Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

42 Cards in this Set

  • Front
  • Back
does not to need to be chemically altered to act (usually weak carcinogens)
needs metabolic conversion from PROCARCINOGEN to ULTIMATE CARCINOGEN
What are the 2 stages of chemical carcinogenesis?
1. initiation (carcinogenic agent irreversibly damages DNA (is mutagenic))
2. promotion (acts (reversibly) to stimulate cell proliferation and enhance carcinogenic process, but not carcinogenic in itself)
How does UV radiation cause cancer? What is the extreme disease example of this process?
induces thymine dimers; XERODERMA PIGMENTOSUM (failure of DNA excision repair mechanisms)
What gene does v-sis mimic?
gene for beta chain of PDGF
What the 4 classes of regulatory genes are the principal targets of genetic damage?
proto-oncogenes, cancer suppressor genes, genes that regulate apoptosis, DNA repair genes
How do oncoproteins differ from the protein products of proto-oncogenes?
oncoproteins are devoid of important regulatory elements, their production is not dependent on growth factors or external signals
What are some examples of cancers that result from ionizing radiation?
-skin cancer/myeloid leukemias in radiologists
-lung cancer in uranium miners
-thyroid cancer in pts w/head/neck radiation therapy
-acute and chronic myeloid leukemias in atomic blast survivors
-osteosarcoma in radium watch-dial workers
What are the 3 oncogenic DNA viruses?
HPV (human papillomavirus), HBV (hep B), EBV (epstein-barr)
What is the general carcinogenic mechanism of DNA viruses?
integrate viral DNA into host genomes, resulting in host expression of viral mRNA coding for specific proteins
What are the major types of neoplasms implicated by HPV?
genital tract neoplasms, esp. premalignant lesions and cancers of cervix (sexually transmitted); laryngeal papillomas; benign squamous papillomas (warts)
What major types of neoplasms are implicated by EBV?
-Burkitt's lymphoma = tumor of B lymphocytes (stimulates prolif of B cells, inc opportunity for translocation and oncogene activation)
-nasopharyngeal cancer
What major types of neoplasms are implicated by HBV?
hepatocellular carcinoma
What is the general carcinogenic mechanism of retroviruses?
transcription of viral genomic RNA into DNA by viral reverse transcriptase (can encode for a viral oncogene itself, or encode for a promoter sequence that is inserted near a protooncogene)
What is the only known oncogenic retrovirus? What type of neoplasm does it cause?
human t-cell leukemia virus type I (HTLV-1); t cell leukemia/lymphoma
What are the general downstream effect of ras?
activates regulators of proliferation, including kinases, which flood nucleus w/signals for cell prolif
What protein mediates the "on-off" activity of ras, by making sure ras turns off shortly after activation?
GAP (GTPase-activating protein) -- hydrolyzes ras-GTP to ras-GDP
What is the resulting defect when there is a mutation of the ras gene?
mutant ras proteins bind GAP but fail to be inactivated, thus signal is always on
What is the single most common oncogene abnormality in human tumors?
mutation of ras gene (25-30%)
What are some examples of oncogenes that regulate transcription of DNA in the nucleus?
myc, fos, myb
How does pRB regulate the cell cycle?
guardian of G1->S checkpoint; CDKs (activated by cyclin) phosphorylate pRB which allows entry of cells in to S phase
What is an example of oncogene activation by point mutation?
What is insertional mutagenesis?
insertion of retroviral promoter or enhancer sequence into host genome that leads to inc expression of nearby oncogene
What is the translocation that occurs in Burkitt's lymphoma?
8:14; c-myc proto-oncogene is translocated adjacent to Ig heavy chain (region w/hectic transcriptional activity), and inc expression of c-myc
What is the translocation that occurs in chronic myeloid leukemia (CML)?
9:22; c-abl protooncogene is translocated adjacent to bcr locus; the c-abl-bcr hybrid (on the "Philadelphia chromosome") encodes for a protein with inc tyrosine kinase activity
What is the translocation in acute promyelocytic leukemia?
15:17; results in fusion of retinoic acid receptor (RAR-alpha) and transcriptional unit PM

*can induce remission w/all-trans retinoic acid (vit A analogue)*
What do "double-minutes" and "homogenous staining regions" on chromosomes indicate?
extensive gene amplification
What are 2 types of neoplasms which involve amplification, and what genes are amplified?
neuroblastoma (N-myc) -> correlates strongly w/disease progression
breast cancers (c-erbB2) -> associated w/poor prognosis
What is the two-hit hypothesis of Knudson?
2 mutations are required to express neoplastic phenotype (both alleles must be inactivated)
What is the prototypic cancer suppressor gene for which the two-hit hypothesis applies?
Rb gene--inactivation causes retinoblastoma (childhood tumor)
How is the cell cycle affected if the Rb gene is inactivated?
normally, cell cycle can only move to S phase if pRb is phosphorylated, setting free transcription factors. if pRb is absent, "molecular breaks" of cell cycle are gone, cells proceed easily into S phase
What is the most common target for genetic alteration in human tumors?
What is the normal function of p53?
causes cell cycle arrest in G1 when there is DNA damage, so it can be repaired. if damage is not repaired, p53 induces apoptosis
What syndrome results from familial loss of p53, and what is this syndrome characterized by?
Li-Fraumeni syndrome; wide variety of tumors (breast, soft tissue carcinomas, brain tumors, leukemias, etc)
What are some major cancer suppressor genes?
Rb, p53, WT-1, BCRA-1, APC, NF-1
What syndrome results from deletion or inactivation of WT-1?
Wilms tumor (most common renal neoplasm in children)

(WT-1 = Wilms Tumor-1)
What types of neoplasms result from inactivation of APC?
familial polyposis coli and adenocarcinoma of colon

(APC = adenomatous polyposis coli)
What types of neoplasms result from inactivation from BRCA-1?
familial propensity to breast and ovarian cancers

(BRCA-1 = BReast CAncer-1)
What are some common genes associated with apoptosis?
bcl-2, bax, p53 (by increasing transcription of bax)
What is the molecular defect in hereditary nonpolyposis colon carcinoma (HNPCC or Lynch syndrome)?
mutation in DNA mismatch repair genes
What is the genetic defect in von Recklinghausen neurofibromatosis type 1?
mutations in NF-1 tumor suppressor gene (which fns as a GAP protein that inactivates ras)
What is the genetic defect in multiple endocrine neoplasia type IIa?
mutations in ret protooncogene transmitted in germline