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Biochemistry: Block 4 > Cancer Genetics > Flashcards

Cancer Genetics Flashcards

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”

A

p53

25
Q

What is the role of wild-type p53?

A

It senses genomic damage, halts the cell cycle, and initiates repair or apoptosis

26
Q

What is the double negative effect?

A

When a mutant form of a protein inhibits the activity of the functional, normal, wild-type protein

27
Q

What is the physiologic process by which new blood vessels form from pre-existing vessels

A

Angiogenesis

28
Q

What molecule produced by tumor cells initiates a signal cascade resulting in expression of genes required for promoting angiogenesis?

A

Vascular endothelial growth factor (VEGF)

29
Q

What is anoikis?

A

Form of programmed cell death that is induced when anchorage dependent cells detach from the ECM

30
Q

What is epithelial to mesenchymal transition?

A

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
Q

What enzymes are required for epithelial to mesenchymal transition?

A

Matrix metalloproteases and tissue inhibitors of matrix matalloproteinases

32
Q

What are the seven basic steps of metastasis?

A

Localized invasion, intravasation, transport, arrest, extravasation, formation of micro-metastasis, and angiogenesis

Biochemistry: Block 4 (11 decks)

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