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Pharmacy Practice 5 > Cancer Biology > Flashcards

Cancer Biology Flashcards

1
Q

define neoplasm

A

new growth, proliferation of cells

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2
Q

define neoplasia

A

formation of a neoplasm

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3
Q

define metaplasia

A

an adaptive substitution of one type of adult tissue to another type of adult tissue

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4
Q

define metastasis

A

spreading of neoplasm to distant sites

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5
Q

define adenoma

A

a benign epithelial neoplasm which produces a gland-like pattern or derives from glands

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6
Q

define papilloma

A

benign tumor of surface epithelium

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7
Q

define polyp

A

benign growth from mucosal surface of intestine or nose

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8
Q

what are the T,N,M staging associated with the stage of cancer?

A

T= size and extent of invasion
N= presence and number of lymph nodes involved
M= presence of distant metastasis

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9
Q

define stage 0 cancer

A

carcinoma that has not invaded into other tissue

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10
Q

define stage 1 and 2 cancer

A

variable, depends on tumor type and location

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11
Q

define stage 3/4 cancer

A

cancer has spread throughout the body

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12
Q

the epidermis of the skin consists of what cell type?

A

keratinocytes

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13
Q

the dermis of the skin consists of what cell type?

A

fibroblast

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14
Q

the hypodermis of the skin consists of what cell type?

A

adipocytes

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15
Q

which type of cancer cell is responsible for the bulk of tumor cell proliferation and is susceptible to cancer therapy?

A

TA cells

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16
Q

what are the cancer stem cell markers in the breast?

A

CD44, CD24

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17
Q

what is the cancer stem cell marker in melanoma?

A

CD20

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18
Q

what are the cancer stem cell markers in the prostate?

A

CD44, a2b1, CD133

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19
Q

what are the cancer stem cell markers in pancreatic cells?

A

CD44, EpCam, CD24

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20
Q

what are the different methods of how our body repairs DNA?

A

base-excision repair
nucleotide-excision repair
transcription-coupled repair
mismatch repair
double-strand-break repair

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21
Q

what is required to allow accumulation of sufficient mutations to generate cancer?

A

chromosomal instability

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22
Q

what is xeroderma pigmentosum?

A

an autosomal recessive disorder causing severe light sensitivity, severe pigmentation irregularities, and early onset of skin cancer

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23
Q

why are patients with xeroderma pigmentosum so vulnerable to skin cancer?

A

they cannot repair damage caused by UV rays

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24
Q

which factors are associated with familial melanoma?

A

p16/INK4a
CDKN2A
CDK4
12q14

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25
Q

which chromosomes are associated with burkitt’s lymphoma?

A

8q24, 14q, 22q, and 2p

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26
Q

how do epigenetic alterations affect gene epxression?

A

alters without changing DNA sequences, thereby turning gene expression on or off
also causes histone methylation, de-acetylation and phosphorylation

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27
Q

what are 2 main causes of human cancer?

A

loss of histone acetylation by histone deacetylase
or
induction of histone methylation by histone methyltransferase

28
Q

what are epigenetic factors that cause tumorigenesis?

A

DNA methylation
histone methylation
histone deacetylation

29
Q

how can we reverse DNA methylation?

A

inhibitors of DNA methyltransferase

30
Q

how do we reverse histone methylation?

A

inhibitors of histone methyltransferase (HMAT)

31
Q

how do we reverse deacetylation?

A

inhibitors of histone deacetylase (HDAC)

32
Q

list the examples of genetic lesions that usually affect only one gene during tumorigenesis

A

Point Mutations
Frame Shift Mutations
Insertions/Deletions
Amplification

33
Q

list the examples of Major Chromosome Abnormalities during tumorigenesis

A

Translocations
Chromosomal Loss

34
Q

how is the C-Myc gene associated with Burkitt’s lymphoma?

A

C-Myc gene is normally off, but is kept on by immunoglobulin gene enhancer due to chromosomal translocation in B-cell tumors

35
Q

chromosomal translocation is found in most cases of?
what forms as a result and causes said formation to not be under normal control?

A

chronic myelogenous leukemia (cancers of bone marrow and white blood cells)
BCR-ABL gene

36
Q

what does the ABL1 gene do?

A

encodes tyrosine kinase ABL. it is activated in response to negative factors like growth factors and DNA damage to stimulate cell proliferation or differentiation, or survival or death

37
Q

cancer is caused by alterations in? (these are our targets for therapeutic interventions)

A

tumor-suppressor genes, oncogenes, and tumor modifier genes (microRNAs)

38
Q

what do tumor-suppressor genes do?

A

they encode proteins to inhibit cell proliferation and stabilize the genome

39
Q

genetic alterations of tumor suppressor genes during tumorigenesis are classified as what kind of mutation? are they dominant or recessive?

A

loss of function
recessive

40
Q

what is retinoblastoma?

