Exam 4 Lesson 42 Flashcards Preview

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Flashcards in Exam 4 Lesson 42 Deck (54):
1

How are cancers classified?

Based on tissue of origin

2

carcinoma

Cancers arising from epithelial cells (most common)

3

sarcomas

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

4

leukemias

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

5

Lymphomas and myeloma

Cancers that begin in the cells of the immune system

6

melanomas

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

7

carcinogens

Substances that cause DNA mutations that cause cancer

8

Non- hereditary cancer

Somatic mutations cause most cancers

9

Hereditary cancer

Germline mutations , rare (~5% of cancers)

10

What kind of disease is cancer?

A genetic disease. Caused by gene mutations.

11

Where do most cancers originate?

From a single aberrant cell

12

What kind of mutations cause cancer?

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

13

clonal evolution theory

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

14

What are the two kinds of mutation events?

Genetic change and epigenetic change

15

What are the two kinds of genetic changes?

Small scale and large scale

16

Small scale genetic changes

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

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Large scale genetic changes

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

18

Epigenetic change

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

19

What is Gleevec?

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

20

What are oncogenes?

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.

21

What are tumor suppressor genes.

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.

22

What causes loss of gene activity?

A genetic change or an epigenetic change

23

tumorigenesis

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

24

Invasion/metastasis

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

Six proposed hallmarks of cancer

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

What does cell proliferation require?

1. Progression through the cell cycle
2. Cell growth

27

What do normal cells require for proliferation?

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

28

How do cancer cells proliferate?

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

29

proto-oncogenes

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

What loss of function mutations promote proliferation pathways?

Loss of function mutations in Rb and PTEN

31

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

The inactivation of Rb

32

What happens if Rb is active?

It inhibits E2F and expression of S-phase genes

33

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

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

34

What is role of p16, or p15INK4?

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

35

What is role of apoptosis?

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

36

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

1. Controls cell cycle arrest
2. Controls apoptosis

37

What does p53 bind to?

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

38

Why does FAK interact with growth factor receptors?

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

39

Do animal stem cells need to attach to lamina?

Yes. They must to survive apoptosis signals.

40

Why do somatic cells have a finite replicative potential?

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

41

senescence

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

42

How do cancer cells maintain replicative potential?

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

intravasion

From cell into a capillary or lymph vessel

44

extravasion

From capillary or lymph vessel into cell

45

How is success rate for each step in metastasis?

slow

46

What must new tumors in new locations do?

Recruit a blood supply and recruit surrounding cells to create a "niche"

47

Epithelial-mesenchymal transition (EMT)

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

How are normal epithelial cells kept in place?

By cell-cell and cell-ECM interactions

49

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

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

angiogenesis

Growth of new blood vessels from pre-existing vessels

51

Why do tumors rely on angiogenesis?

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

52

How do cancer cells respond to hypoxia?

They release factors that stimulate the proliferation of endothelial cells.

53

VEGF

Positive factor for angiogenesis

54

How can vascularization be suppressed?

By a VEGF receptor inhibitor