1- hallmarks Flashcards

1
Q

Name three tumor suppressor genes involved in the negative regulation of proliferation.

A

p53, RB1, TGF-B

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2
Q

What activates p53, and what are the two main mechanisms through which p53 responds to cellular stress?

A

Activated by damaged DNA or cells; mechanisms include regulating target genes for metabolic homeostasis, antioxidant defense, DNA repair, or inducing apoptosis.

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3
Q

What experiment with mice provided insights into how the immune system can prevent cancer, and what were the key findings?

A

Transplanting tumors from immunodeficient mice to immunocompetent hosts and vice versa; tumors were destroyed in immunocompetent hosts but not in immunodeficient hosts.

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4
Q

What is the role of telomerase in cancer cells, and how does it allow them to divide indefinitely?

A

Telomerase adds telomeres to chromosomes, preventing cells from entering senescence and allowing them to divide indefinitely.

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5
Q

How does chronic inflammation contribute to the development and progression of cancer, and what is the role of COX2?

A

Chronic inflammation can cause pro-neoplastic mutations and resistance to apoptosis; COX2 generates inflammatory mediator PGE2, overexpressed in many tumor cells.

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6
Q

Describe the process of metastasis and the key steps involved.

A

Local invasion, intravasation, survival in circulation, arrest in distant organ, extravasation, micrometastasis, macrometastatic growth.

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7
Q

What are the two main growth factors involved in angiogenesis, and how do they contribute to the development of new blood vessels in tumors?

A

Vascular Endothelial Growth Factor (VEGF) and Basic Fibroblast Growth Factor (bFGF); they promote the formation of new blood vessels in the tumor.

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8
Q

Name three genes associated with genome instability and mutation in cancer cells.

A

BRCA1, BRCA2, P53, RB1

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9
Q

What is the fine balance controlling cell death, and name two pro-apoptotic and two anti-apoptotic proteins.

A

Balance between pro-apoptotic (Bax, Bac, Bim, PUMA) and anti-apoptotic (Bcl-2, Bcl-XL, MCL1) proteins.

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10
Q

What is “aerobic glycolysis” in cancer cells, and how does it differ from normal glycolysis?

A

Cancer cells convert glucose to lactate in the presence of oxygen; less efficient than normal glycolysis.

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11
Q

How do tumor cells sustain proliferative signaling, and what are three growth factors they may produce?

A

Through autocrine, paracrine, or endocrine signaling; VEGF, bFGF, CXCL8 (IL8) + CXCR2.

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12
Q

Explain the role of p53 in controlling cell growth.

A

p53 is activated in response to DNA damage and regulates target genes involved in metabolic homeostasis, antioxidant defense, DNA repair, and growth arrest. It can also induce apoptosis depending on the degree of cellular stress.

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13
Q

What is the significance of RB1 in controlling cell cycle progression?

A

RB1 regulates the cell cycle by blocking cells between G1 and S phase. It controls the function of cyclin and cyclin-dependent kinase (CDK) complexes, preventing uncontrolled cell division.

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14
Q

What is angiogenesis, and how does it contribute to tumor growth?

A

Angiogenesis is the formation of new blood vessels. In tumor growth, angiogenesis, stimulated by factors like VEGF and bFGF, allows tumors to establish a network of blood vessels, providing oxygen and nutrients for sustained growth.

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15
Q
A
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