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Radiation Biology > Hall 18 - Cancer Biology > Flashcards

Hall 18 - Cancer Biology Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

What are proto-oncogenes?

A

Positive growth regulators

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2
Q

What are four mechanisms of oncogene activation?

A
  1. Retroviral integration near proto-oncogene causes increased expression via viral promoter (LTR)
  2. Gain of function mutations in only one copy > dominant oncogene (ex, RAS)
  3. Gene amplification leading to increased DNA copy number and expression (ex, MYC)
  4. Chromosome translocation can place a proto-oncogene under control of a strong promoter or aberrant fused proteins (ex, BCR-ABL)
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3
Q

What are tumor suppressor genes?

A

Negative growth regulators (in the same signaling networks as proto-oncogenes)

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4
Q

Tumor suppressor phenotype is _______ at the cellular level but inherited between generations in an autosomal ______ fashion.

A

Recessive, dominant

*Two-hit hypothesis: lose one = increase cancer risk; lose second one = transformation

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5
Q

How do sporadic cases of cancer from tumor suppressor loss happen?

A

Loss of heterozygosity
One copy lost, other chromosome suffers a deletion and replicates

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6
Q

What is the defective gene and inheritance pattern for retinoblastoma? What cancers do these people get?

A

RB1
Dominant
Retinoblastoma, sarcoma

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7
Q

What is the defective gene and inheritance pattern for Li-Fraumeni? What cancers do these people get?

A

p53 (or CHK2)
Dominant
Breast, lung, brain, sarcoma

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8
Q

What is the defective gene and inheritance pattern for familial Wilms tumor? What cancers do these people get?

A

WT1 or WT2
Dominant
Wilms tumor

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9
Q

What is the defective gene and inheritance pattern for neurofibromatosis 1? What cancers do these people get?

A

NF1
Dominant
Neurofibroma, MPNST, cafe au lait spots, Lisch iris nodules

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10
Q

What is the defective gene and inheritance pattern for neurofibromatosis 2? What cancers do these people get?

A

NF2
Dominant
Schwannoma, meningioma, ependymoma

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11
Q

What is the defective gene and inheritance pattern for familial adenomatous polyposis (FAP)? What cancers do these people get?

A

APC
Dominant
Colon, stomach, small bowel

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12
Q

What is the defective gene and inheritance pattern for von Hippel Lindau? What cancers do these people get?

A

VHL
Dominant
Kidney, adrenal, hemangioblastomas

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13
Q

What is the defective gene and inheritance pattern for familial gastric cancer? What cancers do these people get?

A

E-CAD
Dominant
Stomach, breast (lobular)

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14
Q

What is the defective gene and inheritance pattern for Gorlin syndrome? What cancers do these people get?

A

PTCH
Dominant
Basal cell carcinoma

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15
Q

What is the defective gene and inheritance pattern for Cowden syndrome? What cancers do these people get?

A

PTEN
Dominant
Hamartomas, increased cancer risk

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16
Q

What is the defective gene and inheritance pattern for multiple endocrine neoplasia? What cancers do these people get?

A

MEN1 and MEN2
Dominant
Pituitary, pancreatic, parathyroid

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17
Q

What is the most critical cell cycle checkpoint?

A

G1 to S
Commits cell to mitosis
Controlled by Rb

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18
Q

What are the 6 phenotypic hallmarks of cancer?

A
  1. Uncontrolled proliferation
  2. Failure to respond to growth-restrictive signals
  3. Failure to undergo apoptosis
  4. Escaping senescence
  5. Angiogenesis
  6. Invasion and metastases
19
Q

What is required to evade apoptosis and senescence?

A

Loss of tumor suppressors

20
Q

How do cancer cells survive crisis related to p53?

A

Activate telomerase
Telomere shortening normally causes senescence via p53

21
Q

What is a key molecule involved in local invasion of tumor cells?

A

Loss of E-cadherin (E-CAD)

22
Q

What results from loss of E-CAD, change in integrins, affinity switch from cell-cell to cell-matrix?

A

Local invasion
*Epithelial to mesenchymal transition (EMT)

Promoted by Snail, Slug, Twist, Zeb1/2

23
Q

Defect in what DNA stability gene leads to ataxia telangiectasia? How is it inherited?

A

ATM (DSB repair)
Recessive

24
Q

Defect in what DNA stability gene leads to ataxia telangiectasia-like disorder? How is it inherited?

