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3 Principles of Neoplasia > 3.2 Carcinogenesis > Flashcards

3.2 Carcinogenesis Flashcards

1
Q

Carcinogenesis: categories of disrupted systems (3)

A
  1. Oncogenes
  2. Tumor suppressor genes (p53, Rb, APC)
  3. Regulators of apoptosis (Bcl2)
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2
Q

Categories of oncogenes (5). Picture sequence of cell growth signalling.

A
  1. Growth factors
  2. Growth factor receptor
  3. Signal transduction proteins
  4. Nuclear transcription factors
  5. Cell cycle regulators
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3
Q

Oncogenes: growth factors

  • example (1)
  • associated tumor?
A
  1. PDGF, overexpression

- Astrocytoma (glial cell)

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4
Q

Oncogenes: growth factor receptors

  • examples (1 major + 2 others)
  • associated tumor
A
  1. ERBB2 [HER2/neu]–Human Epidermal GF Receptor
    - breast carcinoma
    - blocked by Trastuzumab
  2. RET–neural GF receptor
    - MEN (multiple endocrine neoplasia)
  3. KIT–stem cell GF receptor
    - GI stromal tumor
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5
Q

Oncogenes: signal transducers

  • examples (1 major, 1 other)
  • mech
A
  1. Ras.
    - signal transducer through nuclear membrane
    - in 25% of tumors (carcinoma, lymphoma, melanoma) have defect in this.
    - activated by GTP; overactivated when GAP has defect, so increased growth signals
  2. ABL–tyrosine kinase
    - CML, some types of ALL
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6
Q

Oncogenes: Nuclear transcription factors

  • examples (1 major, 2 others)
  • mech/etiology
  • associated tumor
A
  1. c-Myc
    - t(8:14) with IgH
    - Burkitt’s lymphoma (B cells)
    - “starry sky appearance”
  2. N-Myc
    - Neuroblastoma
  3. L-Myc
    - Lung carcinoma
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7
Q

Oncogenes: Cell cycle regulators

  • examples (1 major, 1 other)
  • mech/etiology
A
  1. CCND1 (cyclin D1)
    - controls G1 to S by making a complex (binds with CDK4–a cyclin dependent kinase) that activates Rb to release “the key” of E2F
    - t(11:14) with IgH, causes overexpression of CCND1
    - Mantle cell carcinoma (subtype of B Cell lymphoma)
  2. CDK4–cyclin-dependent kinase
    - see above, binds with cyclin D1 for same effect on Rb
    - Melanoma
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8
Q

Tumor suppressor genes:

  • classic examples (2) + 1 other
  • mech
A
  1. p53
    - 2 traffic cops: “show me your DNA” before going from G1 to S
    - if errors repairable, increase expression of repair enzymes
    - if errors not repairable, induce apoptosis with BAX, which inhibits Bcl2, allowing Cyt C to leak.
  2. Rb
    - also regulates G1 to S
    - Rb “tightly holds the key” of E2F, a TF necessary for transition to S
    - E2F is released normally when Rb is phosphorylated by a complex (cyclin D1/CDK4)
    - Familial retinoblastoma (in eyes)
  3. APC
    - reduces beta catenin
    - familial adenomatous polyposis
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9
Q

Li-Fraumeni syndrome

A
  • One of the 2 p53 genes has germline mutation
  • remember, p53 is the 2 traffic cops that check G1 to S
  • more likely to develop a variety of tumors
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10
Q

Knudson 2-hit hypothesis

A
  • Both of the classic tumor suppressors contain 2 copies
  • p53
  • Rb
  • APC
  • so, both require double ‘hit’ to disable
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11
Q

BAX

A
  • Bcl2 Associated X protein
  • released by p53 (traffic cops) when a cell needs to undergo apoptosis
  • inhibits Bcl2, allowing Cytc C to leak
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12
Q

PDGF

  • what is it
  • associated cancer
A
  • oncogene, GF category
  • Platelet derived growth factor
  • Astrocytoma (glial cell)
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13
Q

ERBB2 (HER2/neu)

  • what is it, mech
  • associated tumor
A
  • Epidermal GF receptor, oncogene
  • (Human Epidermal GF Receptor 2). overexpressed in cancer
  • associated with breast carcinoma
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14
Q

Ras

  • what is it
  • mech
A
  • family of signal transducer genes (GTP-binding protein)
  • oncogenes; 25% of tumors have defect in Ras
  • activated by GTP. GAP converts GTP to GDP.
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15
Q

c-Myc

  • what is it
  • mech of disorder
  • associated tumor
A
  • “michael burkitt, born August 14”
  • oncogene, nuclear TF
  • t(8:14) with IgH causes overexpression of c-Myc.
  • Burkitt’s lymphoma (also associated with EBV)
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16
Q

Cyclin D1 (CCND1)

  • what is it
  • mech of disorder
  • associated cancer
A
  • ‘November 14: division 1 cyclist bikes through the earth’s mantle’
  • oncogene, cell cycle regulator
  • complexes with CDK4 to activate Rb, making it release its “key” of E2F, allowing cells to undergo G1 to S
  • Mantle cell lymphoma, 11:14
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17
Q

Familial retinoblastoma

A
  • One of the 2 Rb tumor suppressor genes has germline mutation
  • retina cells develop tumors if the remaining copy of Rb becomes defective
  • remember, Rb holds on to the “key” of E2F that controls G1 to S
18
Q

