Exam 3: Cancer II

Question 1

mutations in genes that control the cycle of cell division: control of the cell cycle

Answer 1

cyclin-dependent kinases (CDKs), cyclins

Question 2

mutations in genes that control the cycle of cell division: G1 to S transition

Answer 2

retinoblastoma protein (RB)

Question 3

mutations in genes that control the cycle of cell division: G2 to M transition

Answer 3

mitosis-promoting factor (MPF)

Question 4

progression through the G2/M checkpoint is regulated by

Answer 4

cyclin B

Question 5

signal-transduction pathways

Answer 5

• signals trigger a cascade of intracellular reactions producing a specific response
• Ras protein

Question 6

receptors

Answer 6

inappropriate activation leads to dysregulation/stimulation of gene expression

Question 7

The Ras signal-transduction pathway conducts signals from

Answer 7

growth factors and hormones to the nucleus and stimulates the cell cycle. mutations in this pathway often contribute to cancer

Question 8

mutations in genes that control cell division =

Answer 8

oncogenes

Question 9

how Ras works

Answer 9

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

Question 10

genes that regulate telomerase

Answer 10

reactivation of telomerase expression helps protect chromosome ends

Question 11

genes that promote vascularization help with the

Answer 11

spread of tumors

Question 12

lynch syndrome

Answer 12

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

Question 13

mutations in genes that control cell division =

Answer 13

oncogenes; mutations can occur at any of the points during the cell cycle

Question 14

spindle assembly checkpoint and cancer

Answer 14

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.

Question 15

colorectal cancer arises through the

Answer 15

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

Question 16

when telomere length is critically short _ stops

Answer 16

cell division

Question 17

alterations to DNA methylation or chromatin structure are seen in may cancers; hyper/hypomethylation. reversible? are these mutations?

Answer 17

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

Question 18

genetic mutations in epigenetic modifiers in cancer

Answer 18

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

Question 19

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

Answer 19

false; big impact in cancer progression

Question 20

t/f mutations that alter chromatin may cause genome-wide epigenetic consequences that promote cancer growth

Answer 20

true; big contributor

Question 21

genes that acquire traditional mutations (activation, deactivation, aa change) leads to

Answer 21

significant epigenetic modifications which leads to certain kinds of uncontrolled cell growth

Question 22

_ is a general feature of cancer cells

Answer 22

chromosomal instability (genomic and chromosomal instability are the primary hallmarks of cancer)

Question 23

types of chromosomal instability features

Answer 23

deletions, inversions, aneuploidy (chromosome # changes), and translocations

Question 24

a _ translocation of chromosomes 9 and 22 causes _

Answer 24

reciprocal translocation that causes myelogenous leukemia; Bcr and Abl arms translocate which positions these 2 genes together and causes cancer (philadelphia chromosome)

Question 25

a _ translocation of chromosomes 8 and 14 causes _

Answer 25

reciprocal translocation that causes Burkitt lymphoma; repositions Bcl2 (oncogene) behind a strong promoter, Bcl2 blocks apoptosis so when hyper activated, it prevents apoptosis from happening

Question 26

the hallmark of follicular lymphoma is the

Answer 26

chromosomal translocation btwn chromosome 14 and 18 chromosomes; that lead to hyper-upregulation of Bcl2 expression in tumor cells

Question 27

chromosomal translocation btwn 14 and 18 places

Answer 27

the Bcl2 gene next to the immunoglobulin heavy chain locus, making it constitutively active. Bcl2 encodes an integral outer mitochondrial membrane protein that blocks apoptotic death (ie cell fail to die) of cells such as lymphocytes and they propagate exponentially

Question 28

Bcl2 is an important anti-apoptotic protein and thus classified as an

Answer 28

oncogene

Question 29

cancer cells often possess chromosome abnormalities including:

Answer 29

extra chromosomes, missing chromosomes, and chromosome rearrangements

Question 30

melanoma biomarkers

Answer 30

a fast rising cancer worldwide and validation of immunological biomarkers may have clinical applications in assisting prognosis, assessing endpoints in therapy, and monitoring responses during treatment

Question 31

microRNAs and cancer

Answer 31

miRNAs are ubiquitous small non-coding RNA molecules that function in RNA silencing and post-transcriptional regulation of gene expression; most cancers have inappropriately activated miRNAs that target tumor suppressor genes

Question 32

miRNAs and chemotherapy resistance

Answer 32

miRNAs represent an alternative bc of genomic instability helps figure out a way for cancer cells to survive/natural selection impacting progression of disease; use our knowledge of miRNAs to target oncogenes/tumor promoting genes = novel therapeutic intervention

Question 33

p53 is a _ gene

Answer 33

tumor suppressor gene and is the most frequently mutated gene (>50%) in human cancer

Question 34

p53 becomes activated in response to myriad stressors:

Answer 34

DNA damage (induced by either UV, IR, or chemical agents) oxidative stress, osmotic shock, ribonucleotide depletion, and deregulated oncogene expression

Question 35

statins and p53

Answer 35

through high-throughput screening, identify statins, cholesterol-lowering drugs, as degradation inducers for conformational or mis-folded p53 mutants w/ minimal effects of WT p53 and DNA contact mutants statins support elimination of mutated p53

Question 36

why elephants do not get cancer?

Answer 36

elephants have close to 20 copies of p53 in their genome; animals that big usu have more mitotic events to get to their mass size and extra copies of p53 lead to elimination of cancer

Question 37

why is cancer a genetic disease, but most are not inherited

Answer 37

cancer is the conseq of accum of mutations that overrides organism ability to inactivate these fast growing cells but despite that critical underpinning of cancer, there is still a lot of environmental contributions to cancer