PHYSICAL CARCINOGENS 1. RADIATION 2. NONRADIATION AGENTS

1. PHYSICAL CARCINOGENS1.RADIATION 2.NONRADIATION AGENTS

2. RADIATION CARCINOGENESISI .ULTRAVIOLET LIGHTII .IONISING RADIATION

3. I .ULTRAVIOLET LIGHTMAIN SOURCE OF UV LIGHT IS SUNLIGHTOTHERS ARE UV LAMPS AND WELDER’S ARCSUV LIGHT PENETRATES ONLY FEW MILLIMETRES OF THE SKIN

4. MELANIN PIGMENT PROTECTS CAUSE VARIOUS FORMS OF SKIN CANCERS 1.SQUAMOUS CELL CARCINOMA2.BASAL CELL CARCINOMA3.MALIGNANT MELANOMA

5. WHITE RACEASTRALIANEW ZEALAND AND THOSE LIVING CLOSE TO THE EQUATOR WHO RECEIVE MORE SUNLIGHTFARMERS AND OUTDOOR WORKERS DUE TO THE EFFECT OF ACTINIC LIGHT RADIATION

6. MECHANISM OF ACTION OF UV LIGHTDNA DAMAGE –MUTATIONNORMALLY DAMAGED DNA GETS REPAIRED

7. CERTAIN RECESSIVE HEREDITARY DISEASES CHARACTERISED BY A DEFECT IN DNA REPAIR MECHANISM AND ASSOCIATED WITH INCREASE RISK OF CANCER

8. 1. XERODERMA PIGMENTOSUMSKIN CANCERS AT EARLY AGE2.ATAXIA TELANGIECTASIA –LEUKAEMIA3. BLOOMS SYNDROME-PREDISPOSED TO ALL TYPES CANCERS

9. 4.FANCONI’S ANAEMIA WITH INCREASED RISK TO DEVELOP CANCERMUTATION OF PROTO-ONCOGENE RAS GENE AND ANTI-ONCOGENETP53

10. II . IONISING RADIATION LIKEa. X – RAYSb. β – RAYSc.GAMA RAYSd.RADIOACTIVE ISOTOPESe.PROTONSf.NEUTRONSTHE RISK INCREASES WITH HIGHER DOSAGE

11. X RAY WORKERS,RADIOTHERAPIST-SKIN CANCERSWATCH WORKERS ENGAGED IN PAINTING THE DIALS WITH LUMINOUS RADIUM- OSTEOSARCOMAMINERS WORKING WITH RADIOACTIVE ELEMENTS

12. JAPANESE ATOM BOMB SURVIVERS OF THE TWIN CITIES OF HIROSHIMA AND NAGASAKI AFTER WORLD WAR 2

13. CHERNOBYL NUCLEAR POWER LEAKAGE-USSR-(1985)DAMAGE TO DNA DIRECTLY OR BY FORMATION OF HIGHLY REACTIVE FREE RADICALS WHICH BRING ABOUT DNA DAMAGE

14. NONRADIATION PHYSICAL CARCINOGENSMECHANICAL INJURY LIKESTONES IN THE GALL BLADDER,URINARY TRACT

15. HEALED SCARS,ASBESTOSISIMLANTS OF INERT MATERIALS SUCH AS PLASTIC,GLASS IN PROSTHESIS

16. VIRAL CARCINOGENESISASSOCIATION WAS FIRST OBSERVED BY ITALIAN PHYSICIAN SANARELLI IN 1889

17. ONCOGENIC VIRUSES ARE TRANSMITTED BY ONE OF 3 ROUTES1.VERTICAL TRANSMISSION-GENETICALLY TRANSMITTED

18. 2. HORIZONTAL TRANSMISSION DIRECT CONTACT LIKE CONTAGIOUS DISEASES

19. 3.BY INOCULATIONONCOGENIC VIRUSES ARE CLASSIFIED INTO1.DNA ONCOGENIC VIRUSES2.RNA ONCOGENIC VIRUSES

20. DNA ONCOGENIC VIRUSES5 GROUPS 1. PAPOVA VIRUSES2. HERPES VIRUSES 3. DENO VIRUSES4.POX VIRUSES5 HEPADNA VIRUSES

21. 1.PAPOVAVIRUSESA.PAPILLOMA VIRUSESABOUT 70 TYPES HAVE BEEN IDENTIFIED

22. HIGH RISK HPV-16,18-CAUSEINVASIVE SQUAMOUS CELL CARCINOMA OF CERVIX,ANUS,PERIANAL REGION,VULVA,PENIS AND ORAL CAVITY

23. LOW RISK HPV-1,2,4 AND 7CAUSE SQUAMOUS CELL PAPILLOMAS,HPV 6 AND 11CAUSE GENITAL WARTS

24. B. SV 40 VIRUS A PAPOVA VIRUS?MESOTHELIOMA OF PLEURA IN HUMAN BEINGS

25. 2 . HERPES VIRUSESA. EPSTEIN-BARR VIRUS(EBV) a.BURKTT’S LYMPHOMA( A B CELL LYMPHOMA)FIRST NOTICED IN AFRICAN CHILDREN BY BURKITT IN 1958.