E2F

A
  • the “key” protein held tightly by the 2 Rb tumor suppressor proteins
  • E2F allows cells to undergo G1 to S
19
Q

Bcl2

  • mech
  • what inactivates it
  • associated cancer
A
  • Controller of apoptosis
  • keeps Cyt C in mito from leaking out to cause apoptosis
  • BAX (Bcl2 activating X factor) released from p53 inactivates Bcl2, leading to apoptosis
  • Bcl2 is overexpressed in follicular lymphoma–t(14:18)–B cells destined to die accumulate in lymph node follicle
20
Q

Angiogenesis factors

A
  1. FGF (fibroblast GF)

2. VEGF

21
Q

ABL

  • what is it
  • mech of disorder
  • associated tumor
  • Tx
A
  • ‘Able company was sent to fight the camels of the 9-22 terrorist attack on Philadelphia’
  • signal transducer gene (tyrosine kinase)
  • t(9:22)– 22 is Philadelphia chromosome
  • CML, some types of ALL
  • Tx with imatinib mesylate (Gleevec)
22
Q

KIT

  • what is it
  • mech of disorder
  • associated tumor
  • tx
A
  • ‘kit kat bar in the stomach’
  • stem cell GF receptor gene
  • point mutation
  • overexpression leads to Gastrointestinal stromal tumor (GIST)
  • Tx with Imatinib mesylate (Gleevec)–tyrosine kinase inhibitor
23
Q

APC

  • mech
  • associated cancer
A
  • ‘2 APCs attacking a fapping beta cat’
  • tumor suppressor gene
  • 2 genes, 2 ‘hits’
  • down-regulates beta-catenin, which is a TF and mediates cell-cell adhesion
  • Familial Adenomatous polyposis (FAP) from loss of APC
24
Q

HPV

  • role in oncogenesis
  • identify the low and high risk types
A

-cervical cancer
-E6, E7
E6: inhibits p53
E7: inhibitis Rb and p53

low risk: 6, 11 (A6, F1111)
high risk: 16, 18, 31, 33 (F16, F18, Su33, Mig31)

25
Q

EBV

-role in oncogenesis

A
  • infects B cells.
  • can cause Burkitt’s lymphoma if 8:14 c-myc overexpression also occurs.
  • also cause other B cell problems
26
Q

Hep B, C

-role in oncogenesis (2 mechs)

A
  • liver cancer, 2 mechs:
    1. chronic regeneration, aka regenerative nodular hyperplasia (B, C)
    2. HBx protein inhibits p53, activates growth genes (B only)
27
Q

H. Pylori

-role in oncogenesis

A

2 tumors:

  1. gastric adenocarcinoma
  2. MALToma

-host inflamm response leads to carcinogenesis–metaplasia

28
Q

Microorganisms associated with oncogenesis

-list them and ex of associated cancer

A
  1. EBV–Burkitt’s lymphoma
  2. HHV-8–Kaposi’s sarcoma
  3. Hep B, Hep C–hepatocellular carcinoma
  4. HTLV-1: Adult T-cell leukemia/lymphoma
  5. HPV–cerical carcinoma
29
Q

HTLV-1

-associated with what?

A
  • oncogenic virus (human T lympotropic virus)

- associated with Adult T-Cell leukemia/lymphoma

30
Q

HHV-8

-associated with what?

A
  • Onocogenic virus (human herpes virus 8)

- associated with Kaposi sarcoma

31
Q

proto-onconegenes vs oncogenes: difference?

A

Oncogenes are mutated proto-oncogenes

32
Q

Trastuzumab

A
  • monoclonal Ab, blocks ERBB2 (HER2) receptor, a GF receptor in breast cancer
  • tx in breast cancer
33
Q

Imatinib mesylate (Gleevec)

A

-tyrosine kinase inhibitor

34
Q

Burkitt’s lymphoma

-etiology: factors

A
  • increased expression of c-MYC

- associated with EBV

35
Q

N-MYC

-associated tumor

A
  • nuclear TF, onocogene

- Neuroblastoma when N-MYC is overexpressed

36
Q

Mantle cell lymphoma

A
  • on november 14, a Division 1 cyclist bikes through the earth’s mantle.
  • cyclin D1, 11;14
37
Q

Familial adenomatous polyposis (FAP)

A
  • 2 APCs attack the fapping beta cat

- loss of APC leads to high levels of beta catenin, activating growth TFs

38
Q

beta-catenin

A
  • think :’fapping beta cat attacked by 2 APCs’
  • 2 functions: TF and mediates cell-cell adhesion
  • accumulation causes cancer
  • accumulation occurs when both APC genes are mutated.
39
Q

polycyclic aromatic hydrocarbons

  • what are they
  • how metabolized and detoxified?
A

-carcinogen in smoke

  • CYP1A1–metabolizes polycyclic aromatic hydrocarbons into toxic form
  • 10% of caucasians have highly-inducible form
  • glutathione S-transferase–detoxifies it
  • 50% of caucasians have deletions
40
Q

initiator vs promoter in carcinogens

A
  • initiator: directly causes permanent mutation

- promotor: allows proliferation of mutated cells

3 Principles of Neoplasia (5 decks)

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