Exam 3: Cancer II Flashcards
mutations in genes that control the cycle of cell division: control of the cell cycle
cyclin-dependent kinases (CDKs), cyclins
mutations in genes that control the cycle of cell division: G1 to S transition
retinoblastoma protein (RB)
mutations in genes that control the cycle of cell division: G2 to M transition
mitosis-promoting factor (MPF)
progression through the G2/M checkpoint is regulated by
cyclin B
signal-transduction pathways
- signals trigger a cascade of intracellular reactions producing a specific response
- Ras protein
receptors
inappropriate activation leads to dysregulation/stimulation of gene expression
The Ras signal-transduction pathway conducts signals from
growth factors and hormones to the nucleus and stimulates the cell cycle. mutations in this pathway often contribute to cancer
mutations in genes that control cell division =
oncogenes
how Ras works
binding of growth factor to receptor causes adaptor molecules bind and link Ras which binds GTP and becomes activated. activated Ras triggers a signalling cascade which causes active MAP kinase to move into the nucleus and activate transcription factors
genes that regulate telomerase
reactivation of telomerase expression helps protect chromosome ends
genes that promote vascularization help with the
spread of tumors
lynch syndrome
inherited disorder (autosomal dominant) that incr the risk of many types of cancer esp colorectal cancer. mutations in any of the DNA repair mech genes, ex MLH1, prevent the proper repair of DNA replication mistakes
mutations in genes that control cell division =
oncogenes; mutations can occur at any of the points during the cell cycle
spindle assembly checkpoint and cancer
abnormal chromosome # or aneuploidy; deregulated spindle assembly checkpoint (SAC) is thought as one of the mechanisms that drive aneuploidy. In normal cells, SAC prevents anaphase onset until all chromosomes are correctly aligned at the metaphase plate thereby ensuring genomic stability.
colorectal cancer arises through the
sequential mutation of a number of genes (tumor progression model); mutations in multiple genes contribute to the progression of colorectal cancer. colon cancers are very treatable IF caught before metastasis
when telomere length is critically short _ stops
cell division
alterations to DNA methylation or chromatin structure are seen in may cancers; hyper/hypomethylation. reversible? are these mutations?
epigenetic changes for continued cell growth; changes in gene expression patterns. if they can change in somatic tissues, we can change them back. these are changes in chromatin structure so not mutations in traditional sense as not a change in DNA seq
genetic mutations in epigenetic modifiers in cancer
mutations in 3 classes of epigenetic modifiers (DNA methylation, nucleosome remodeling, and histone modification) is frequently observed in various types of cancers highlighting the crosstalk btwn genetics and epigenetics; the mutations of epigenetic modifiers probably cause genome-wide epigenetic alterations in cancer
t/f: incr # of genes being modified w/o genetic change (methylation of a tumor suppressor gene); changing the packing of chromatin has no impact in cancer progression
false; big impact in cancer progression
t/f mutations that alter chromatin may cause genome-wide epigenetic consequences that promote cancer growth
true; big contributor
genes that acquire traditional mutations (activation, deactivation, aa change) leads to
significant epigenetic modifications which leads to certain kinds of uncontrolled cell growth
_ is a general feature of cancer cells
chromosomal instability (genomic and chromosomal instability are the primary hallmarks of cancer)
types of chromosomal instability features
deletions, inversions, aneuploidy (chromosome # changes), and translocations
a _ translocation of chromosomes 9 and 22 causes _
reciprocal translocation that causes myelogenous leukemia; Bcr and Abl arms translocate which positions these 2 genes together and causes cancer (philadelphia chromosome)
