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SFM Quiz 2 > Cell Cycle pt. 2 > Flashcards

Cell Cycle pt. 2 Flashcards

1
Q

tumors

A

lesions that may or may not be neoplasms

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2
Q

neoplasms

A

abnormal growth with abnormal regulation, benign or malignant

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3
Q

cancer

A

malignant neoplasm

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4
Q

metastasis

A

secondary growth of cancer at a different location

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5
Q

initiation of carcinogenesis

A

simple mutation in one or more genes that control key regulatory pathways of cells

genotitic even (change in DNA sequence)

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6
Q

Promotion of carcionigenesis

A

selective functional enhancement of signal transduction pathways that were induced by initiator by continous exposure

epigenetic event, change in gene regulation

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7
Q

Progression of carcinogenesis

A

continuiing change of the basically unstable karyotype

clastogenic event

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8
Q

Things to know about initiation

A

irreversible

no threshold

caused by chemicals, radiation, ROS, viruses

change in cellular DNA

single mutation, chromosomal translocation, gene amplification

can lead to activation of onocogenes and inactivation of tumor supressor genes

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9
Q

Things to know about promotion

A

occurs over long span of time

reversibly in early stages, lifestyle changes may prevent

involves gene activation or repression such that latent phenotyp of intiated cell becomes expressed through cellular selection and clonal expansion

there is a threshold

can inhibit cell death of initiated cells

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10
Q

monoclonal tumors

A

come from one type of cell

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11
Q

polyclonal tumors come from

A

many typs of cells

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12
Q

Things to know about progression

A

complex genetic changes

irreversible gene expression changes

evolution of karyotypic instability

selection for optimal growth in repsonse to cellualr environment

results in the conversion of benign tumors to malignat ones and maybe metastasis

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13
Q

Cancer cells evade death by

A

being self sufficient, using growth signals, becoming insensitive to inhibitory signals, acquire limitiless replcaition potential, avoid immunology, promote inflamation, reprogram metabolism, sustain angiogenesis, so cool

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14
Q

oncogenes

A

cellular genes that stimulate cell division and/or growth

loss of regulation can lead to enhanced expression of these proteins and tell the cell “Divide! Divide!” (unregulated cell division and growth)

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15
Q

tumor supressors

A

cellular genes that serve to check or inhibit cell division

loss of expression of these proteins leads to cell growth or cell division

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16
Q

oncogenes are always

A

dominant mutations/overexpressions

they result from a gain of function mitation

only one of the two alleles needs to be activated for it to affect cell

rarely in germline inheritance

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17
Q

Three forms of oncogenes

A

cellular proto-oncogenes that have been captured by retrovirus

virus specific genes that behave like cellular proto-oncogenes that have been mutated

cellular proto-oncogenes that have been mutated

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18
Q

Raus Sarcoma

A

chicken
src oncogene
non-receptor TK
colon carcinoma

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19
Q

oncogeneic element in type 1 transducing viruses

A

cellular oncogene carred in retrovirus

basically, when retroviruses go into cellular DNA, they leave and take oncogenes with them

20
Q

oncogenic element in type 2 non-transducing viruses

A

cellular oncogene activated by proviral insertion/integration

basically, virus goes into genome and changes promoter (oncogenese can be promoted)

21
Q

oncogenic element in type 3 non-transducing long latency viruses

A

retroviral transactivating protein disrupting normal regulation of cellular transcription

retrovirus activates disrupting DNA (?)

22
Q

oncogenic element in type 4 retroviruses that contain an envelope that signal

A

inappropriate cellular signaling resulting from viral enveleop/cell receptor interactions

acts like a mitogen

23
Q

conversion of protooncogenes to oncogenes: truncatoin

A

loss of regulatory domain

product is over active

24
Q

conversion of protonocogenes to oncogenes: point mutation

A

in coding region-unregulated product

in promoter or enhancer-overproduced

25
Q

conversion of protooncogenes to oncogenes: insertion

A

viral promoter or enhancer-overprocued product

26
Q

conversion of protooncogenes to oncogenes: gene amplification

A

amplifies DNA, overproduced product

27
Q

conversion of protooncogenes to oncogenes: translocation

A

to a strong enhancer-overproduced product

with gene fusion-fusion with protein with abnormal properties

28
Q

growth factor oncogenes

A

PDGF
EGF
M-CSF

29
Q

GTP bining proteins oncogenes

A

ras

30
Q

transcription factors oncogenes

A

myc
fos
jun
TR, RAR

31
Q

too much myc or ras and the cell

A

will continue dividing!

32
Q

k-ras

A

chrom: 12p12.1
cancers: lung, ovarian, colorectal, bladder, carcinomas (5-20%)
protein: small G protein

33
Q

N-ras

A

chrom: 1p13
cancers: head and neck cancers (30%)
protein: small G protein

34
Q

H-ras

A

chrom: 11p15
cancers: colorectal cancers
protein: small G protein

35
Q

c-myc

A

chrom: 8q24
cancers: various leukemias, carcinomas (10-50%)
protein: TF

36
Q

L-myc

A

chrom: 1p32
cancers: lung cancer
protein: TF

37
Q

Tumor Supressor Genes

A

recessive

repress gorwth

inactivating mutations, deletions, loss of expression=carcinogenesis

germline inheritance frequent in cancer development

no known virus involvement

38
Q

Types of tumor suppressor genes

A

p53, Rb, p16/ink4a (p53 controls ccc in G1 and G2, mutated lose control of division)
all proteins are cell cycle regulatory proteins

39
Q

P16/INK4A

A

many studies show inactivation of the ink4a locus on chromsome 9p21 in cancers

2nd most common inactivated gene

via gene mutation, deletion, CpG island methylation in promoter region

40
Q

Rb (retinoblastoma)

A

not limited to loss of both allele to cause Rb

Rb is the gaurdian of the restriction point

can be genetic loss or other reasons

41
Q

inactivation of Rb gene by mutation

A

retinoblastoma, osteosarcoma, small cell lung carcinoma

42
Q

methylation of Rb gene promoter

A

brain tumors, others

43
Q

sequestration of pRb by Id1, Id2

A

diverse carcinomas, neuroblastoma, melanoma

44
Q

sequestration of pRb by the HPV e7 viral oncoprotein

A

cervical carcinoma

45
Q

cancer needs several ___ for cancer to result

A

mutations in several gene products or genes

SFM Quiz 2 (25 decks)

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