The document discusses oncology and cancer epidemiology, etiology, biology, pathology, diagnosis, staging, and treatment. It provides statistics on common cancer types and mortality rates by sex. Cancer results from uncontrolled cell growth and can spread locally or metastasize. Diagnosis involves clinical exams, imaging, biopsies and laboratory tests. Staging classifies cancer extent and guides treatment which may include surgery, radiation, chemotherapy, or a combination. The goal is cure for localized cancer or symptom control and quality life for advanced cancer.

1. SURGICAL ONCOLOGY James Taclin C. Banez, MD, FPSGS, FPCS, DPBS, DPSA

2. Study of neoplastic diseases: ONCOS = tumor LOGOS = study Neoplasm : Altered cell population characterized by an excessive, non-useful proliferation of cells that are unresponsive to normal control mechanisms and to organizing influences of adjacent tissue.

3. Neoplasm: Malignant: Cancer cells that exhibit uncontrolled proliferation and impair the function of normal organs by local tissue invasion and metastatic spread to distant anatomic sites. Benign: Composed of normal appearing cells that do not invade locally or metastasize to other sites

4. EPIDEMIOLOGY: Overall cancer death rates shows slow steady increase Lower death rates during past 50yrs: Stomach Uterus Increase death rates: Lung Pancreas

5. EPIDEMIOLOGY: Cancer incidence by sites and sex: Male Female Lung 20% Breast 27% Prostate 20% Colon & Rectum 16% Colon & Rectum 14% Lung 11% Urinary 10% Uterus 10% Leukemia & Lymphoma 8% Leukemia & Lymphoma 7% Skin, pancreas and oral 3-4% Skin, pancreas and oral 3-4%

6. EPIDEMIOLOGY: Cancer death by sites and sex: Male Female Lung 36% Lung 20% Colon & Rectum 11% Breast 18% Prostate 10% Colon & Rectum 14% Leukemia & Lymphoma 9% Leukemia & Lymphoma 9% Pancreas & Urinary 5% each Pancreas & Ovary 5% Urinary & Uterus 4% each

7. The most significant 5 yrs survival rates are achieved in patients w/ cancer of skin, thyroid, cervix, uterus and bladder ; w/ the lowest survival w/ pancreatic cancer Females tend to have a greater number of 5yrs survival w/ cancer of any given primary site than males, reason (?) 5 yr survival female = 50% 5 yr survival male = 31%

8. ETIOLOGY: Chemical carcinogens : Hydrocarbons from coal tar = skin, larynx & bronchial CA Aromatic amines = urinary tract CA Benzene = leukemia Asbestos = mesothelioma Physical carcinogens: Ionizing radiations = bone cancer Multiple x-rays = skin/thyroid CA Atomic bomb (Japan) = leukemia

9. ETIOLOGY: Mechanical (chronic irritation): Marjolin’s ulcer = burn scar cancer Infection: Parasitic: Schistosomas – Liver & bladder CA Viruses: Hepatitis B – hepatocellular CA Epstein-Barr virus – Burkitts lymphoma Herpes simplex virus 2 – cervical CA Aids

10. ETIOLOGY: Geographic factors: Inc. CA of stomach – Scandinavian, Iceland and Japan Inc. CA of liver – South & West Africa Inc. CA of Nasopharynx – China Inc. CA of urinary bladder – Egypt Dec. CA of colon – Black/Africa Dec. CA prostate / breast – Japan Dec. CA of uterine/cervix – Israel/Jewish Dec. CA of skin – Blacks customs & environment plays an important role in the development of CA. migration of populations usually causes a shift towards the patterns of cancer incidence of the host country

11. ETIOLOGY: Precancerous conditions: Leucoplakia Actinic keratosis Polyps of colon & rectum Neurofibromas Dysplasia of cervix, bronchial Chronic ulcerative colitis Hereditary factors: Familial polyposis – colonic CA Breast CA – 2-3x in daughters and in younger age

12. ETIOLOGY: Oncogenes & Growth Factors: RNA tumor viruses cause: Carcinomas Sarcoma Leukemia Lymphomas Retrovirus have an enzyme that alters genomic RNA resulting to abnormal growth and differentiation of the cell. Multi-factorial: Lung / breast CA

