Surgical Oncology

• 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:

• Cancerincidencebysites 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:

• Cancerdeathbysites 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 ofskin, thyroid, cervix, uterusandbladder ; 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):

• • Marjolins 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 & environmentplays 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:

• • Brodersclassified 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 ex