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Block 1 WK 6 > 2013 Perrino Cancer > Flashcards

2013 Perrino Cancer Flashcards

1
Q

cancers of epithelium are called?

A

carcinomas

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2
Q

Cancers of connectve tissues or muscles cells are called?

A

sarcomas

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3
Q

What is kaposi’s sarcoma connected to?

A

AIDS

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4
Q

what are cells that arise form hemopoietic cells and cancers derived from cells of the nervous system?

A

leukemias, lymphomas

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5
Q

what is the most common cancer?

A

reproductive cancer

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6
Q

What are the two cancers that have a near 100% death rate/new occurance rate?

A

nervous system, connective tissue, muscles and vasculature

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7
Q

most cancers are classified as what?

A

eptihelial cancers so carcinomas

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8
Q

Cancer cells often maintain characteristics of their (blank) ,and cancers originating from different cell types are usually very different diseases.

A

tissue of origin

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9
Q

What is a tumor growing at the anatomical site where the tumor originated and tumor progression began and proceeded to yield a cancerous mass called?

A

primary tumor

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10
Q

Most cancers arise from a (blank)

A

single abnormal cell

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11
Q

What showed evidence that cancer arises from single abnormal cell?

A
  • all cells of a particular cancer have same chromosome breakage point (phili 9-33 CML)
  • all cells of particular cancer have same x-inactivation
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12
Q

carcinogenesis is linked with (blank)

A

mutagenesis

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13
Q

Correlation between carcinogens and mutations

(blank) generally cause point mutations in a DNA sequence

A

chemical carcinogens

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14
Q

Correlation between carcinogens and mutations

(blank) generally cause chromosome breaks and translocations

A

ionizing radiation x-rays

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15
Q

Correlation between carcinogens and mutations

(Blank) introduce foreign DNA into cells

A

transforming viruses

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16
Q 
Tumor progression: the development of cancer requires the accumulation of mutations
In many (blank)
A

genes

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17
Q

What are the stages in development of cervical carcinoma?

A

normal->low-grade epithelial neoplasia-> invasive carcinoma

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18
Q

Incidence of bladder cancers in workers exposed to 2-napthylamine showed what?

A
  1. Cancers arise years after exposure to chemical carcinogens
  2. It takes Years of exposure are required for cancers to develop
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19
Q

the tumor (blank) plays an important role in tumor survival and growth.

A

microenvironment

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20
Q

What is the key property of all cancer cells?

A

1) They disregard the external and internal signals that regulate cell proliferation
2) avoid suicide by apoptosis
3) They circumvent programmed limitations to proliferation escaping replicative senescence and/or avoiding differentiation
4) genetically unstable (p53)
5) they escape from tissue of origin (invasive)
6) they survive and proliferate in foreign sites (they metastasize)
7) cancer stem cells maintain many tumors

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21
Q

a class of about 100 genes that have been identified that are repeatedly altered in different cancers are called the cancer (blank).

A

critical genes

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22
Q

What can radiation chemotherapy target?

A

fast growing cells that have the same structure

23
Q

Are environmental poisons causing cancer?

A

no, smoking and old age

24
Q

Who made the war on cancer?

A

nixon

25
Q

What are the two broad classes of cancer critical genes?

A

gain of function mutation and loss of function mutation

26
Q

What is the type of gene that has a gain of function mutation and is dominant?

A

oncogene

27
Q

What is the type of gene that has a loss of function mutation and is recessive?

A

tumor suppressor gene

28
Q

If you have an oncogene proliferating then you have cells expressing constitutively active (blank) receptor.

A

PDGF

29
Q

What was the first onocogene to be discovered and causes 30% of all cancers?

A

RAS

30
Q

Many signaling proteins can become oncogenes, but a particular pathway mutation can lead to this. Which pathway am I referring to?

A

map kinase pathway

31
Q

What was the first tumor suppressor gene discovered?

A

retinoblastoma

32
Q

(blank) is when a gene product normally functions to suppress cell proliferation; so when the gene product has too little activity, carcinogenesis is
favored.