13. CANCER BIOLOGY Morphologic changes: Rise from a single cell Revert to more primitive cell types Normal orderly tissue patterns are lost or replaced by the random pilling up of malignant cells w/o definite pattern High index of mitoses Invasion of adjacent structures

14. CANCER BIOLOGY Biochemical changes: Changes in DNA, RNA and chemical architecture results to LOSS of CONTACT INHIBITION to proliferation and intercellular adhesiveness Reversion of normal cellular biochemistry to that of the embryonal cells that produces EMBRYONAL subs. (CEA, alpha fetoprotein)

15. CANCER BIOLOGY Biochemical changes: Also produced biologically active subs. Normally produced by the cells. (hyperparathyroidism); also that are not normally produced by the cells of origin (bronchogenic CA=ACTH) Growth rates of neoplasm: Doubling time is doubled Takes 30 doubling time to produce 1cm nodule

16. CANCER BIOLOGY Effector mechanism in tumor immunity: Host provides a number of effector mechs. that destroys the tumor: Tumor-antigen-specific antibodies Mononuclear phagocytes Natural killer cells Cytotoxic T lymphocytes Neutrophils K cells

17. CANCER BIOLOGY Effector mechanism in tumor immunity: Tumor Necrosis Factor (TNF): Cytokines produced by monocytes, machrophage, endothelial cells, large granular lymphocytes and neutrophils Properties: Direct cytotoxicity for certain cells Stimulation of procoagulant activity by vascular endothelial cells Induction of fever by direct effect on the hypothalamic thermoregulatory center

18. CANCER PATHOLOGY Classification of Neoplasm: Carcinoma – arising from epithelial cells Sarcoma – arise from connective tissue and cells of mesenchymal origin (fibrous, muscular, fatty, vascular & skeletal).

19. CANCER PATHOLOGY Grading of malignancy: Broders classified carcinoma into 4 grades according to: Degree of differentiation Appearance of cells, their nuclei and the number of mitotic figures Grade I – least malignant Grade IV – most malignant

20. CANCER PATHOLOGY Carcinoma in Situ: Has cytologic characteristic of malignant tumors but w/ no detectable invasion into the surrounding tissue or infiltration into deeper cell layers

21. ROUTES OF SPREAD: Metastasis may entirely dominate the clinical picture, while the primary tumor remains latent and asymptomatic Direct extension Lymphatic spread Common in epithelial neoplasms of all types (except for basal cell CA)

22. ROUTES OF SPREAD: Vascular spread Either thru the thoracic duct or by the invasion of blood vessels Capillaries are almost invaded, veins invaded frequently but arteries rarely. More common in sarcomas Spread through serous cavities Peritoneal seedings (gastrointestinal CA)

23. CLINICAL MANIFESTATION : The onset of neoplastic state is difficult to date (asymptomatic). Seven Danger Signals of Cancer (Direct manifestation): Change in bowel or bladder habits A sore that does not heal Unusual bleeding or discharge Thickening or lump in breast or elsewhere Indigestion or difficult in swallowing Obvious change in wart or mole Nagging cough or hoarseness

24. CLINICAL MANIFESTATION : Indirect or Systemic Manifestation : Secondary to metastasis Cachexia Secondary to none metastatic: Ectopic production of known hormones Secretion of unidentified, hormone like substances Toxic substances secreted from the tumor Autoimmune – host is sensitized to an antigen from the tumor

25. CLINICAL MANIFESTATION : Signs of Expansile growth: Obstruction Destruction Signs of Infiltrative Growth: Tumor infiltrates the nerves Pain Numbness paralysis

26. CLINICAL MANIFESTATION : Signs of Tumor necrosis (Bleeding & Infection): Tumor may become necrotic, ulcerate and bleed Fatigue and weakness in right colon cancer due to anemia Inflammation caused by cecal CA can mimic the clinical symptoms of acute AP or cholecystitis. Unknown primary tumors presenting as metastases

27. DIAGNOSIS OF CANCER: Clinical History: Warning signs for Cancer: Weight loss Loss of Appetite Bleeding or a discharge from any body orifice or nipple Sore that is slow to heal

