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54 Cards in this Set

  • Front
  • Back
What is xeroderma pigmentosum?
-autosomal recessive disorder
-extreme sensitivity to sunlight
-development of skin cancer in exposed areas of skin
-locus heterogeneity
What is XP-C? What does it do?
-tumor suppressor (caretaker)
-recognizes thymidine dimers in DNA
-loss leads to xeroderma pigmentosum
What is XP-G? What does it do?
-tumor suppressor (caretaker)
-helicase + endonuclease in nucleotide excision repair
-loss leads to xeroderma pigmentosum
What is XP-F? What does it do?
-tumor suppressor (caretaker)
-endonuclease in nucleotide excision repair
-loss leads to xeroderma pigmentosum
What are the seven abnormal characteristics of cancer cells?
-self sufficiency in growth signals
-insensitivity to antigrowth signals
-evasion of apoptosis
-limitless replicative potential
-tissue invasion and metastasis
-genomic instability
-sustained angiogenesis
What events could lead to loss of heterozygosity for the Rb gene?
-somatic recombination
-loss and duplication
-chromosome loss
What is Rb? What does it do?
-tumor suppressor (gatekeeper)
-inhibits E2F, a transcription factor
-loss leads to retinoblastoma
What is APC? What does it do?
-tumor suppressor
-negative regulator of Wnt/β-catenin/TCF pathway (degrades β-catenin)
-loss leads to familial adenopolyposis, or sporadic colorectal cancer
What are MSH2 and MSH6? What do they do?
-tumor suppressors (caretakers)
-in mismatch repair, bind to a mispaired segment in order to distinguish the template and new strands
-loss leads to hereditary nonpolyposis colon cancer
What is MLH1? What does it do?
-tumor suppressor (caretaker)
-in mismatch repair, acts as endonuclease
-loss leads to hereditary nonpolyposis colon cancer
What is p53? What does it do?
-tumor suppressor
-activates transcription of p21 and GADD45
-activates Bax
-loss leads to Li-Fraumeni syndrome, or common sporadic cancer
What are BRCA 1 and 2? What do they do?
-tumor suppressors (caretakers)
-in double strand break repair, help to form nucleoprotein filaments
-loss leads to risk for breast cancer
What is Ras? What does it do?
-oncogene (G-protein)
-activates Raf in response to growth signal
-mutated to constitutively active (unable to hydrolyze GTP) leads to cancer
In what ways can N-myc be amplified? What are the consequences?
-double minute chromosomes
-homogenous staining region
Amplification can lead to neuroblastomas.
What is HER2? What does it do?
-part of the EGR receptor family
-does not have a ligand, but heterodimerizes with EGFR (HER1), a receptor tyrosine kinase which does
-amplification leads to breast cancer
What does c-myc do?
-transcription factor that promotes cell cycle progression
-(8;14)(q24;q32) translocation to Ig heavy chain promoter leads to Burkitt lymphoma
What does Bcl2 do?
-(14;18)(q32;q21) translocation to Ig heavy chain promoter leads to follicular lymphoma
What is mantle cell lymphoma caused by?
(11;14)(q13;q32) translocation of cyclin D1 gene to Ig heavy chain promoter → disregulated progression through G1
What does c-abl do? What is the Philadelphia chromosome?
-regulated tyrosine protein kinase
-Philadelphia chromosome = t(9;22)(q34;q11) → Bcr-ABL gene → chronic myelogenous leukemia
What does TGFβ do? What happens if its receptor is mutated?
-inhibits cell proliferation
-interacts with a cell surface receptor → activation of receptor-associated protein kinase → activation of Smads
-loss of TGFβ receptor leads to uncontrolled proliferation
What do Smads do?
-activate transcription of growth inhibitors such as p15
-loss leads to uncontrolled growth
What does PAI-1 do? What regulates it?
-inhibits protease that degrades extracellular matrix proteins
-transcription activated by Smads
-loss leads to increased metastasis
How do cancer cells achieve limitless replicative potential?
