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Cell Biology > Exam 4 Lesson 42 > Flashcards

Exam 4 Lesson 42 Flashcards

1
Q

How are cancers classified?

A

Based on tissue of origin

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2
Q

carcinoma

A

Cancers arising from epithelial cells (most common)

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3
Q

sarcomas

A

Cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue

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4
Q

leukemias

A

Cancer that starts in blood-forming tissue such as the bone marrow and causes large numbers of abnormal blood cells

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5
Q

Lymphomas and myeloma

A

Cancers that begin in the cells of the immune system

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6
Q

melanomas

A

Arise from the cells that produce the dark pigment in skin, hair

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7
Q

carcinogens

A

Substances that cause DNA mutations that cause cancer

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8
Q

Non- hereditary cancer

A

Somatic mutations cause most cancers

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9
Q

Hereditary cancer

A

Germline mutations , rare (~5% of cancers)

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10
Q

What kind of disease is cancer?

A

A genetic disease. Caused by gene mutations.

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11
Q

Where do most cancers originate?

A

From a single aberrant cell

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12
Q

What kind of mutations cause cancer?

A

cancer is caused by a progressive accumulation of random mutations in a single lineage of cells

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13
Q

clonal evolution theory

A

Accidental production of mutant cell
Cell proliferates and there are two mutations
Cell proliferates and there are three mutations
Can lead to dangerous cell proliferation

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14
Q

What are the two kinds of mutation events?

A

Genetic change and epigenetic change

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15
Q

What are the two kinds of genetic changes?

A

Small scale and large scale

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16
Q

Small scale genetic changes

A

A small gene in one or a few nucleotides; point mutation, insertion, deletion

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17
Q

Large scale genetic changes

A

In chromosomal structure; duplication, amplification, deletion, insertion, inversion, translocation

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18
Q

Epigenetic change

A 
Histone modification (heterochromatin pathway; not inherited);
DNA methylation (an inherited pattern of methylation of C nucleotides in CpG sequence)
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19
Q

What is Gleevec?

A

A drug that targets a protein kinase that promotes development of leukemia.

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20
Q

What are oncogenes?

A

They have a gain-of-function mutation. They produce overactive proteins that drive the cell cycle or contribute to some other aspect of the cancer process.

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21
Q

What are tumor suppressor genes.

A

They suffer a loss-of-function mutation. The loss of both copies of the normal gene leads to cancer. Loss of gene activity may come from a genetic change or an epigenetic change.

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22
Q

What causes loss of gene activity?

A

A genetic change or an epigenetic change

23
Q

tumorigenesis

A

Evolution of a normal cell into a tumor cell. A process by which normal cells are transformed into cancer cells.

24
Q

Invasion/metastasis

A

Evolution of benign into a malignant cancer cell. Cancer cells break loose, enter blood or lymphatic vessels, and form secondary tumors at other sites in body.

25
Q

Six proposed hallmarks of cancer

A
  1. Self- sufficiency in growth signals
  2. Insensitivity to anti-growth signals
  3. Evading apoptosis
  4. Tissue invasion and metastasis
  5. Limitless replicative potential
  6. Sustained angiogenesis
26
Q

What does cell proliferation require?

A
  1. Progression through the cell cycle

2. Cell growth

27
Q

What do normal cells require for proliferation?

A

Signals in the form of cytokines, ECM components, and cell-cell interactions.

28
Q

How do cancer cells proliferate?

A

They generate their own cell proliferation signals (mutagens, growth factors) or they recruit nearby stromal cells, causing them to release growth factors.

29
Q

proto-oncogenes

A

Receptors for mutagens or growth factors that may be unregulated. Downstream signaling molecules that may be unregulated like mutant form of Ras, mTOR, or Akt.

30
Q

What loss of function mutations promote proliferation pathways?

A

Loss of function mutations in Rb and PTEN

31
Q

What do anti-proliferative and anti-growth signals usually block?

A

The inactivation of Rb

32
Q

What happens if Rb is active?

A

It inhibits E2F and expression of S-phase genes

33
Q

How are cancer cells insensitive to anti-growth or antiproliferation signals?

A

They may downregulate receptors for anti-proliferative signals, have loss-of-function mutations in Cdk inhibitors or loss of function mutations in Rb

34
Q

What is role of p16, or p15INK4?

A

It inhibits CDk4 from binding to cycling D, inhibiting the complex

35
Q

What is role of apoptosis?

A

It maintains constant cell number and eliminates cells that have become abnormal because of genetic mutations or other stresses.

36
Q

What does p53 protein do in response to DA damage and stress?

A
  1. Controls cell cycle arrest

2. Controls apoptosis

37
Q

What does p53 bind to?

A

It binds to regulatory region of p21 gene. p21 is a Cdk inhibitor protein.

38
Q

Why does FAK interact with growth factor receptors?

A

To control the ERK/MAPK pathway in regulation of cell proliferation.

39
Q

Do animal stem cells need to attach to lamina?

A

Yes. They must to survive apoptosis signals.

40
Q

Why do somatic cells have a finite replicative potential?

A

Because of a lack of telomerase activity. Telomeres shorten with each replication cycle.

41
Q

senescence

A

As telomeres shorten, chromosomal ends become unprotected, leading to cell cycle arrest.

42
Q

How do cancer cells maintain replicative potential?

A

Normally, telomerase expression is largely repressed in postembryonic cell lineages. Cancer cells are able to maintain the expression of telomerase for continued telomerase activity.

43
Q

intravasion

A

From cell into a capillary or lymph vessel

44
Q

extravasion

A

From capillary or lymph vessel into cell

45
Q

How is success rate for each step in metastasis?

A

slow

46
Q

What must new tumors in new locations do?

A

Recruit a blood supply and recruit surrounding cells to create a “niche”

47
Q

Epithelial-mesenchymal transition (EMT)

A

Shutdown of E-cadherin expression enables cancer cells to extricate themselves from the keratinocyte neighbors in the epidermis, while its replacement by expression of N-cadherin allows these tumor cells to interact with mesenchymal cells

48
Q

How are normal epithelial cells kept in place?

A

By cell-cell and cell-ECM interactions

49
Q

What do cancer cells do to cell-cell and cell-ECM interactions?

A

They alter these interactions via changes in gene expression. For example, they alter cell-cell adhesion molecules (CAMs), by losing E-cadherin and gaining N-cadherin.

50
Q

angiogenesis

A

Growth of new blood vessels from pre-existing vessels

51
Q

Why do tumors rely on angiogenesis?

A

They increase in size and need new blood vessels to supply all cells with oxygen and nutrients.

52
Q

How do cancer cells respond to hypoxia?

A

They release factors that stimulate the proliferation of endothelial cells.

53
Q

VEGF

A

Positive factor for angiogenesis

54
Q

How can vascularization be suppressed?

A

By a VEGF receptor inhibitor

Cell Biology (35 decks)

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