Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Carcinogenesis
| Question | Answer |
|---|---|
| What are carcinogens?Name few | Agents that damage DNA- chemicals, oncogenic virus and radiation. |
| Why are aflatoxins carcinogenic? | They cause hepatocellular carcinoma- Aspergillus harms grains |
| Why is Alkalating agent carcinogenic? | They cause Leukemia and Lymphoma (chemotheraphy) |
| Why is Alcohol carcinogenic? | Squamous cell carcinoma of oropharynx and upper esophagus, pancreatic carcinoma, and hepatocellular carcinoma |
| Why is arsenic carcinogenic? | Arsenic is in cigarette and causes lung cancer |
| Why is asbestos carcinogenic? | Lung cancer mainly but also mesothelioma |
| Cigarette smoke is carcinogenic? | More dangerous -Carcinoma of oropharynx, esophagus, lung,kidney, and bladder. (carcinogens to blood to urine and hang out there) |
| Nitrosamines are carcinogenic? | stomach cancer- |
| Naphthylamine are carcinogenic? | Urothelial carcinoma of bladder - cigarette |
| Vinyl chloride is carcinogenic? | angiosarcoma of the liver- Vinyl chloride in pipes |
| Nickel, chromiwn, beryllium, or silica are carcinogenic? | lung carcinoma |
| Oncogenic Viruse: EBV | Nasopharyngeal carcinoma, Burkitt lymphoma, and CNS lymphoma in AIDS |
| Oncogenic Viruse:HHB8 | Kaposi sarcoma- cancer of endotheliel cells |
| Oncogenic Viruse: HBV and HCV | Hepatocellular carcinoma |
| Oncogenic Viruse: HTLV-1 | T cell lymphoma/leukemia |
| Oncogenic Viruse:HPV | Squamous cell carcinoma of vagina, anus, and cervix; adenocarcinoma of cervix |
| Oncogenic radiation: ionizing | AML, CML, and papillary carcinoma of the thyroid- free radicals |
| Oncogenic radiation: non inonizing radiation UBV sunlight | Basal cell cardnoma, squamous cell carcinoma, and melanoma of skin. Results in formation of pyrimidine dimers in DNA, which are normally excised by restriction endonuclease |
| The mechanism behind the working of the carcinogens involves 3 main methods-name them | Proto oncogenes - tumor suppressor gene Regulator of apoptosis |
| how do Proto oncogenes cause cancer ? | They are important for cell growth and differentiation. If proto oncogene is mutated it becomes an oncogene.-leads to unregulated cell growth. |
| how do growth factors effect cell division? | when there needs to be some division of a cell. The growth factor acts on the growth factor receptor and sends a signal transduction to the nucleus for nuclear regulators and cell cycle regulators. All these are proto oncogene and if mutations=oncogene. |
| proto oncogene becoming cancerous= Platelet derived growth factor B | in an astrocyte has a PDGFR. When PDGF binds to the receptor then the astrocyte divides. If there is a mutation then over production of the PDGF which activates itself in an ongoing loop.= Astrocytoma. |
| proto oncogene becoming cancerous= Platelet derived growth factor receptor | if there is a mutation in expression of the receptors then there is a presentation of a multiple receptors an the GF acts in all of them and the cell goes out of control with all the signals comming in |
| Examples of Platelet derived growth factor receptor that can be cancerous | ERBB2 [HER2/ Epidermal growth factor receptor Amplification- breast carcinoma RET Neural growth factor receptor point mutation- Men2 A 2b, medullary carcinoma of thyroid KIT Stem cell growth factor receptor point mutation- gastrointestinal stromal tumor |
| proto oncogene becoming cancerous= signal transduction | The signal that is comming in after the receptor has been activated is mutated and it causes multiple signals to the nucleus to divide. |
| Examples of signal transduction that can become cancerous. | RAS - GTP binding protien point mutation- melanoma lymphoma carcinoma ABL- tyrosine kinase -translocation(9;22)-- CML- ALL |
| Describe in detail what happens in RAS and how does signal transduction mutation lead to cancer? | GF acts on growth factor receptor,Ras which is associated with the receptor and bound to GDP gets activated and GDP converts to GTP. once signal goes thru, GAP converts GTP to GDP to avoid multiple signals. HERE GAP is mutated= multiple signals |
| Examples of Nuclear regulators that can be cancerous | c-MYC Transcription factor- translocation(8:14)- Burkits N-MYC Transcription factor- Amplification- neuroblastoma L-MYC Transcription factor-Amplification- lung cancer |
| Describe in detail what happens in c-MYC and how does Nuclear regulator mutation lead to cancer? | c-MYC is on the 8 chromosome and it is translocated to chromosome 14 of the immunoglobulin HEavy chain which in in "ON" position. Thus over poduction of the c-MYC=burkits lymphoma. |
| proto oncogene becoming cancerous= cell cycle regulators | G1 ,S, G2 and M. G1 to S is highly regulated. |
| Examples of cell cycle regulatrs that can become cancerous. | Cyclin D1 Cyclin translocation(11:14)igH -mantle cell lymphoma(B cells have 3 layers in them -Follicle, mantle and margin) CDK4 Cyclin-dcpcndent kinase amplication melanoma |
| Describe in detail what happens in cyclin D1 and how does cell cycle mutation lead to cancer? | CyclinD1 is on the 11 chromosome and is translocated to chromosome 14 of immunoglobulin Heavy chain which in in "ON" position. Thus over poduction of the Cyclin D=G1->s phase.Mutation increase. |
| What is a tumor suppression gene? | Regulate cell growth and, hence, decrease ("suppress") the risk of tumor formation; p53 and Rb (retinoblastoma) are classic examples. |
| describe the functioning of the p53 gene | In response to DNA damage, p53 slows the cell cycle and upregulates DNA repair enzymes. If DNA repair is not possible, p53 induces apoptosis. i. p53 upregulates BAX, which disrupts Bcl2. ii. Cytochrome c leaks from the mitochondria activating apoptosis |
| How does p53 lead to cancer? | Both copies of the p53 gene must be knocked out for tumor formation (Knudson two-hit hypothesis). one Germline mutation results in Li-Fraumeni syndrome (2nd hit is working), characterized by the propensity to develop sarcomas and carcinomas |
| How does Rb gene regulate cell cycle? | G1 to S is regulated by E2F transcription factor. E2F is regulated by RB. Phosphorylated(by cyclinD/CDK4) Rb stops G1 to go to S. If RB is mutated. G1 to S is easy= no tumor suppression |
| How does Rb mutation lead to cancer | Both copies of Rb gene must be knocked out for tumor formation . Sporadic mutation (both hits are somatic =unilateral retinoblastoma Germline mutation results in familial retinoblastoma (2nd hit is somatic),= bilateral retinoblastoma and osteosarcoma. |
| What is the process of apoptosis? | Bcl2 normally stabilizes the mitochondrial membrane, blocking release of cytochrome c. 2. Disruption ofBcl2 allows cytochrome c to leave the mitochondria and activate apoptosis |
| describe follicular lymphoma | t(l4;18) moves Bcl2 (chromosome 18) to the Ig heavy chain locus (chromosome 14),resulting in increased Bcl2=no apoptosis B cells that normally undergo apoptosis during somatic hypermutation in the lymph node accumulate, leading to follicular lymphoma |
| Cancer cells have increased inmmortality why? | Normally, telomeres shorten with serial cell divisions, eventually resulting in cellular senescence. Cancers often have upregulated telomerase, which preserves telomeres Angiogenesis is upregulated Cancer cell downgrade MHC1 so no immune response |
Created by:
atayal
Popular Biology sets