Cancer Genetics Flashcards

(32 cards)

1
Q

What is a tumor?

A

An abnormal mass of cells resulting from a defect in cell proliferation and survival control

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2
Q

What is a benign tumor? A malignant one?

A

Benign- similar to surrounding cells, slow growing, non-invasive, no metastasis; Malignant- rapid growth, undifferentiated, invasive, potentially metastatic

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3
Q

What is responsible for about 90% of cancer-related deaths?

A

Metastasis

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4
Q

What is the general classification of cancers of epithelial tissues?

A

Carcinoma

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5
Q

What is the general classification of cancers of connective and fibrous tissues?

A

Sarcoma

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6
Q

What are cancers of circulating blood cells of the bone marrow classified as?

A

Leukemias

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7
Q

What classification of cancer makes up 90% of human cancers?

A

Carcinoma

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8
Q

According to the multiple hit model of molecular cancer development, what are the six capabilities the original, non-cancerous cell must aquire through mutations or alterations?

A

Independence from external growth signals, Insensitivity to external anti-growth signals, Evading apoptosis and cellular death, Immortalization (infinite replication and division), Promotion of angiogenesis, Capability of tissue evasion and metastasis

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9
Q

What is the difference between a monoclonal and polyclonal tumor?

A

Monoclonal tumors derive from a single cell; polyclonal tumors derive from several individual cells within a similar tissue type all receiving a series of mutations

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10
Q

What is an oncogene?

A

A gene whose normal activity promotes cellular proliferation or division

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11
Q

What is a tumor supressor?

A

A gene whose wild type protein product functions to block cell division or promote cellular death

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12
Q

What is the non-mutant or wildtype version of an oncogene?

A

Proto-oncogene?

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13
Q

What kind of mutation activates a proto-oncogene to an oncogene?

A

Gain of function mutation

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14
Q

By what mechanisms can mutations result in activation of oncogenes?

A

Point mutation resulting in a constiutively active form of the protein; Amplification (more copies of gene present); Higher transcription (insertion into transcriptionally active area); translocation resulting in fused proteins

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15
Q

What is the mechanism by which Ras becomes an oncogene?

A

A single point mutation is intriduced (Gly–>Val) resulting in a protein that hydrolyzes GTP very inefficiently, effectively making it excessively active promoting genes important for growth and survival

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16
Q

Through what mechanism does Myc become oncogenic?

A

Amplification of the c-Myc gene

17
Q

What kind of protein is Myc?

A

Transcription factor

18
Q

What is the Philadelphia chromosome? With what cancer is it associated?

A

It results from a translocation between the p34 region of chromosome 9 and the p11 region of chromosome 22; chronic myelogenous leukemia

19
Q

What is the protein product of the Philadephia chromosome?

A

Fused Bcr-Abl gene

20
Q

What are the functions of tumor suppressor genes?

A

Regulators of cell cycle; inducer of apoptosis; transcription factors (repressors or activators)

21
Q

What concept can serve as a general paradigm for how loss of tumor surpressors must occur for cancer to develop?

A

Two-Hit Model

22
Q

What are the mechanisms by which a tumor suppressor can become inactive?

A

Loss of heterozygosity; silencing through epigenetics

23
Q

How are genes silecenced through epigenetics?

A

Methylaton at promoters

24
Q

What is the “guardian of the genome”

25
What is the role of wild-type p53?
It senses genomic damage, halts the cell cycle, and initiates repair or apoptosis
26
What is the double negative effect?
When a mutant form of a protein inhibits the activity of the functional, normal, wild-type protein
27
What is the physiologic process by which new blood vessels form from pre-existing vessels
Angiogenesis
28
What molecule produced by tumor cells initiates a signal cascade resulting in expression of genes required for promoting angiogenesis?
Vascular endothelial growth factor (VEGF)
29
What is anoikis?
Form of programmed cell death that is induced when anchorage dependent cells detach from the ECM
30
What is epithelial to mesenchymal transition?
A process by which epithelial cells lose their polarity and cell-cell adhesion and gain migratory and invasie properties to become mesenchymal stem cells
31
What enzymes are required for epithelial to mesenchymal transition?
Matrix metalloproteases and tissue inhibitors of matrix matalloproteinases
32
What are the seven basic steps of metastasis?
Localized invasion, intravasation, transport, arrest, extravasation, formation of micro-metastasis, and angiogenesis