A

cancer caused by alterations of tumor-suppressor genes. it forms retinoblastoma protein which is a substrate for cyclin-dependent kinase

41
Q

what is the function of a transcription factor?

A

to help transcribe genes by converting DNA to RNA

42
Q

what is E2F?

A

an important transcription factor that helps cells enter S phase

43
Q

what is p53?`

A

a transcription factor that binds with DNA to activate or repress the expression of genes involved in growth arrest, apoptosis, DNA repair, and angiogenesis

44
Q

what are oncogenes?
what type of mutation are they? is it dominant or recessive?
how do they progress?

A

altered proteins deriving from proto-oncogenes (normal genes) with increased expression
gain of function
dominant
by viral infections or exposure to carcinogens

45
Q

proto-oncogenes encode for what signaling proteins?

A

receptors associated binding proteins, serine/threonine kinases, and non-receptor tyrosine kinases

46
Q

how are oncogenes activated?

A

Point mutation
Amplification
Chromosome translocation
Overexpression due to DNA demethylation

47
Q

why is the Ras gene important and what does it do?

A

it’s the most commonly mutated gene. it stimulates cell growth

48
Q

what are tumor modifier genes (MicroRNAs)?
how do the interact with oncogenes?

A

genes which don’t encode proteins. they produce RNA to block gene expression by causing mRNA degradation or block protein translation
they suppress their expression

49
Q

what is the deterministic pathway to cancer?

A

different tumors of same cancer type occur via mutation of each gene

50
Q

what is the plastic pathway to cancer?

A

different tumors evolve along variable pathways via mutation of many possible sites

51
Q

how does telomere erosion work?

A

a slow process of telomere shortening, leading to decreased proliferation of tumor cells

52
Q

how does telomere uncapping work?

A

a rapid pathway to increase apoptosis and DNA damage response to decrease proliferation of tumor cells

53
Q

what is GRN163L?

A

an anti-telomerase agent which targets the telomerase RNA template to affect telomere erosion and induce telomere uncapping

54
Q

what are examples of direct vessel signaling inhibition of tumor angiogenesis?

A

VEGF ligand inhibitors
VEGFR receptor inhibitors
growth factor inhibitors

55
Q

what drug class used for tumor angiogenesis inhibition blocks endothelial and pericyte cell activation to block proliferation?

A

tyrosine kinase inhibitors

56
Q

what is paget’s theory of metastasis?

A

Cells are dispersed randomly but only grow in organs
that provide the correct factors necessary for growth

57
Q

what is ewing’s theory of metastasis?

A

The first site to which a cancer metastasizes is the
closest one in which there are small blood vessels.

58
Q

An aberrant proliferation of cells is _______, and discontinuous spread of a neoplasm to distant sites through lymphatic channels, blood vessels
etc. is ________.
A. Adenoma and Papilloma
B. Hepatoma and melanoma
C. Neoplasm and metastasis
D. Papilloma and Polyp
E. Neoplasm and metaplasia

A

C

59
Q

Skin cancer progression is a multi-stage process that involves
I. Initiation stage by mutation of the K-Ras gene
II. Activation of the Ras-Raf-MAPK pathway
III. Promotion and progression stage to invasive carcinoma
A. I only
B. III only
C. I and II only
D. II and III only
E. I, II and III

A

D

60
Q

What is “false” about Tumor suppressor genes ?
A. Encode proteins that inhibit cell-proliferation and
ensure stability of the genome.
B. “gain of function” genetic alterations occur in this
class of genes.
C. Usually recessive in nature.
D. Includes RB and p53 proteins.
E. RB is controlled through phosphorylation

A

B

61
Q

An adenocarcinoma of the colon diagnosed at Stage
I is a:
A. Benign neoplasm that can be treated by surgical
removal and no further treatment.
B. Malignant neoplasm that has spread widely
throughout the body showing distant metastasis
C. Malignant neoplasm of glandular origin which is
restricted at the site of origin in colon (carcinoma in situ)
D. Epithelial cancer that has invaded into the
underlying connective tissue.
E. Aggressive colon cancer containing a combination of
epithelial and stromal cells

A

C

62
Q

Which of the following is true for p53?
I. Is a transcription factor that binds to DNA in a sequence specific manner.
II. Activation and stabilization of p53 occurs by
phosphorylation and acetylation.
III. Cellular responses to activated p53 include growth
arrest, DNA repair and apoptosis.
IV.A downstream target of p53 is p16.
A. II, III
B. I, II, III
C. I, III, IV
D. II, III, IV
E. I, II, III, IV

A

B

63
Q

define carcinoma

A

Arise from epithelial precursor cells

64
Q

define sarcoma

A

Arise from stromal or mesenchymal components of organs

65
Q

define carcinosarcomas and malignant teratomas

A

mixture of epithelial and mesenchymal cells

66
Q

list tumors that are undifferentiated and highly metastatic

A

Squamous cell carcinoma
Adenocarcinoma
Fibrosarcoma

Pharmacy Practice 5 (8 decks)

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