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Biochem 1502 > Cancer > Flashcards

Cancer Flashcards

1
Q

Most common new case of cancer in men

A

Prostate

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2
Q

Most fatal cancer in men

A

lungs/bronchus, prostate, GI

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3
Q

Most common new case of cancer in females

A

Breast

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4
Q

Most fatal cancer in females

A

lungs/bronchus, breast, GI

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5
Q

Primary prevention

A

Smoking cessation, polypectomy (GI)

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6
Q

Prostate measure for cancer

A

PSA

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7
Q

Breast cancer measure for cancer

A

mammogram

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8
Q

Theory of Clonal Evolution

A

initial mutation occur sin a single cell that gives this cell a selective growth advantage, this populates and a single cell within the clonal population acquires a second mutation giving it a selective growth advantage. Repeated cycles lead to a malignant tumor with mutations in KEY genes

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9
Q

Cancer is due to multiple genetic changes that allow it to

A

be freed of programmed restraints and lead to abnormal progeny

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10
Q

5 Hallmarks of cancer

A

Self-sufficiency for growth signals
Insensitivity to growth inhibitory signals
evasion of apoptosis
limitless replicative potential (immortal)
sustained angiogenesis

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11
Q

Neoplastic transformation occurs only when the mutations occur in

A

KEY genes

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12
Q

regulation of cell growth occurs via

A

Growth factors, growth factor receptors, signal transduction and cascade, transcription factors

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13
Q

Proto-oncogene

A

gene whose protein product controls cell growth and differentiation

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14
Q

oncogene

A

mutation in a proto-oncogene that causes qualitative or quantitative changes in gene products, in which expression results in NEOPLASTIC TRANSFORMATION

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15
Q

Tumor Suppressor genes

A

genes whose reduced function can lead to neoplastic changes, they normally negatively regulate growth

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16
Q

proto-oncogene protein products _______ cell growth and division

A

stimulate

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17
Q

Tumor suppressor protein products _______ cell growth and division

A

repress

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18
Q

Mutations to tumor suppressor genes can lead to

A

transformations by removing the restraints on growth

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19
Q

Examples of tumor suppressor genes

A

Retinoblastoma, p53 (inhibit cell cycle), BCRA1 and 2 (breast cancer - DNA repair pathways)

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20
Q

p53

A

most COMMON mutated gene in cancer, due to its unique functions. contributes to genomic instability

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21
Q

Oncogenes are _____ in their action

A

dominant - meaning only one copy of the gene needs to be mutated bc activation will result in unregulated function

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22
Q

tumor suppressors are ______ in action

A

recessive - meaning both copies must be mutated in order to be inactivated by mutations to lose function

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23
Q

DNA repair and mutations

A

increase in DNA errors or decreases in DNA repair, mutations in pro to-oncogenes and tumor suppressors lead to cancer

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24
Q

Follicular lymphoma

A

Translocation of BCL-2 to a chromosome where it is constitutively overexpressed, causing resistance to apoptosis

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25
Q

Limitless replication in cancer cells is achieved by

A

reappearance of telomerase, which lengthens telomeres evading shortening chromosomes

26
Q

Two examples of diseases caused by mutation in DNA repair genes

A

Xeroderma pigmentosum and Hereditary Nonpolyposis Coli

27
Q

In a quiescent vessel, inhibitors of angiogenesis exist that off-set the inducers. In cancer,

A

lack of inhibitors or overexpression of inducers allows recruitment of vessels

28
Q

Possible mechanism for recruitment of vessels to cancer cells

A

mutation in p53 gene; p53 normally suppress angiogenesis by inducing a angiogenesis inhibitor

29
Q

How do cancer cells evolve the metastatic ability

A

acquiring genes that allow them to break down tissue structure and invade the basement membrane to allow migration to other side of vessel

30
Q

Angiogenesis inhibitor

A

induced by p53

31
Q

Energy shift in cancer cells

A

Cancer cells shift to glycolysis followed by lactic acid formation even in AEROBIC conditions

32
Q

Lower efficiency of energy production in cancer cells is offset by….

