Flashcards in Neoplasia 3 Deck (26)
Causes of cancer
Polycyclic aromatic hydrocarbons, nitrosamines, metals, aflatoxin, insecticides
UV, x-rays, asbestos
DNA: Papillomavirus, Epstein-Barr, hepatitis B
RNA: HTLV-I, HTLV-II
Oncogenes: Ras, c-myc, c-abl
Tumor suppressor genes: p53
Hereditary Tumor Genes: BRCA1, Rb, HNPCC, APC
Cancer targets DNA stability/function:
cell cycle regulation & DNA repair.
Asbestos from insulation can cause
Lung, mesothelioma cancers
Radon -decay from uranium (quarries) can cause
Vinyl chloride (Refrigerant, adhesive) can cause
Liver, angiosarcoma cancers
-Group consists of diverse chemical structures
-Most are indirect-acting or procarcinogens that need metabolic activation to become ultimate carcinogen (polycyclic hydrocarbons, nitrosamines, plant and microbial antgens, e.g., aflatoxin B1)
-All are highly reactive electrophiles that react with electron-rich atoms in RNA, proteins, DNA.
-Human cancers usually are not caused by retroviruses, but via insertional mutagenesis:
insertion of a strong viral promoter adjacent to a cellular protooncogene resulting in overexpression of that normal or mutated protooncogene.
human papilloma, Epstein-Barr, hepatitis B and C are
Oncogenic DNA viruses
DNA viral carcinogenesis
Viral integration into host cell, but incomplete replication
Transcription of early genes drive host cell immortalization
Normal gene (involved in cell proliferation/differentiation) that can become an oncogene due to mutations or increased expression.
Genes that promote autonomous cell growth in cancer cells and are created by mutations in proto-oncogenes that have the ability to promote cell growth in the absence of normal growth-promoting signals.
Product of oncogene expression which resemble the normal products of proto-oncogenes. Many times lack important internal regulatory elements, and their production in the transformed cells does not depend on growth factors or other external signals.
__ translocation comprising the Philadelphia chromosome creates a Bcr/Abl fusion protein with active ______
Abl tryosine kinase activity
________ are small fragments of extra chromosomal DNA, seen in tumors including breast, lung, ovary, colon, and most notably, _______.
Double minutes; neuroblastoma
Hereditary Tumor Genes:
Retinoblastoma, Adenomatous polyposis coli (APC)
Adenomatous polyposis coli (APC)
-Germ line mutation associated with FAP w/thousands of polyps developed by teen years-early adulthood with one or more undergoing malignant transformation after second mutation.
-70-90% of non-familial colorectal carcinomas and sporadic adenoma have a mutation in the APC gene.
-ß-catenin-E-cadherin germline mutations increase risk of familial gastric carcinomas.
Mutagenic effect occur at the chromosomal level include DNA damage as ds & ss breaks, translocations, point mutations
Long latent period suggests accumulation of additional mutations (environmental or genetic)
Target DNA stability/function: cell cycle regulation & DNA repair
Sonography: Ultrasound can distinguish between
solid and hollow structures
Cancer Treatment/Failure: Surgery & Drug resistance
-Surgical debulking may miss micrometastases.
-Chemotherapy suffers from drug toxicity, drug specificity and, especially, the development of drug resistance.
-Development of drug resistance.
-Lack of tumor immunity
Symptom complexes that cannot readily be explained by the tumor or by the elaboration of hormones indigenous to the tissue from which the tumor arose, are known as
examples of paraneoplastic syndromes
Symptoms that result from rupture or infarction
Cachexia or wasting