Express telomerase, which extends the telomeres and the cell avoids senescence.
How do cancer cells achieve sustained angiogenesis?
-bFGF (basic fibroblast growth factor)
-TGFα (transforming growth factor)
-VEGF (vascular endothelial growth factor)
What is the proposed pathway for malignant transformation in colorectal cancer?
-APC mutation
-Ras gene mutation
-DCC tumor suppressor loss
-p53 loss
-other chromosome losses
How does the incidence of various cancers in Japan compare with that of the U.S. and what contributes most to the discrepancy?
Japan has higher incidence of:
-stomach cancer (H. pylori)
-liver cancer (hepatitis)
U.S. has higher incidence of:
-colon cancer (diet)
-prostate cancer (diet)
What combination of carcinogen application and tumor promoter is necessary for tumor formation?
-carcinogen followed by high frequency (e.g. twice-weekly) application of tumor promoter
-it is not necessary to apply tumor promoter immediately after carcinogen (initiator)
What do intercalating agents look like, in general? How do they interact with DNA?
-flat conjugated polycyclic aromatic ring system
-bind between stacked base pairs inside the double helix
How do alkylating agents damage DNA?
-bind covalently to nucleophilic sites in DNA (N7 of guanine), via SN1 or SN2 reactions
-DNA is damaged when it tries to divide
What are some examples of alkylating agents?
-nitrogen mustard
What are some examples of procarcinogens (that require metabolic activation)?
-aflatoxin B1
What are some examples of carcinogens that are both intercalating agents and react covalently with DNA?
-benzo[a]pyrene 7,8-dihydrodiol-9,10-epoxide
What are some known and suspected tumor promoters?
-microbial infections
-bile acids
-reproductive hormones
What is the effect of childbearing on risk of breast cancer?
Women who have children at a young age (< 30) are at a lower risk for breast cancer than women who have children at an older age or who do not have children.
What is Gleevec for? How does it work?
-treatment of chronic myelogenous leukemia
-binds to the active site on the chimeric Bcl-ABL kinase, inhibiting it
What is an osteoma?
benign neoplasm of bone
What is a melanoma?
malignant neoplasm of melanocytes
What is an adenoma?
benign neoplasm of a gland
What are the two major routes of metastasis?
Where does colon cancer metastasize to? How does it get there?
Colonic veins eventually drain into the portal vein, which drains into the liver.
What is a sarcoma?
malignant neoplasm of connective tissue, muscle, or bone
What is a carcinoma?
malignant neoplasm of epithelial tissue
What is the difference between cancer staging and grading?
Staging refers to spread, grading refers to cell differentiation.
Why is cancer bad?
-tissue destruction
-cancer cachexia (ill health, malnutrition, wasting due to cytokines)
-hormonal effects
How does the nuclear:cytoplasmic ratio change in cancerous cells?
The normal N:C ratio is 1:4 or 1:6. In cancer it is often 1:1.
What is PSA?
Prostate specific antigen - tumor marker for prostate cancer.
Which extracellular apoptosis sensors signal death and which signal survival?
How do NF-κB and I-κB influence apoptosis?
NF-κB induces anti-apoptotic genes. I-κB will therefore promote apoptosis.
What factors are inhibitors of angiogenesis?
What types of tissues make up a tumor?
-non-neoplastic supportive connective tissue
-blood vessels
-lymphatic vessels
parenchymal tissue:
-transformed malignant cells
Where are the most likely sites for breast cancer to metastasize to?
-GI tract
in that order
Cancers from which sites are likely to metastasize to bone?
-multiple myelenoma
What is PET scanning? What are the limitations?
-use FDG, it becomes metabolized to 2-FDG-6-phosphate
-it is a radioactive compound, cancer cells will have a larger amount because they undergo glycolysis more
-limitations are that benign inflammatory processes and muscle also take it up
What is the most dangerous side effect of chemotherapy?
bone marrow suppression