A

upregulation of GLUT1 glucose transporters

33
Q

PET

A

visualize glucose uptake to look for tumors

34
Q

What genes are associated with glycolytic fueling

A

Ras, myc, and p53

35
Q

HYPOXIC conditions result in

A

upregulation of GLUT1 glucose transporters and upregulation in glycolytic enzymes

36
Q

Why do cancer cells switch to glycolysis

A

to generate intermediates for biosynthetic processes (nucleosides and amino acid production)

37
Q

Colon cancer is well understood and is known to be a

A

multistep process of accumulated mutations

38
Q

Stem Cell Theory of Cancer

A

Tumors contain cancer stem cells with indefinite proliferative potentials, they are self-renewing and responsible for all components of the tumor; drug resistant

39
Q

Inherited mutations in tumor suppressor genes occur

A

in 5-10% of al cancers

40
Q

Inherited malignant tumors most commonly occur in

A

breast and colon cancer

41
Q

BRCA1-2

A

mutated BRCA1(50%)-2(30%) mutation accounts for hereditary forms of breast cancer, predisposes ind to breast and ovarian cancer and at a younger age (often involving both breasts); repair of DOUBLE STRANDED DNA breaks

42
Q

Adenomatous Polyposis Coli (APC)

A

5-10% inherited colorectal cancer, accounting for Familial Adenomatous Polyposis (FAP), multiple polyps in the rectum at a young age, but normal rate of carcinoma formation from polyp

43
Q

APC protein role

A

inhibition of beta-catenin in normal cells in which beta-catenin is adhered to cell-cell surface proteins and cadherins. In cancer, no inhibition of beta-catenin results in free movement into the nucleus and transcription of genes for proliferation

44
Q

Hereditary Non-Polyposis Colorectal Carcinoma (HNPCC)

A

polyp rapidly transforms into carcinoma but rate of polyp formation is normal

45
Q

Predisposition for HNPCC is due to inherited mutations in

A

Mismatch repair genes

46
Q

Chemical carcinogenesis - INITIATION

A

carcinogen induces alterations in the genetic makeup that confers a neoplastic growth potential

47
Q

Chemical carcinogenesis - PROMOTION

A

mediated by chemicals that are not carcinogenic but promote tumor development (hormones, high fat diet, alcohol) transform the initiated cell into a population of cancer cells (MODIFIABLE)

48
Q

Enzymes important in carcinogen metabolism

A

Cytochrome p450 oxidase, and N-acetyl transferase (drugs may become active or inactive by metabolism to cause cancer)

49
Q

Examples of environmental carcinogens

A

Polycyclic aromatic hydrocarbons (PAH) and aromatic amines from cigarette smoke leave residues on DNA (fingerprinting exposure and indicating DNA damage)

50
Q

PAH and aromatic amines contribute to which cancer types

A

lung, bladder, and breast depending on exposure

51
Q

Polymorphisms in drug metabolizing enzymes

A

explain differences in susceptibility within populations to carcinogens

52
Q

polymorphisms is the new susceptibility factor that may be the best predictor of cancer risk

A

inter-inividual variation in P450, glutathione transferase and N-acetyl transferase gene influence individual response

53
Q

Susceptibility factors include:

A

polymorphisms, predisposition, age, ethnicity, gender, health impairment, nutritional impairment

54
Q

p53 mutation occurring in lung, head, and neck cancers

A

mutation in specific codon caused by benzopyrene to bind DNA, mirrored by aflatoxins, hepatitis B

55
Q

p53 mutation occurring in basal cell carcinoma

A

hallmarks of UV exposure, thymine dimers

56
Q

p53 mutation occurring in cervical tumors

A

due to HPV which targets p53 and causes its inactivation by rapid degradation of the protein

57
Q

p53 and its link to hypoxia and tumor evolution

A

hypoxic cells at the center of a tumor mass should undergo apoptosis indicating p53 must be mutated to circumvent apoptosis

58
Q

p53 and its link to angiogenesis and tumor evolution

A

p53 directs the synthesis of thrombospondin a anti-angiogenic factor, p53 mutation would no longer make the anti-angiogeneic factor and allowing recruitment of vessels via endothelial growth factor

59
Q

Thrombospondin

A

antiangiogeneic factor whose synthesis is directed by p53

60
Q

Treatment for cancer is considered once the TNM and genetic modifications have been discovered

A

T: tumor, N: node, M; metastasis

Biochem 1502 (14 decks)

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