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Cancer (Bio152) > Final > Flashcards

Final Flashcards

1
Q

What are the traditional cancer managements?

A

surgery, chemotherapy and radiotherapy

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2
Q

How is cancer stratified?

A

using gene expression arrays allows survillence of expression levels which classify cancers into subgroups

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3
Q

What are the three types of B lymphomas stratified with gene expression arrays?

A

primary mediastinal, germinal-center, and activated

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4
Q

How has the NFKB pathways used to target b cell lymphoma?

A

by targeting upstream IKK

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5
Q

What is the future hope of genomics and proteomics?

A

to assign each patient’s tumor to a specific subtype of disease and to apply drug therapies that are proven to be effective

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6
Q

What is the difference between Pharmacokinetics and pharmacodynamics?

A

PK is the study of the rate at which drugs are administered. PD is the study at which cells or molecular targets actually respond to administered drugs

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7
Q

What are most drugs targeting?

A

most drugs are targeting oncogenic receptor downstream tyrosine kinase pathway

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8
Q

What is does the term druggability imply?

A

that the target molecule has structure that should make it vulnerable to attack and inhibition by low molecule-weight compounds,

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9
Q

What is necessary for a protein to be considered druggable?

A

a well-defined catalytic cleft which allow small organic molecules to bind

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10
Q

What is meant by the ideology of “rational drug design?’

A

drugs should be targeted against specific proteins know to be malfunctioning within cells, the candidacy of these proteins as attractive targets for therapeutic intervention, detailed molecular structures of such target proteins should inform the design of the chemical structures of the drugs that are to be developed

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11
Q

what is a teratoma

A

benign tumor formed by an embryonic stem cell in which a wide variety of differentiated cell types are formed

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12
Q

what is warburg effect?

A

aerobic glycolysis

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13
Q

what type of cancer derives from connective tissues?

A

sarcomas

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14
Q

what type of cancers derive from secreting epithelium?

A

adenocarcinoma

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15
Q

what are some characteristics of cancer?

A

evading apoptosis, insensitivity to antigrowth signals, sustained angiogenesis, tissue invasion and metastasis, limitless replicative potential

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16
Q

what are the classification of cancer cells according to cellular growth?

A

normal, hyperplasia, mild dysplasia, severe dysplasia, and metastasis

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17
Q

how is cancer graded according to the differentiation of the tumor?

A

G1: well differentiated
G4: undifferentiated

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18
Q

what was the conclusion of Rous sarcoma virus?

A

he broke a sarcoma into piece which was then filtrated and injected into anther chicken which then developed a sarcoma. this concluded that RSV was able to be multiplied and cause cancer

19
Q

true or false. the src antigen is also resent in uninfected cells

A

true

20
Q

what does src encode?

A

tyrosine kinase

21
Q

true or false, c-src is a proto-oncogene

A

true

22
Q

Describe the process that was used to detect oncogenes in the DNA of cancer cells?

A

DNA is extracted from cancer cells which is then into a phosphate buffer with Ca forming crystals. The crsytals are added to normal mouse fibroblasts. If a transforming gene is present the donor DNA would become incorporated into the genome and then proliferation occurs. the cells are then injected into a mouse to determine if a tumor will form

23
Q

What are the pleiotropic actions of a protein kinase

A

GSK-3B- proliferation
BAD-apoptosis
HIF-1a-angiogenesis
TSC2- protein synthesis

24
Q

what are the types of cell communication systems?

A

autocrine- a cell signaling to itself
paracrine- cell signaling to a nearby tissue
endocrine- cell signaling to a distant cell

25
Q

Explain the Patched-Smoothened signaling system

A

when a hedgehog ligand binds to the patched receptor allowing Gli to move into the nucleus to induce transcription. without the ligand patched inhibits smoothened from moving into the primary cilia creating gli to act as repressor

26
Q

What is the Hayflick phenmenon

A

the number of times a normal human cell population will divide until cell division stops (senescence)

27
Q

true or false. senescent cells may remain metabolically active but the lost the ability to reenter the cell cycle

A

true

28
Q

which two cdks are increased during the onset of senescence

A

p16 and p21

29
Q

what is crisis?

A

state arising when cells lose telomeres of adequate length, resulting i end to end fusion of chromosomes and widespread death of apoptosis

30
Q

what are telomeres

A

repeating hexanucleotide sequence

31
Q

how do cancer cells escape crisis?

A

by expression of telomeraseTERT

32
Q

By what mechanism can telomeres be maintained

A

by the ALT mechanism which is used by human tumor cells that lack significant telomerase activity

33
Q

True or False. Age does not play a large factor in the incidence of cancer.

A

False. Age plays a large factor

34
Q

What is the alternative model

A

many steps of tumor progression are driven by heritable alterations accumulated by developing tumor cells, notably somatic mutations and promoter methylation events

35
Q

what is field cancerization?

A

organs affected by sporadic tumors occasionally sprout multiple, apparently independently arising tumors

36
Q

what causes the genetic alteration in the field of cancerization?1

A

somatic mutations

37
Q

what is the cellular Darwinian Evolution theory?

A

Random mutations are presumed to create genetic variability in a cell population. Forces of selection may favor the outgrowth of individual cells that have mutatnt alleles, favoring proliferating and survival

38
Q

Combining Darwin’s evolution theory with multi-step tumorgenesis what can researchers can conclude?

A

tumorgenesis is a succession of clonal expansion

39
Q

What must the Darwinian evolution be modified?

A

events during tumorgenesis are epigenetic and the rate of genetic diversification can occur very rapidly

40
Q

what is the cause and effect of clonal diversification?

A

it caused by high mutation rates which leads to tumor heterogeneity

41
Q

What is heterotypic signaling?

A

communication between dissimilar cell types used to encourage proliferation of the other type of cells nearby

42
Q

In normal cell types what does heterotypic signaling depend on?

A

mitogenic growth factors, growth-inhibitory signals, trophic factors

43
Q

what causes stromalization of many advanced tumors?

A

the level of PDGF expression increases

44
Q

What are the sequences of the invasion-metastasis cascade?

A

primary tumor formation, localized invasion, intravasation, transport throughout circulation, extravasation, micrometastasis, macrometastasis

Cancer (Bio152) (2 decks)

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