W07_03 Molecular pathogenesis of cancer - common genes Flashcards

1
Q

what kinds of mutations are there in cancer?

A

point;
insertion/deletion;
amplification/copy number alteration;
translocation/chromosomal rearrangement

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2
Q

define oncogene

A

promotes autonomous growth in cancer cells, in the absence of cell growth-promoting signals

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3
Q

define proto-oncogene

A

non-mutated, “normal” gene with the potential to become oncogenic.

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4
Q

define oncoprotein

A

the product of an oncogene

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5
Q

typically, oncoproteins can be of these signalling types

A
growth factors;
growth factor receptors;
signal transduction molecules;
nuclear regulatory proteins;
cell cycle regulators
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6
Q

what class of signalling is Her2-neu?

A

growth factor receptor

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7
Q

what happens to Her2-neu in cancer?

A

gene is amplified, and the receptor is increased as a result

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8
Q

what’s the clinical significance of a Her2-neu mutation?

A

gives rise to breast cancer;

25-30% of breast cancers express this on the surface

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9
Q

treatment for Her2-neu+ breast cancer?

A

trastuzumab (Herceptin) targeted therapy

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10
Q

what class of signalling is Ret?

A

growth factor receptor (normally a glial-derived neurotrophic factor receptor)

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11
Q

when is ret normally expressed?

A

during neural development, and also in neuroendocrine cells

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12
Q

where is ret normally expressed?

A

C-cells of thyroid, adrenal medulla, parathyroid cells

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13
Q

which clinical diseases are caused by ret mutation (usually germ-line mutation)?

A

multiple endocrine neoplasia type ii,

familial medullary thyroid cancer

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14
Q

what class of signalling is Ras?

A

receptor-associated signal transduction molecule

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15
Q

what are the three most well known Ras oncogene types?

A

HRas,
KRas,
NRas

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16
Q

how can Ras become problematic?

A

if the pathway of GTPase is blocked, then Ras will stay constitutively active

17
Q

ras helps us guide treatment for which type of cancer?

A

lung

18
Q

what class of signalling is Abl?

A

non-receptor associated tyrosine kinase

19
Q

what mutation leads to a problem with abl?

A

when abl translocates onto chromosome 22 and makes bcr-abl

20
Q

what disease results from bcr-abl?

A

cml and all

chronic myeloid leukemia and acute lymphoblastic leukemia

21
Q

therapy for bcr-abl?

A

imatinib mesylate

22
Q

what class of signalling is Myc?

A

nuclear regulatory protein

23
Q

how can myc go wrong?

A

thru amplification or translocation

24
Q

n-myc is amplified to in which cancer?

A

neuroblastoma

25
Q

l-myc is amplified in which cancer?

A

SCLC

26
Q

what’s a “double minute”?

A

copies of a gene that float around, independent of a chromosome

27
Q

what’s the molecular cause of burkitt’s lymphoma?

A

translocation of the myc gene to the IgH gene

28
Q

what class of signalling is cyclin D?

A

cell cycle regulator

29
Q

cyclin D associates with which two factors to help cell cycle regulation?

A

CDK4 and CDK6