A

MRE11
Recessive

25
Q

Defect in what DNA stability gene leads to Nijmegen breakage syndrome? How is it inherited?

A

NBS (part of MRE complex)
Recessive

26
Q

Defect in what DNA stability gene leads to hereditary breast cancer? How is it inherited?

A

BRCA1 or BRCA2 (HR repair)
*Dominant

27
Q

Defect in what DNA stability gene leads to Fanconi anemia? How is it inherited?

A

FANCD2 and FANC (associates with BRCA1/2)
Recessive

28
Q

Defect in what DNA stability gene leads to HNPCC/Lynch syndrome? How is it inherited?

A

MSH2, MSH6, MLH1, PMS1, PMS2 (mismatch repair)
*Dominant

29
Q

Defect in what DNA stability gene leads to Seckel syndrome? How is it inherited?

A

ATR (activated by ssDNA)
Recessive

30
Q

Defect in what DNA stability gene leads to Bloom syndrome? How is it inherited?

A

BLM (RecQ helicase that unwinds stalled DNA replication fork)
Recessive

31
Q

Defect in what DNA stability gene leads to Werner syndrome? How is it inherited?

A

WS (RecQ helicase + interacts with DNA-PKcs, Ku in NHEJ)
Recessive

32
Q

Defect in what DNA stability gene leads to Rothmund-Thomson syndrome? How is it inherited?

A

RECQL4 (RecQ helicase)
Recessive

33
Q

Defect in what DNA stability gene leads to xeroderma pigmentosum? How is it inherited?

A

XP (genome wide NER)
Recessive

34
Q

Defect in what DNA stability gene leads to Cockayne syndrome? How is it inherited?

A

CSA, CSB (transcription-coupled NER)
Recessive

35
Q

How does PI3K lead to cancer?

A

Phosphorylates PIP2 to PIP3 (reversed by PTEN) > docking site and recruits Akt > active phosphorylated Akt promotes protein synthesis and cell growth (mTORC1), cell cycle progression (activates MDM2, inhibits p21/27, Wee1, Chk1), and escapes apoptosis (activates IAPs, inhibits pro-apoptotic proteins)

PI3K/Akt/mTOR pathway

36
Q

How is Akt implicated in cancer?

A

PI3K phosphorylates PIP2 to PIP3 (reversed by PTEN)&raquo_space; docking site and recruits Akt&raquo_space; active phosphorylated Akt promotes protein synthesis and cell growth (mTORC1), cell cycle progression (activates MDM2, inhibits p21/27, Wee1, Chk1), and escapes apoptosis (activates IAPs, inhibits pro-apoptotic proteins)

PI3K/Akt/mTOR pathway

37
Q

How is EGFR activated?

A

Ligand binding
It is a canonical RTK
Recruits SOS to activate Ras-GTP (from inactive Ras-GDP)

38
Q

What is the EGFR pathway and how does it lead to cancer?

A

EGFR binding by ligand > SOS activates Ras-GTP > Raf > MEK > MAPK (ERK) > increased cyclin-CDK activity and transcription of target genes promoting cell proliferation

39
Q

What are activators of the Ras/Raf/MAPK pathway?

A

GPCRs, integrins, SRc family kinases
Anything that shuts down Ras GTPase activity to hydrolyze GTP (ex, *NF1)

40
Q

What are the PI3K/Akt/mTOR, JAK/STAT, and Ras/Raf/MAPK pathways all downstream of?

A

RTKs

41
Q

What normally happens without Wnt ligand?

A

APC/Axin complex promotes ubiquitination of beta-catenin > proteosomal degradation

Otherwise, Wnt can bind to Frizzled and eventually stabilize beta-catenin > translocates to nucleus and promotes gene transcription

42
Q

When TGF-beta binds to type II receptor dimer and activates the pathway, what gets phosphorylated to effect transcription?

A

SMAD2/3 > SMAD4 goes to nucleus

(SMAD6/7 are inhibitory)

43
Q

What are the effects of the TGF-beta pathway?

A

Activated SMAD2/3/4» gene transcription
» increased inflammation (pneumonitis)
» decreased growth of epithelial cells
» increased fibrosis

44
Q

What pathway is stimulated by proinflammatory cytokines TNF-a and IL-1, binding of Toll-like receptors, and UV radiation?

A

NF-kB

IKK complex&raquo_space; phosphorylates IkB (also possibly by ATM)&raquo_space; degradation&raquo_space; free NF-kB&raquo_space; gene transcription (pro-survival)

Radiation Biology (29 decks)

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