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Molecular Biology Exam 3 > Cancer 1 > Flashcards

Cancer 1 Flashcards

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1
Q

Cancer in which organ is the deadliest?

A

Lung Cancer

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2
Q

Breast and lung cancer have the same incidence, but why does breast cancer have a better survival rate?

A

Can remove tumor in breast - can’t remove lung.

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3
Q

What are the two most common ways to die?

A

cancer and heart attacks

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4
Q

What is the definition of cancer?

A

A disease in which an individual mutant clone of cells begin by prospering at the expense of its neighbor cells.

the descendants of these clones can destroy the whole cell society in your body

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5
Q

List the properties of cancer cells.

A

> cells growing out of control
become self-sustaining, do not need signals to grow
release autocrine growth factor signals
these cells should stop growing with anti-growth signals - but cancer cells ignore them
cancer cells ignore apoptosis signals
defective in cell cycle control mechanisms to stop cell cycle
gets help from stromal cells
induces angiogenesis
invasive to other tissues
do not show replicative-senescence but are immortal

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6
Q

What is erythropoeitin?

A

A small protein growth factor - remember that cell growth is controlled by growth factors.

Produced by kidney when RBC numbers are low.

Stimulates bone marrow to produce more RBCs.

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7
Q

What is the important biological distinction between normal cells and cancer cells?

A

Cancer cells require little growth factors.

**Normal cells - have strong requirement for growth factors.

**Cancer cells - become independent of stimulation that is normally required by cells to proliferate.

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8
Q

What are the two heritable properties of cancer cells?

A

(1) Reproduce in defiance of normal restraints on cell division and cell growth.
(2) Invade areas normally reserved for other cells.

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9
Q

How does cancer actually kill?

A

As a tumor grows and spreads, it squeezes or destroys blood vessels, nerves - until an organ can no longer do its job - death results.

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10
Q

What is the pathology definition of cancer?

A

An abnormal cell that grows (increases in mass) and proliferates (divides) out of control will give rise to a tumor or neoplastic growth.

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11
Q

What happens if neoplastic cells do not become invasive?

A

The tumor is benign - can surgically remove local mass as cure.

benign tumor = NO cancer

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12
Q

When is a tumor considered malignant?

A

If cells have the ability to invade surrounding tissues.

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13
Q

What is the most common classification of cancer?

A

carcinoma

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14
Q

What are carcinomas derived from?

A

Carcinomas are cancer of epithelial cells (most common).

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15
Q

What are sarcomas derived from?

A

Sarcomas are cancer of connective tissue and muscle tissue.

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16
Q

What are leukemias and lymphomas derived from?

A

Leukemias and lymphomas are cancer of white blood cells and their precursors.

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17
Q

What is the nomenclature for benign tumors?

A

Adenoma - which is a benign epithelial tumor with glandular organization.

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18
Q

What is the nomenclature for a malignant epithelial tumor with glandular organization?

(hint: benign tumor of this type is called adenoma)

A

Malignant tumor of same type is adenocarcinoma.

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19
Q

What are basal-cell carcinomas derived from?

A

Basal-cell carcinoma is cancer of a keratinocyte stem cell in the skin.

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20
Q

What are melanomas derived from?

A

Melanoma is cancer of the pigment cells in the skin (melanocytes).

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21
Q

Besides the origin of cell type, what is the difference between basal-cell carcinomas and malignant melonomas?

A

> Basal-cell carcinomas - rarely metastasize.

> Malignant Melonomas - metastasize widely (more deadly).

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22
Q

What is the definition of metastases?

A

Cancer cells can break loose, enter into blood or lymph, travel to new areas and form secondary tumors.

** In cancer, metastases kills patients.**

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23
Q

True or False:

All tumors arise from a single ancestor.

A

True

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24
Q

A mutation in what gene causes colon cancer?