26. 90% BURKITT ‘S LYMPHOMA TUMOUR CELLS HAVE EBV DNA HIGH ANTIBODY TITERS.OCCURS IN IMMUNOSUPRESSION CASES AS IN MALARIA AND HIV.

27. b.ANAPLASTIC NASOPHARYNGEALCARCINOMA-SOUTH EAST ASIA CHINA, ESKIMOS

28. 100% CASES CARRY EBV DNA IN TUMOUR CELLS.HIGH TITERS OF ANTIBODY TO EBV ANTIGENS

29. B . HUMAN HERPES VIRUS 8 (HHS 8)OR KAPOSI’S SARCOMA ASSOCIATED HERPES VIRUS(KSHS)A VASCULAR NEOPLASM COMMON IN AIDS PATIENTS

30. HHS 8 VIRUS ALSO CAUSE B CELL LYMPHOMA3 . ADENOVIRUSES NOT IN HUMAN BEINGS4.POXVIRUS-SQUAMOUS CELL PAPILLOMA - MOLLUSCUM CONTAGIOSUM

31. 5.HEPADNAVIRUSHBV BELONGS TO THIS FAMILYCAUSE HEPATOCELLULARCARCINOMA CONTINUED HEPATOCYTE DESTRUCTION

32. FOLLOWED BY PROLIFERATION WHICH MAKES THEM VULNERABLE TO THE ACTION OF AFLATOXIN FROM ASPERGILLOUS FLAVUS MUTATION-HCCHCV – 50% CASES OF HCC

33. RNA ONCOGENIC VIRUSRETROVIRUSES - HAVING ENZYME REVERSE TRANSCRIPTASE(RT)3 SUB-GROUPS1.ACUTE TRANSFORMING VIRUSES2 . SLOW TRANSFORMING VIRUSES

34. 3. HUMAN T CELL LYMPHOTROPIC VIRUSES(HTLV).RNA VIRUSES HAVE 3 GENESgag,pol,env genes

35. ACUTE TRANSFORMING VIRUSESTRANSFORM ALL THE INFECTED CELLS INTO MALIGNANT CELLS RAPIDLY.

36. THEY ARE DEFECTIVE VIRUSES WHERE v-onc HAS SUBSTITUTED gag,pol AND env AND THESE DEFECTIVE VIRUSES CANNOT REPLICATE BY THEMSELVES

37. UNLESS THE HOST CELL IS INFECTED BY ANOTHER HELPER VIRUS.NOT FOUND TO BE ONCOGENIC TO HUMANS.

38. 2.SLOW TRANSFORMING VIRUSESMOUSE MAMMARY TUMOUR VIRUS(BITTNER MILKFACTOR)INSERTIONAL MUTAGENESIS-NEOPLASTIC TRANSFORMATIONNOT ONCOGENIC TO HUMANS

39. 3.HUMAN T CELL LYMPHOTROPIC VIRUSES(HTLV)ONLY RETROVIRUS IMPLICATED IN HUMAN CANCER1.HTLV 1- ADULT T CELL LEUKKAEMIA LYMPHOMA SYNDROME2.HTLV II –T CELL VARIANT OF HAIRY CELL LEUKAEMIA

40. 3. HTLV III(HTLV-III is an outdated term for HIV-1)4. HTLV IVIMMUNOSUPPRESSION PLAYS A SUPPORTIVE ROLE IN NEOPLASTIC TRANSFORMATIONNO v-oncogene MEDIATIONNO INSERTIONAL MUTAGENESIS

41. HTLV I - HAS tat geneIN ADDITION TO gag,pol,env genestat gene STIMULATES NEOPLASTIC CELL PROLIFERATION OFT CELLS.

42. FIRST POLYCLONALTHEN MONOCLONALPROLIFERATION -LEUKAEMIALYMPHOMA

43. HTLV II- TRANSFORMATION BY PROMOTER INSERTION-ONCOGENESIS BY ONCOGENES AND GROWTH FACTORS

44. MODE OFDNA VIRAL ONCOGENESISa . INFECTION –REPLICATION-CYTOLYSIS-RELEASE OF VIRUSESb . INTEGRATION –VIRAL DNAINTEGRATES INTO HOST DNA-NEOPLASTIC TRANSFORMATION

45. MODE OF RNA VIRALONCOGENESISRETROVIRUS CONTAIN 2 IDENTICAL RNA STRANDSAND ENZYME REVERSE TRANSCRIPTASE

46. RT ACTS AS A RNA DEPENDENT DNA SYNTHETASEACT AS TEMPLATE TO SYNTHESIS OF ASINGLE STRAND OF MATCHING VIRAL DNA.

47. SINGLE STRAND OF VIRAL DNA IS THEN COPIED BY DNA DEPENDENT DNA POLYMERASE TO FORM ANOTHER STRAND OF COMPLIMENTARY DNA

48. THIS RESULTS IN DOUBLE STRANDED VIRAL DNA FORMATION OR PROVIRUS FORMATION

49. PROVIRAL DNA GETS INTEGRATED INTO HOST CELL GENOME - NEOPLASM

50. SUMMARY OF VIRUSES AND HUMAN CANCERI.BENIGN TUMOURSa.HUMAN PAPILLOMA VIRUS -HUMAN WARTSb. POXVIRUS - MOLLUSCUM CONTAGIOSUM