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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
Limitless replication in cancer cells is achieved by
reappearance of telomerase, which lengthens telomeres evading shortening chromosomes
26
Two examples of diseases caused by mutation in DNA repair genes
Xeroderma pigmentosum and Hereditary Nonpolyposis Coli
27
In a quiescent vessel, inhibitors of angiogenesis exist that off-set the inducers. In cancer,
lack of inhibitors or overexpression of inducers allows recruitment of vessels
28
Possible mechanism for recruitment of vessels to cancer cells
mutation in p53 gene; p53 normally suppress angiogenesis by inducing a angiogenesis inhibitor
29
How do cancer cells evolve the metastatic ability
acquiring genes that allow them to break down tissue structure and invade the basement membrane to allow migration to other side of vessel
30
Angiogenesis inhibitor
induced by p53
31
Energy shift in cancer cells
Cancer cells shift to glycolysis followed by lactic acid formation even in AEROBIC conditions
32
Lower efficiency of energy production in cancer cells is offset by....
upregulation of GLUT1 glucose transporters
33
PET
visualize glucose uptake to look for tumors
34
What genes are associated with glycolytic fueling
Ras, myc, and p53
35
HYPOXIC conditions result in
upregulation of GLUT1 glucose transporters and upregulation in glycolytic enzymes
36
Why do cancer cells switch to glycolysis
to generate intermediates for biosynthetic processes (nucleosides and amino acid production)
37
Colon cancer is well understood and is known to be a
multistep process of accumulated mutations
38
Stem Cell Theory of Cancer
Tumors contain cancer stem cells with indefinite proliferative potentials, they are self-renewing and responsible for all components of the tumor; drug resistant
39
Inherited mutations in tumor suppressor genes occur
in 5-10% of al cancers
40
Inherited malignant tumors most commonly occur in
breast and colon cancer
41
BRCA1-2
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
Adenomatous Polyposis Coli (APC)
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
APC protein role
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
Hereditary Non-Polyposis Colorectal Carcinoma (HNPCC)
polyp rapidly transforms into carcinoma but rate of polyp formation is normal
45
Predisposition for HNPCC is due to inherited mutations in
Mismatch repair genes
46
Chemical carcinogenesis - INITIATION
carcinogen induces alterations in the genetic makeup that confers a neoplastic growth potential
47
Chemical carcinogenesis - PROMOTION
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
Enzymes important in carcinogen metabolism
Cytochrome p450 oxidase, and N-acetyl transferase (drugs may become active or inactive by metabolism to cause cancer)
49
Examples of environmental carcinogens
Polycyclic aromatic hydrocarbons (PAH) and aromatic amines from cigarette smoke leave residues on DNA (fingerprinting exposure and indicating DNA damage)
50
PAH and aromatic amines contribute to which cancer types
lung, bladder, and breast depending on exposure
51
Polymorphisms in drug metabolizing enzymes
explain differences in susceptibility within populations to carcinogens
52
polymorphisms is the new susceptibility factor that may be the best predictor of cancer risk
inter-inividual variation in P450, glutathione transferase and N-acetyl transferase gene influence individual response
53
Susceptibility factors include:
polymorphisms, predisposition, age, ethnicity, gender, health impairment, nutritional impairment
54
p53 mutation occurring in lung, head, and neck cancers
mutation in specific codon caused by benzopyrene to bind DNA, mirrored by aflatoxins, hepatitis B
55
p53 mutation occurring in basal cell carcinoma
hallmarks of UV exposure, thymine dimers
56
p53 mutation occurring in cervical tumors
due to HPV which targets p53 and causes its inactivation by rapid degradation of the protein
57
p53 and its link to hypoxia and tumor evolution
hypoxic cells at the center of a tumor mass should undergo apoptosis indicating p53 must be mutated to circumvent apoptosis
58
p53 and its link to angiogenesis and tumor evolution
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
Thrombospondin
antiangiogeneic factor whose synthesis is directed by p53
60
Treatment for cancer is considered once the TNM and genetic modifications have been discovered
T: tumor, N: node, M; metastasis

Biochem 1502 (14 decks)

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