A

loss of function mutations

33
Q

Explain the Rb pathway

When does this all happen?

A

1-CDk is active and phosphorylates RB protein which allows it to leave the E2F protein. The E2f protein then begins DNA synthesis.
G1 and S phase

34
Q

Explain the BAD pathway?

A

PI3->PDK PKB->bad gets phosphorylated and inactivated and you get cell proliferation.

35
Q

How can BAD allow a cancer to escape cell death?

A

it loses its ability to inactivate the death inhibitory protein (which means that bad will constantly be inactive which will inhibit apoptosis and increase cell proliferation)

36
Q

cancer cells require two pathways to really proliferate, what are these two pathways?

A

a cell proliferation pathway and a pathway to provide nutrients ( mitogen and growth factor)

37
Q

If you do a Ct scan of a malignant invasive cancer what can you expect to see besides a mass?

A

increased uptake of glucose in the body indicating incredible amounts of cell growth and need for nutrients

38
Q

What are three basic categories of genetic alterations that turn a cancer-critical gene into an oncogene?

A 
deletion or point mutation in coding sequence (RAS, EGF)
gene amplification (src, myc)
chromosome rearrangement (myc, burkitt's lymphoma Abl CML)
39
Q

What are the two types of chromosome rearrangment that can lead to an oncogene?

A

1) Nearby regulatory DNA sequence causes normal cell to overproduce protein (myc, burkitt’s lymphoma)
2) fusion to actively transcribed gene greatly overproduces fusion protein (abl, CML)

40
Q

What is myc?

A

is a regulator gene that codes for a transcription factor.

41
Q

What does p53?

Why is it bad if p53 is mutated

A

it stops damaged cells from replicating.

p53 wont be able to stop the damage cell from replicating so you will get lots of bad cells

42
Q

How often do you find a p53 mutation in cancer patients?

A

50%

43
Q

Does p53 allow cells to escape apoptosis

A

yes

44
Q

What does gleevic do?

A

prevents leukemia cuz it binds to BCR and keeps BCR from getting phosphorylated and initiating proliferation.

45
Q

What is a rational cancer treatment?

A

small molecule pathway inhibitors

46
Q

What does Iressa do?

A

Iressa inhibits the Map kinase pathway by binding to Tyrosine Kinase receptors.

47
Q

(blank) is the first selective inhibitor of epidermal growth factor receptor’s (EGFR) tyrosine kinase domain.
The target protein (EGFR) is also sometimes referred to as Her1 or ErbB-1. Effective against many breast
cancers. also approved for some lung cancers

A

Iressa

48
Q

What does salirasib do?

What cancer does it really work in?

A

inhibits RAS binding to galectin

pancreatic cancer

49
Q

What does Zelboraf do?

What cancers does it really work for?

A

inhibits Raf from phosphorylating the rest of the Map kinase pathway.
Melanoma

50
Q

How many phases in a clinical trial?

A

4

51
Q

What phase of clinical trials is this?
Initial studies to determine the metabolism and pharmacologic actions of drugs in humans, the side effects associated with increasing doses, and to gain early evidence of effectiveness; may include healthy participants and/or patients.

A

Phase I trial

52
Q

What phase of clinical trials is this?
Controlled clinical studies conducted to evaluate the effectiveness of the drug for a particular indication or indications in patients with the disease or condition under study and to determine the common short-term side effects and risks.

A

Phase II trials

53
Q

What phase of clinical trials is this?
Expanded controlled and uncontrolled trials after preliminary evidence suggesting effectiveness of the drug has been obtained, and are intended to gather additional information to evaluate the overall benefit-risk relationship of the drug and provide and adequate basis for physician labeling.

A

Phase III trials

54
Q

What phase of clinical trials is this?

Post-marketing studies to delineate additional information including the drug’s risks, benefits, and optimal use.

A

Phase IV trials

Block 1 WK 6 (10 decks)

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