1. staging Clinico_pathological staging is important for: 1.It gives estimate of prognosis. 2.It is useful in planning of treatment. 3.It is useful in comparison of outcome from different centers. Histological diagnoses is done by biopsy Types of biopsies : 1.Incisional biopsy: removal of a small portion of a tumour by.. : a. Endoscopic biopsies b. core-needle biopsy by tru-cut needle. c. fine-needle aspiration biopsy 2.Excisional biopsy : the whole tumour is removed with the draining lymph node

5. TNM staging system T: size of primary tumour. T: size of primary tumour. N: extent of spread to regional L.N. N: extent of spread to regional L.N. M: presence or absence of distant metastases. M: presence or absence of distant metastases. Histological grading It assesses the degree of differentiation : a. : well-differentiated (good prognosis) b. :moderately differentiated (bad prognosis) c. : poorly differentiated (worst prognosis) Screening for cancer Is the detection of disease in an asymptomatic population to improve outcomes by early diagnosis

7. Criteria for screening 1. The disease : a. recognizable at early stage b. treatment at early stage is beneficial. C. common disease. 2.The test : a. sensitive and specific. b. acceptable by people. c. safe and inexpensive. 3.The program :a. Adequate further diagnostic tools. b. beneficial treatment is available. c. benefit more than physical and psychological harm. E.g.. Breast and colorectal cancer.

9. The multi disciplinary team in cancer treatment 1. surgery : the main aim of cancer surgery is local control of tumour, surgery can be : a. diagnostic. b. curative. c. palliative. d. preventive. e.reconstructive. A. diagnostic surgery, e.g. obtaining tissue for diagnosis like in laparoscopy. B. curative surgery : removal of the primary tumour and as much as possible of the surrounding tissue and L.N. C. palliative surgery : like in inoperable carcinoma of head of pancreas, we anastamose the G.B to jejunum to alleviate.obst. Jaundice. D. preventive surgery : like in F.A.P. treated by pan procto- colectomy. E. reconstructive surgery : to restore the continuity of G.I.T.

11. 2.Radiotherapy Is the use of mega voltage x-ray or gamma rays which generates energy more than 1.1 million volt. Its advantages: 1.it can treat deeply –seated tumours. 2.it causes minimal skin reaction. 3.absorption of radiation is similar in all tissues. Molecular effects of ionising radiation ionising radiation interacts with tissue by tow ways : 1.direct action : primary ionisation of macromolecules. 2.indirect action : by production of reactive species from breakdown of water which then causes damage to macromolecules (moving an electron from H2O to form H2O+ ‘ this is called free radical which causes most of the damage to the DNA. The biological effect of radiation is enhanced by oxygen which reacts with the free radical. Radiation dosage : is prescribed by Gray which is the absorption of :1. joule (J) of energy by one Kg of tissue.

12. Radiobiology (the four Rs) 1.Repair after radiation damage there are two patterns of repair: A. sublethal damage repair (SLD) takes 4-6 hrs after afraction of radiotherapy then the cell will be repaired. This happens to the normal cells. B. potentially lethal damage (PLD) happens after 4-6 hrs of radiation. Cells will not be repaired (killed). This happens to cancer cells. 2.repopulation,after killing cancer cells by radiotherapy in growth fraction this gives stimuli to cells inclonogenic fraction to start and repopulate tumour, so, tumour will shrink. 3.redistribution : cells G2 or M are more sensitive to radiotherapy than cells in late S phase. This will synchronise the cells. 4.reoxygenation : hypoxic cells are radio-resistant. So, every time we use radiothearpy oxygenated cells are killed. And the portion of hypoxic cells becomes oxygenated, this takes 24 hrs. These four factors provides the reason for fractionation of radiotherapy.

13. Tumour factors determining the success of radiotherapy 1.radio sensitivity : tumours are variable In their sensitivity to radiotherapy e.g. : seminoma and lymphoma are more sensitive than soft tissue sarcoma. 2. tumour volume: the larger the tumour is the higher proportion of cells that are hypoxic or anoxic. So more resistant to R.T. 3.the site of the tumour : tumours which lie adjacent to organs which are easily damaged by R.T are difficult to treat. Complications of R.T It arises from inevitable damage to normal tissue adjacent to the tumour. The most sensitive tissues are : 1.bone marrow. 2.gonads.3.eyes. 4.mucosa of GIT. 5.lungs.6.kidneys.7.liver.

14. Treatment planning Aims : 1.maximum required dose is reached to the Tu. 2.minimal dose to nearby organs. To do so, we have to know : A. the volume that needs to be treated. B. the required dose to kill the Tu. C. the arrangement of RT. fields

15. 1.gross Tu. Volume (GTV) : is the actual Tu. Volume. 2.clinical target volume (CTV) Tu. + microscopical Tu. Cells around Tu. 3.planning target volume (PTV) is the above + extra margine to allow for variation in shape and position of Tu. 4.treatment volume (TV) : is the practical volume treated by the machine. 5.irradiated volume : is all the above plus small margine due to scatter of R.T. Volume of Tu.

16. Dosage of R.T Is the over all dose in Grays divided by the over all time of treatment : 1.normal fractionation is Five fraction per week. 2.hypo fractionation is fewer than four fractions per week. 3. hyper fractionation two fractions per day = ten fractions per week. Field arrangement 1. single field : is used for palliation. 2.parallel opposed fields: is used for head and neck Tu. 3.multiple field for deeply seated TU. Like prostate. U. Bladder.

17. 3.chemotherapy Classification of C.T agents are : 1.alkylating agents.e.g. cyclophos phamide and melphalan. Action : it binds to protein or DNA and inhibit their function. (non – cycle specific) 2.anti-metabolites, e.g. 5-fluorouracil and methotrexate. Action : they inhibit DNA synthesis leading to cell death. They work through the (S phase ) (cycle specific). 3.vinca alkaloids, e.g. vinicristine,vinblastine. Action : arrest cell in mitosis (act at M) (cycle specific). 4.anti-biotics, e.g. adriamycin, bleomycin. Action : binds to double stranded DNA preventing its replication (non- cycle specific).

18. C.T drug resistance 1.interinsic resistance : the TU. from the start is resistant to C.T by its own nature, e.g. lipo - sarcoma. 2.acquired resistance : it arises after several exposures to the drug due to selection of resistant cells by destruction of sensitive cells. Why C.T must be given intermittently and in combination and over apro-longed period Each time C.T is used growth fraction (G.F) is killed, by time clonogenic fraction (C.F) will transfer to be ( G.F) and TU. Shrinks. This needs C.T to be given intermittently and over apro-longe period and in combination to overcome drug resistance

22. Combination C.T How to choose combination C.T : 1.each drug must be active against the TU. If used alone. 2.drugs must not be similar in toxicities. 3.they must have different mechanisms of action. 4. they must be used close to their maximum tolerable dose. Response to C.T 1.cure : H.D,acute childhood leukaemia, chorio carcinoma, E.sarcoma, willms TU. 2.improved survival : overian CA., breast CA., M.M. 3.non-responsive CA. :malignmant melanoma thyroid carcinoma, R.C.C.

23. Complications of C.T A. mild : nausea, vomiting, mucositis, alopecia. B. moderate leucopenia, thrombocytopenia. C. sever : cardiac toxicity, (ADM), lung fibrosis (bleomycin), nephro toxicity (cisplatin), second cancer formation.