A

mutation in APC gene (tumor suppressor)

  • *cells with APC mutation gain an advantage in growth**
  • *form polyps**
  • *at this stage the tumor is a benign tumor**
  • *mutation in Ras - becomes a “cancer” gene**
  • *lose p53 = carcinoma (epithelial cells)**
  • *tumor moves into bloodstream**
  • *gains capacity to invade**
  • *now a malignant tumor**
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25
Q

What results in the production of a Philadelphia chromosome?

A

translocation between Chr 9 + 22

Philadelphia chromosome is a smaller chromosome

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26
Q

What disease does the Philadelphia chromosome cause?

A

Chronic Myelogenous Leukemia

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27
Q

What are the two types of carcinogens?

A
  • chemical carcinogens

- radiation (X-rays, UV)

28
Q

What 3 types of natural mechanisms does our body have in helping to prevent cancer?

A
  • DNA repair mechanism
  • cell cycle controls
  • apoptosis
29
Q

What develops into a carcinoma to cause cervical cancer?

A

> cell proliferation begins in the basal epithelia
low grade or high grade intraepithelial neoplasia

at this stage - surgical removal will cure

30
Q

What is the best weapon that we have against cancer?

A

early detection

31
Q

Why is obesity related to a higher incidence of cancer?

A

more cells/more chance of mutations

32
Q

True or False:

The loss of programmed cell death or DNA repair leads to progeny cells that continue to accumulate mutations leads to cancer.

A

True

33
Q

What is the most deadliest aspect of cancer?

A

Metastasis - can’t eradicate by surgery or irradiation.

34
Q

What percentage of invading cells the become invasive and form new colonies to cause cancer survive?

A

1/1,000 invading cells survive.

35
Q

What is angiogenesis?

A

The formation of new blood vessels that sprout from pre-existing blood vessels.

36
Q

What is neovascularization?

A

The formation of new blood vessels basically from scratch.

37
Q

Tumors need cross talk between what types of cells?

A

> Tumors are made up of many cells.
Cancer cells, fibroblasts, and stroma: supportive connective tissue.
Tumor needs cross talk between these cells.

**Stromal cells (e.g., fibroblast and WBCs) **

38
Q

True or False:

Cancer is an environmental disease.

A

True

In U.S. and Europe 1 out of 5 people die of cancer.

In Third World countries infectious diseases kill more people - lucky if get cancer cause lived long enough to get it.

39
Q

What percentage of lung, kidney, and bladder cancer does tobacco account for?

A

24%

40
Q

What percentage of bowel, pancreas, prostate, and breast cancer does a high fat/low fiber diet account for?

A

37%

41
Q

What test is used in the laboratory to test potential chemicals to determine if they are carcinogens?

A

Ames test (bacteria needing histidine).

42
Q

What type of cancer can ulcers and Helicobacter pylori cause?

A

stomach cancers

43
Q

What type of cancer can AIDS:HIV cause?

A

Kaposi’s sarcoma

44
Q

What substance is the most important environmental cause of cancer?

A

Tobacco - 90% of patients with lung cancer smoked.

45
Q

What percentage of lung cancer victims survive?

A

13%

46
Q

What are the genetic causes of cancer?

A
  • tumor suppressor genes

- oncogenes

47
Q

What are cancer critical genes?

A

Genes whose alteration frequently results in cancer.

48
Q

What are the two broad types of mutations in cancer?

A

(1) overactivity mutations - gain of function - oncogenes - involves single mutation event and activation of gene causing proliferation (dominant).

(2) underactivity mutations - loss of function - tumor suppressor genes - involve genes that inhibit growth.
mutation event: one gene - no effect; second mutation - causes problems (recessive).

49
Q

Are oncogenes considered a overactivity mutation or underactivity mutation?

A

Overactivity mutations - gain of function - oncogenes - involves single mutation event and activation of gene causing proliferation (dominant).

Oncogenes = gas pedal

Mutation of a single copy of proto-oncogene converts it to an oncogene and has dominant effect.

50
Q

Are tumor suppressor genes a overactivity mutation or underactivity mutation?

