Cancer Flashcards

1
Q

Why are malignant tumours hard to eradicate?

A

Malignant tumors typically give rise to metastases

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2
Q

Benign tumors

A

enclosed by a connective tissue capsule

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3
Q

malignant tumors

A

invasive cancerous gland tubules

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4
Q

the five most common cancers

A

Lung, stomach, breast, colon/ rectum, and uterine cervix

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5
Q

The growth of a typical human tumor

such as a tumor of the breast

A

May take years for the tumor to become noticeable

The doubling time of a typical breast tumor, for example, is about 100 days

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6
Q

What cancer arises from the translocation between chromosomes 9 and 22

A

chronic myelogenous leukemia

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7
Q

Philadephia chromosome

A

The translocation between chromosomes 9 and 22 produces small chromosome

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8
Q

Cancer incidence as a function of age

A

The incidence of cancer rises steeply as a function of age.

Due to it requiring multiple mutations

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9
Q

Cancer following exposure to a carcinogen

A

Delayed

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10
Q

In the normal stratified squamous epithelium, where are dividing cells

A

dividing cells are confined to the basal layer

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11
Q

In low-grade intraepithelial neoplasia, where are dividing cells

A

dividing cells can be found throughout the lower third of the epithelium

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12
Q

In high-grade intraepithelial neoplasia, where are dividing cells

A

cells in all the epithelial layers are proliferating and show no sign of differentiation

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13
Q

When does true malignancy begin?

A

cells move through or destroy the basal lamina and invade the underlying connective tissue.

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14
Q

How does a tumour develop

A

through repeated rounds of mutation and proliferation, giving rise eventually to a clone of fully malignant cancer cells

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15
Q

How does each mutation affect cell proliferation

A

enhances

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16
Q

Genetic instability compared to tumours

A

Normal cells have little instability

cells with too much instability genetic result in failure to survive

cells with optimum genetic instability cause cancerous cells

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17
Q

Two types of derangement that can give rise to the unbridled proliferation characteristic of cancer

A

Stem cell fails to produce one non stem cell daughter in each divsion and thereby proliferates to form a tumour

daughter cells fail to differeciate normallly and instead proliferate to form a tumour

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18
Q

Steps in the process of metastasis

A

Cell growth as benign tumour in epithelium

break through basal lamina

invade capillary

escape to blood vessel and proliferate

Tumor cells may enter the bloodstream directly by crossing the wall of a blood vessel, as diagrammed here, or, more commonly perhaps, by crossing the wall of a lymphatic vessel that ultimately discharges its contents (lymph) into the bloodstream

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19
Q

The Ames test

A

for mutagenicity

see if carinogen is mutagenic and results in colonies formed in independent culture

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20
Q

Metabolic activation of a carcinogen

A

many chemical carcinogens have to be activated by a metabolic transformation before they will cause mutations by reacting with DNA

21
Q

Which cancer has increased/ decreases over the years from 1930-2000

A

lung increased due to smoking. Females more recently due to advertising

stomach has decreased

breast and prostate same

22
Q

Effects of childbearing on the risk of breast cancer.

A

Having children earlier decreased the likelyhood of having breast cancer

23
Q

Oncogenes genes mutation act

A

dominantly

a gain-of- function mutation in a single copy of the cancer-critical gene can drive a cell toward cancer

24
Q

tumour supressor genes mutation act

A

recessive

the function of both alleles of the cancer-critical gene must be lost to drive a cell toward cancer

25
What do mutations of tumour supressor genes and oncogenes result in?
cells that proliferate abnormally
26
Hereditary retinoblastoma
Inherit mutant Rb gene In the hereditary form, all cells in the body lack one of the normal two functional copies of the Rb tumor suppressor gene, and tumors occur where the remaining copy is lost or inactivated by a somatic mutation
27
nonhereditary retinoblastoma
all cells initially contain two functional copies of the gene, and the tumor arises because both copies are lost or inactivated through the coincidence of two somatic mutations in one line of cells
28
Ways proto-oncogenes can be made overactive
deletion or point mutation gene amplifaction chromosome rearrangement
29
overactive proto-oncogenes convert to
oncogenes
30
A cell that is defective in only one of its two copies of a tumor suppressor gene, the Rb gene —usually behaves as a normal, healthy cell; how may it come to lose the function of the other gene copy as well
non disjunction, duplicaiton, recombination, conversion, deletion, point mutation
31
Having two fused oncogenes can result in?
decreased tumor free cells
32
Rb protein affect on cell cycle what phase?
inhibits E2F preventing entry to S phase
33
What does phosphorylated Rb result in
inactive Rb and active E2F leads to expression of S phase genes
34
Damaged DNA pathway
Chk2 activated --> rapid G1/S block P53 stabilized and causes apoptosis, g1/g2 arrest, and DNA repaire
35
Papillomaviruses give rise to
cancer of uterine cerix by E6 and E7 which inhibit Rb and p53 causes cell prolliferation
36
How shortened telomeres may lead to
chromosomal instability and cancer.
37
The barriers to metastasis
difficult for the cells to enter in blood steam
38
Each tumor will generally contain a different set of
genetic lesions
39
Effects of ionizing radiation on normal cells and tumour cells
Cancer cells tend to be more susceptible than normal cells to the damaging effects of ionizing radiation because they lack an ability to arrest the cell cycle and make the necessary repairs
40
The conversion of the Abl proto- oncogene into an oncogene
The chromosome translocation responsible joins the Bcr gene on chromosome 22 to the Abl gene from chromosome 9 in chronic myelogenous leukemia
41
Gleevec
blocks the activity of Bcr-Abl protein and halts chronic myeloid leukemia. Gleevec sits in the ATP-binding pocket of the tyrosine kinase domain of Bcr-Abl and thereby prevents Bcr-Abl from transferring a phosphate group from ATP onto a tyrosine residue in a substrate protein. This blocks onward transmission of a signal for cell proliferation and survival.
42
angiogenesis
A new blood capillary forms by the sprouting of an endothelial cell from the wall of an existing small vessel.
43
What stimulates angiogenesis
Lack of oxygen
44
Von Hippel-Lindau disease
VHL hereditary cancer syndrome | • Germ-line mutation of tumor suppressor gene (VHL)
45
VHL
tumor suppressor gene
46
Somatic VHL mutations common in
in sporadic CNS hemangioblastoma & kidney cancer – Kidney cancer • 3% of all malignancies • Incidence: 4500 new cases/year (Canada) • Mortality: 1500 death/year (Canada)
47
Reintroduction of wild-type VHL in VHL-/- RCC cells
restores their dependency on specific growth factors to proliferate
48
VHL mutants found in patients fail to
ubiquitinate p220 and p100