Carcinogens And Metaplasia Flashcards Preview

CLS 2 > Carcinogens And Metaplasia > Flashcards

Flashcards in Carcinogens And Metaplasia Deck (9)

Chemical carcinogens types

Genotoxic-> direct DNA damage by adding things to it
Mitogenic-> bind cell receptors and stimulate cell division
Cytotoxic-> produce tissue damage leading to hyperplasia
Direct acting-> can directly cause neoplasia
Procarcinogens-> agent requires conversion to an active carcinogen
Initiating agents-> don't directly cause neoplasia but cause genetic abnormality that predisposes it
Promoting agents-> prolonged exposure causes development of neoplasia-> increased cell turnover


Examples of chemical carcinogens

Polycyclic hydrocarbons-> cigarette smoke-> lung cancer
Aromatic amines-> industrial exposure-> con tend to active agents in the liver-> concentrated during excretion-> urothelium cancers
Nitrosamines-> effect gut bacteria
Alkylation agents-> bind DNA so are directly mutagenic-> used in chemo-> treating one cancer but increasing the chance of another


Stages of chemical carcinogensis

1) initiation-> induction of genetic changes
2) promotion-> induction of cell proliferation
3) progression-> persistent cell proliferation causes secondary genetic abnormalities-> lead to dysregulation and then autonomous cell growth


Physical carcinogens

Irradiation-> direct DNA damage, potent-> DNA breaks and instability
-x rays-> bone marrow and exposed skin
-inhalation of radioactive dust/gas
-ingestion of radioactive iodine-> thyroid
-incorporation of radioactive metals into bone
Asbestos-> potent when inhaled-> irritates lungs causing increased cell proliferation-> increased risk of neoplasia


Viral carcinogens

Epstein Barr-> burkits lymphoma, nasopharyngeal carcinoma, other B cell lymphoma, some Hodgkin's
Hep B-> hepatocellular
HPV> cervical and some skin carcinomas
HTLV-> T cell leukaemia/lymphoma
HSV8-> kaposi sarcoma-> systemic


Common cytogenic abnormalities in tumours

Gain or loss of chromosomes
Deletion of chromosomes
Selective amplification
Chronic myeloid leukaemia-> fusion of oncogene bar-abl-> protien with tyrosine kinase activity
Follicular lymphoma-> IgH gene from chr 14 fused to Bcl-2 gene on chr 2-> prevention of apoptosis
Ewing's sarcoma-> fusion of LFT-1 with EWS gene-> protein with high transcriptor activity
Neuronalblastoma-> amplification of n-myc
Burkits lymphoma-> fusion of c-myc with IgH-> c-myc expression


Pre neoplastic conditions

Some non-neoplastic diseases carry increased risk of later development of neoplasia
Hyperplasia can result in dysplasia-> progress to carcinoma
Endometrial layers, breast lobules
Chronic gastritis
Hepatic cirrhosis
Celiac disease
Autoimmune thyroiditis


Inherited neoplastic conditions

MEN syndrome-> chr 10+11 mutation-> multiple tumours in endocrine organs
Polyposis coli-> absent AP-> adenoma tag and carcinomas of colon
Li-fraumeni-> mutated p53-> breast and sarcomas
Xeroderma pigmentosum-> abnormal DNA repair
Neurofibromatosis type 1-> abnormal NF1-> benign and malignant tumours of peripheral nerves


Immune responses and tumour biology

Tumours specific antigens:
Present only in tumour cells
Lymphoid infiltrate in some tumours suggests thee is an immune response to these antigens-> patients who have lymphoid infiltrate have a better prognosis
Vaccines against antigens?
Tumours associated antigens:
Present on both tumour and normal cells
Anfectal antigens-> normally expressed in bone development but are r expressed in neoplastic cells
AFP expressed in hepatocellular cancer
CEA in gastrointestinal cancer

Decks in CLS 2 Class (42):