Chapter 7 Key Concepts pt 2 Flashcards
(58 cards)
3 antitumor effector mechanisms
CTLs
NK cells
macrophages
What can tumor cells express that is recognized by CTLs? (4)
- Product of oncogene or mutated tumor suppressor gene
- Mutated self protein
- Overexpressed or aberrantly expressed self protein
- Oncogenic virus
Oncogene products
mutated RAS, BCR/ABL fusion protein
Tumor suppressor gene products
mutated p53 protein
Overexpressed self protein
tyrosinase, gp100, MART in melanomas
Aberrantly expressed proteins
cancer-testis antigen (MAGE, BAGE)
Oncogenic virus
HPV E6, E7
EBNA in EBV-induced lymphoma
Persons with inherited mutations of genes involving DNA repair system
greatly increased risk for development of cancer
HNPCC syndrome (4)
Defects in mismatch repair system
Leading to carcinomas of the colon
Show microsatellite instability
Changes in length of short repeats throughout the genome
Xeroderma Pigmentosum (3)
Defect in the nucleotide excision repair pathway
Increased risk for development of skin cancers in UV light
Cause- inability to repair pyrimidine dimers
Name of Syndromes that have Defects in Homologous Recombination of DNA repair system
Bloom Syndrome
Ataxia-Telangiectasia
Fanconi anemia
Cause of Syndromes that have Defects in Homologous Recombination of DNA repair system
hypersensitivity to DNA-damaging agents (ionizing radiation)
ex. BRCA1 and BRCA2 are involved in DNA repair
Cause of Mutations in lymphoid cells
expression of gene products that induce genomic instability and cause lymphoid neoplasms
ex. RAG1, RAG2, AID
Oncogenic mutations that tumor cells may acquire (4)
point mutations
translocations
deletions
gene amplifications
Balanced translocations in cancer
Contribute to carcinogenesis by overexpression of oncogenes
Generation of novel fusion proteins with altered signaling capacity
Deletions and cancer
cause loss of tumor suppressor gene function and can activate proto-oncogenes
Gene amplification and cancer
increases the expression and function of oncogenes
Genomic sequencing influence on cancer
revealed numerous “cryptic” rearrangements like small deletions and insertions and chromothrypsis
Chromothrypsis
a chromosome is “shattered” and then reassembles in a haphazard way
Structure and function of chemical carcinogens
Highly reactive electrophile groups
Directly damage DNA, leading to mutations and cancer
Direct-Acting Agents
do not require metabolic conversion to become carcinogenic
ex. alkylating agents used for chemotherapy
Indirect-Acting Agents
not active until converted to a carcinogen by endogenous metabolic pathways ex. cytochrome P450
ex. benzopyrene, azo dyes, aflatoxin
What occurs after exposure of a cell to a mutagen or initiator
tumorigenesis can be enhanced by exposure to promoters to stimulate proliferation of mutated cells
Examples of human carcinogens (5)
direct-acting agents
indirect-acting agents
promoters
agents that cause pathologic hyperplasia of endometrium
agents that cause regenerative activity of the liver
