Hide Notes 

Slide 1: SURGICAL ONCOLOGY James Taclin C. Banez, MD, FPSGS, FPCS, DPBS, DPSA
Slide 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.
Slide 3: Neoplasm: 1. 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. Composed of normal appearing cells that do not invade locally or metastasize to other sites 2. Benign: 
Slide 4: EPIDEMIOLOGY:   Overall cancer death rates shows slow steady increase Lower death rates during past 50yrs: 1. 2. Stomach Uterus Lung Pancreas  Increase death rates: 1. 2.
Slide 5: EPIDEMIOLOGY: Cancer incidence by sites and sex: Male Lung Prostate Colon & Rectum Urinary Leukemia & Lymphoma Skin, pancreas and oral 20% Breast 20% Colon & Rectum 14% Lung 10% Uterus 8% Leukemia & Lymphoma Female 27% 16% 11% 10% 7% 3-4% 3-4% Skin, pancreas and oral
Slide 6: EPIDEMIOLOGY: Cancer death by sites and sex: Male Lung Colon & Rectum Prostate Leukemia & Lymphoma Pancreas & Urinary 36% Lung 11% Breast 10% Colon & Rectum 9% Leukemia & Lymphoma Female 20% 18% 14% 9% 5% 4% each 5% Pancreas & Ovary each Urinary & Uterus
Slide 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%
Slide 8: ETIOLOGY: 1. Chemical carcinogens: a. b. c. d. Hydrocarbons from coal tar = skin, larynx & bronchial CA Aromatic amines = urinary tract CA Benzene = leukemia Asbestos = mesothelioma Ionizing radiations = bone cancer  2. Physical carcinogens: a. Multiple x-rays = skin/thyroid CA b. Atomic bomb (Japan) = leukemia
Slide 9: ETIOLOGY: 1. Mechanical (chronic irritation):  Marjolin’s ulcer = burn scar cancer Parasitic:  2. Infection:  Schistosomas – Liver & bladder CA Hepatitis B – hepatocellular CA Epstein-Barr virus – Burkitts lymphoma Herpes simplex virus 2 – cervical CA Aids  Viruses:    
Slide 10: ETIOLOGY: 1. Geographic factors:           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 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
Slide 11: ETIOLOGY: 1. Precancerous conditions: a. b. c. d. e. f. Leucoplakia Actinic keratosis Polyps of colon & rectum Neurofibromas Dysplasia of cervix, bronchial Chronic ulcerative colitis Familial polyposis – colonic CA Breast CA – 2-3x in daughters and in younger age 2. Hereditary factors:  1.
Slide 12: ETIOLOGY: 1. Oncogenes & Growth Factors:  RNA tumor viruses cause: 1. 2. 3. 4. Carcinomas Sarcoma Leukemia Lymphomas  Retrovirus have an enzyme that alters genomic RNA resulting to abnormal growth and differentiation of the cell. Lung / breast CA 2. Multi-factorial: 
Slide 13: CANCER BIOLOGY 1. 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
Slide 14: CANCER BIOLOGY 1. 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)
Slide 15: CANCER BIOLOGY 1. 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) 1. Growth rates of neoplasm:   Doubling time is doubled Takes 30 doubling time to produce 1cm nodule
Slide 16: CANCER BIOLOGY 1. Effector mechanism in tumor immunity:  Host provides a number of effector mechs. that destroys the tumor: a. b. c. d. e. f. Tumor-antigen-specific antibodies Mononuclear phagocytes Natural killer cells Cytotoxic T lymphocytes Neutrophils K cells
Slide 17: CANCER BIOLOGY 1. Effector mechanism in tumor immunity:  Tumor Necrosis Factor (TNF):   Cytokines produced by monocytes, machrophage, endothelial cells, large granular lymphocytes and neutrophils Properties: a. Direct cytotoxicity for certain cells b. Stimulation of procoagulant activity by vascular endothelial cells c. Induction of fever by direct effect on the hypothalamic thermoregulatory center
Slide 18: CANCER PATHOLOGY A. Classification of Neoplasm: Carcinoma – arising from epithelial cells Sarcoma – arise from connective tissue and cells of mesenchymal origin (fibrous, muscular, fatty, vascular & skeletal).