A

Underactivity mutations - loss of function - tumor suppressor genes - involve genes that inhibit growth.

Mutation event: one gene - no effect; second mutation - causes problems (recessive).

Tumor-suppressor genes = brakes

Tumor suppressor genes have changes causing cancer that is recessive - both copies must be mutated.

51
Q

What is the third type of mutations seen in cancer?

A

DNA maintenance genes.

> subset of tumor suppressor genes
mutations involve inactivation of caretaker genes that create genomic stability
include DNA repair genes, checkpoint genes

52
Q

What does the transformation activity of Rous sarcoma virus (RSV) depend on?

A

v-src oncogene

RSV is a retroviruses which causes cancer

53
Q

What are transformed cells?

A

Small colonies of proliferating cells caused by oncogene.

54
Q

How do retroviruses cause cancer?

A

Virus hijacks c-src, makes a mutation so c-src is activated like crazy.

retroviruses hijack proto-oncogenes and activate them by either over-expression (from a strong viral promoter) or cause mutations of proto-oncogene into oncogene

55
Q

What was the first human oncogene discovered?

A

Ras - which is a monomeric GTPase for signal transduction.

**Ras oncogenes - cannot shut off MAP kinase pathway by hydrolyzing GTP to GDP (remember cholera).

**Intracellular signal transducer molecule overproduction - Ras.

56
Q

What are the 4 mechanisms of oncogene activation?

A

(1) Deletion or Point Mutation
(2) Regulatory Mutation
(3) Gene Amplification
(4) Chromosomal Rearrangement

57
Q

How does deletion or point mutations in the coding sequence activate oncogenes?

A

Deletion of point mutation in coding sequence - makes hyperactive protein (e.g., Ras codon 12 Gly to Val: keeps Ras protein in active state - cannot shut off MAPK pathway).

58
Q

How does a regulatory mutation activate oncogenes?

A

Regulatory mutation - produce more normal protein - promoter mutation.

59
Q

How does gene amplification activate oncogenes?

A

Gene amplification - several copies instead of 1 copy - normal protein overproduced.

60
Q

How does chromosomal rearrangement activate oncogenes?

A

Chromosomal rearrangement - brings new regulatory sequence that causes overproduction OR creates overactive fusion protein.

> e.g., EGF receptor - rearrangement removes extracellular domain.

  • Truncated EGF receptor - becomes active without ligand.
  • Receptors dimerize to fool cell to produce stimulator signal to divide.
  • Associated with glioblastoma - brain tumor.
61
Q

How can ligands cause cancer?

A

If ligands produced constitutively they cause proliferation and grow all the time (cancer cells produce own ligand - autocrine signaling).

62
Q

How can receptors cause cancer?

A

Tyrosine kinase receptors - when RTKs constitutively produced don’t even need a ligand.

63
Q

How can transcription factors cause cancer?

A

In nucleus, these proteins constantly induce transcription - e.g., fos an jun activate gene expression including those important for cell cycle progression - over production can lead to oncogene.

64
Q

How can cell-cycle proteins cause cancer?

A

Anything that can cause cell proliferation - overproduction of these proteins leads to cancer.

65
Q

How do proteins that inhibit apoptosis cause cancer?

A

Like Bcl2 (promotes cell survival despite DNA damage) - overproduction allows cancerous cells to survive and grow.

66
Q

What are the properties and characteristics of Bcl2 oncogene?

A

> example of rearrangement mutation

> B cell lymphoma identified as translocated gene

> in cancer cells Bcl2 locus on Chr 18 undergoes a reciprocal translocation with part of Chr 14 gene (exchange Chr pieces)

> this places Bcl2 gene under control of new enhancer (Ab heavy chain gene) - very active in B cells

> results in expression of Bcl2 in B cells

> instead of expression of Ab makes lots of Bcl2

> so prevents apoptosis of damaged cells - get DNA damage and cell proliferation

Molecular Biology Exam 3 (9 decks)

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