Lecture 5 Flashcards

1
Q

What is Ras? why is it seen in many cancers

A

Small GTPases that act as molecular switches by coupling cell membrane growth factor receptors to intracellular signalling pathways that regulate various cellular processes, monomeric, bind and hydrolyze guanine nucleotides. Seen in so many cancers because it is essential in signal transduction

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2
Q

how do Ras, HER2 and C-myc induce cancer

A

Ras: mutation
HER2-amplification
C-myc: translocation

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3
Q

what is EGFR

A

tyrosine kinase.

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4
Q

What is a tyrosine kinase

A

an enzyme that can transfer a phosphate group from ATP to a protein in a cell. On/off switch in many cellular functions

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5
Q

T/F phosphorylation is reversible

A

True

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6
Q

how does a proto-oncogene become and oncogene

A

Mutation
amplification
Gene translocation

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7
Q

What is EGF?

A

Hormones bind to EGF which cause dimerization of EGF monomers, which begins the activation cascade of the Ras protein

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8
Q

Describe Ras protein activation

A

Hormones bind to EGF monomers which cause dimerization, and phosphorylation of receptor tyrosine residues
GRB2 and Sos couples receptor to inactive Ras
GDP dissociates from Ras, GTP binds and active Ras dissociates from Sos

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9
Q

What’s the function of Sos in the third step of Ras activation

A

Promotes dissociation of GDP

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10
Q

What do GAP and GEF do?

A

GAP: Inactivates Ras
GEF: activates Ras

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11
Q

which codon mutations are the most common in cancer?

A

12

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12
Q

What mutation is responsible for H-ras oncogene activation?

A

V12, single base-pair mutation, glycine to valine, impairs GTPase activity

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13
Q

What is Ras binding to when it is active? inactive?

A

Active: GTP
inactive: GDP

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14
Q

why does the Ras protein activation/inactivation cycle run in one direction?

A

Hydrolysis of GTP to GDP is irreversible

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15
Q

which cancer is the most common to see a point-mutate ras gene

A

pancreatic cancer, 90% of pancreatic cancers have point mutated ras gene

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16
Q

What’s EGFR?

A

tyrosine kinase

17
Q

What is a tyrosine kinase

A

transfers phosphate group from ATP to a protein in a cell. On/off switch in many functions.

18
Q

What does EGFR do in a normal cell?

A

increases gene transcription and cell cycle progression

19
Q

What cancer is HER2 linked to

A

breast & ovarian cancers

20
Q

What is Burkitt’s Lymphoma

A

Malignant neoplasm in bone marrow and lymphatic structures
Cancer in the lymphatic system (B-lymphocytes), extreme proliferation
extremely high proliferation rate
occurs a lot in equatorial Africa
distinct jawbone
three types

21
Q

What are the three types of BL

A

Endemic, Sporadic, Immunodeficiency-associated

22
Q

What is Sporadic BL?

A

affects the whole world, mainly in kids, not linked to EBV, abdomen affected

23
Q

How is c-MYC translocated in BL

A

Translocated from chromosome 8 to IgH on chromosome 14 resulting in abnormal c-MYC expression and cell transformation

24
Q

What is c-Myc? what is it’s function

A

Proto-Oncogene, causes cancer when the gene for c-Myc is translocated, located on chromosome 8, regulates B-cell survival and expression, and controls a variety of cell functions like cell cycle progression

25
Q

how is c-MYC affected when its gene is translocated

A

The IgH enhancer directs high constitutive expression of IgH gene, when the c-MYC is translocated to this chromosome, it starts to produce c-MYC at exceptionally high amounts

26
Q

how are B cells and immunoglobulins related?

A

B cells express IgH on their membranes

27
Q

where are B cells mostly localized

A

cortex of lymph nodes

28
Q

what are lymph nodes

A

filters foreign via lymphatic vessels, foreign antigens are trapped and exposed to immune system for destruction

29
Q

What is CML? How is it caused

A

Chronic myelogenous leukemia, cancer of the white blood cells
Translocation between chromosome 22 and 9 resulting in BCR-ABL gene

30
Q

describe Abl

A

On chromosome 9, non-receptor tyrosine kinase, regualtes cell proliferation, cell migration, actin reorganization, etc

31
Q

Describe BCR

A

On chromosome 22, not a b cell receptor, serine/threonine kinase activity, cell cycle regulation