Slide 19: CANCER PATHOLOGY A. Grading of malignancy:  Broders classified carcinoma into 4 grades according to: 1. 2. Degree of differentiation Appearance of cells, their nuclei and the number of mitotic figures Grade I Grade IV – least malignant – most malignant
Slide 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
Slide 21: ROUTES OF SPREAD:  Metastasis may entirely dominate the clinical picture, while the primary tumor remains latent and asymptomatic 1. Direct extension 2. Lymphatic spread  Common in epithelial neoplasms of all types (except for basal cell CA)
Slide 22: ROUTES OF SPREAD: 1. 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 Peritoneal seedings (gastrointestinal CA) 2. Spread through serous cavities 
Slide 23: CLINICAL MANIFESTATION:  The onset of neoplastic state is difficult to date (asymptomatic). Seven Danger Signals of Cancer (Direct manifestation): 1. 2. 3. 4. 5. 6. 7. 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
Slide 24: CLINICAL MANIFESTATION: Indirect or Systemic Manifestation: 1. Secondary to metastasis  Cachexia 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 2. Secondary to none metastatic: a. b. c. d.
Slide 25: CLINICAL MANIFESTATION: Signs of Expansile growth: 1. Obstruction 2. Destruction Signs of Infiltrative Growth:  Tumor infiltrates the nerves 1. 2. 3. Pain Numbness paralysis
Slide 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
Slide 27: DIAGNOSIS OF CANCER: A. Clinical History:  Warning signs for Cancer: 1. 2. 3. 4. Weight loss Loss of Appetite Bleeding or a discharge from any body orifice or nipple Sore that is slow to heal
Slide 28: DIAGNOSIS OF CANCER: A. Clinical History:  1. 2. 3. 4. 5. 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
Slide 29: DIAGNOSIS OF CANCER: A. Physical Examination:   Palpable masses (movable, nonmovable) LN enlargement Blood examination Radiological procedure:  B. Laboratory Examination:   X-ray, esophagoram, Barium enema, mammography, thyroid scan, CT scan, MRI
Slide 30: DIAGNOSIS OF CANCER: A. Laboratory Examination:  Endoscopy:  Bronchoscopy, esophagoscopy, gastroscopy, proctosigmoidoscopy, colonoscopy, cystoscopy
Slide 31: DIAGNOSIS OF CANCER: A. Laboratory Examination:  Biopsy:   o To document presence of malignancy Types: 1. Needle biopsy (cytological) 2. Incisional biopsy 3. Excisional biopsy Rapid frozen biopsy / exfoliative cytology (Pap smear)
Slide 32: STAGING OF CANCER: A. Clinical Staging of Cancer: TNM: Stage Stage Stage Stage  I = cancer confined to it’s primary site II = more locally advanced disease III = metastasis to regional LN IV = metastasis to distant sites Use all information available prior to 1st definitive treatment:
Slide 33: STAGING OF CANCER: A. 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. Restaging is necessary for additional or secondary definitive treatment after a (disease-free) interval following 1st treatment. Used only when the cancer is 1st diagnosed at autopsy. B. Re-treatment Staging:  C. Autopsy Staging: 
Slide 34: CANCER TREATMENT: Interdisciplinary Approach: Surgical resection 55% (40% alone) 2. Radiation therapy 34% (16% alone) 3. 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. 1.  
Slide 35: CANCER TREATMENT: GOALS of Therapy:  Vary w/ extent of the cancer: 1. Localized w/o evidence of spread:  Eradicate the cancer and CURE THE PATIENT 2. Spread beyond the local site:  Control patient’s symptoms and to maintain maximum activity for the longest possible period of time.
Slide 36: CANCER TREATMENT: CRITERIA of Incurability: 1. 2. 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.
Slide 37: CANCER TREATMENT: SURGICAL RESECTION: A. 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  B. Surgical Palliative Resection: 1. 2. 3. To relieve symptoms To prolong a useful comfortable life Gastrojejunostomy, colostomy
Slide 38: CANCER TREATMENT: RADIOTHERAPY:   Destroy tumor with preservation of anatomic structures Direct toxic effect to cells due to ionization of water
Slide 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
Slide 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
Slide 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
Slide 42: PROGNOSIS: DETERMINANTS: 1. 2. 3. 4. 5. Site of origin of primary tumor Stage of the disease Histologic features of the cancer Host immune factors Age of the patients
Slide 43: THANK YOU