mechanisms and signal uncontrolled proliferation. (c) Some oncogenes, such as RAS result from point mutations. (d) Oncogenes – can result from genetic translocations. The Philadelphia chromosome in chronic myeloid leukemia (CML) result from a translocation that creates a novel protein fusion of the BCR and ABL genes and expression of an unregulated promoter of cell growth. (e) Tumor-suppressor genes must be inactivated in cancer cells by mutations to each allele, one from each parent. (f) A common mutation in cancer cells is inactivation of the tumor-suppressor gene tumor protein p53 (TP53), which controls expression of many genes that repair DNA damage, suppression of cellular proliferation during genome (g) Cancer cells are immortal. (h) When they reach a critical age, cancer cells activate tolemerase to restore and maintain their telomeres, thereby allowing cancer cells to divide repeatedly or become immortal. (i) Like many normal adult tissues, cancers can contain rare stem cells that provide a source of immortal cells. To fully eradicate a cancer, it may be necessary to target the cancer stem cell. (j) Most of the genetic and epigenetic alterations that causes cancer occur within the somatic tissues during the lifetime of the individual. (k) Access to the vascular system is essential for tumor growth. Stromal cells and cancer cells can secrete