28. DIAGNOSIS OF CANCER: Clinical History: Warning signs for Cancer: Persistent cough or wheeze Change in voice Difficulty of swallowing Change in bowel habit Growing lump in the skin, breast, abdomen or muscle

29. DIAGNOSIS OF CANCER: Physical Examination: Palpable masses (movable, non-movable) LN enlargement Laboratory Examination: Blood examination Radiological procedure: X-ray, esophagoram, Barium enema, mammography, thyroid scan, CT scan, MRI

30. DIAGNOSIS OF CANCER: Laboratory Examination: Endoscopy: Bronchoscopy, esophagoscopy, gastroscopy, proctosigmoidoscopy, colonoscopy, cystoscopy

31. DIAGNOSIS OF CANCER: Laboratory Examination: Biopsy: To document presence of malignancy Types: Needle biopsy (cytological) Incisional biopsy Excisional biopsy Rapid frozen biopsy / exfoliative cytology (Pap smear)

32. STAGING OF CANCER: Clinical Staging of Cancer: TNM: Stage I = cancer confined to it’s primary site Stage II = more locally advanced disease Stage III = metastasis to regional LN Stage IV = metastasis to distant sites Use all information available prior to 1 st definitive treatment:

33. STAGING OF CANCER: Post-surgical Resection Staging: Pathological Staging: The extent of disease using all data available at the time of surgery and on examination of a completely resected specimen. Re-treatment Staging: Restaging is necessary for additional or secondary definitive treatment after a (disease-free) interval following 1 st treatment. Autopsy Staging: Used only when the cancer is 1 st diagnosed at autopsy.

34. CANCER TREATMENT: Interdisciplinary Approach: Surgical resection 55% (40% alone) Radiation therapy 34% (16% alone) Chemotherapy 22% (alone or combination) Surgery & radiation tx represents treatment of cancers that remains localized to it’s primary site or regional LN. Chemotherapy and Immunotherapy – tx effective against tumor cells already metastatic to distant organ sites.

35. CANCER TREATMENT: GOALS of Therapy: Vary w/ extent of the cancer : Localized w/o evidence of spread: Eradicate the cancer and CURE THE PATIENT Spread beyond the local site: Control patient’s symptoms and to maintain maximum activity for the longest possible period of time.

36. CANCER TREATMENT: CRITERIA of Incurability: Distant metastasis (most common) Evidence of extensive local infiltration of adjacent organs or structures Pt’s general condition and the presence of any co-existing disease must be considered in planning therapy. The PSYCHOLOGICAL makeup of the patient and the patient’s life situation must be considered.

37. CANCER TREATMENT: SURGICAL RESECTION: Surgical Curative Resection: Wide local resection: Low grade malignancy Basal cell CA of the skin Radical Local Resection: High grade malignancy En Bloc LN dissection for breast, esophagus, gastric, colorectal CA Surgical Palliative Resection: To relieve symptoms To prolong a useful comfortable life Gastrojejunostomy, colostomy

38. CANCER TREATMENT: RADIOTHERAPY: Destroy tumor with preservation of anatomic structures Direct toxic effect to cells due to ionization of water

39. CANCER TREATMENT: CHEMOTHERAPY: Antimetabolites: Inhibit enzymes of nucleic acid synthesis Methotrexate & 5-FU Alkylating agents: Substitute alkyl grp for the hydrogen atom Alkylation of DNA molecule interferes with replication in transcription

40. CANCER TREATMENT: CHEMOTHERAPY: Antibiotics: From soil fungi Forms stable complexes with DNA and inhibit synthesis of DNA and RNA Actinomycin D, Doxorubicin, Bleomycin Vinca Alkaloids: Bind to microtubular proteins necessary for cell division causing cell death during mitosis Vincristine & Vinblastine

41. CANCER TREATMENT: IMMUNOTHERAPY: Inhibit proliferation of cancer cells w/o affecting function of normal cells Stimulates the host to generate specific immune response to its tumor-vaccine from tumor cells TUMOR SPECIFIC ANTISERUM: Murine monoclonal antibodies Immunotoxins None-specific immunotherapy=BCG vaccine

42. PROGNOSIS: DETERMINANTS: Site of origin of primary tumor Stage of the disease Histologic features of the cancer Host immune factors Age of the patients

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