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

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: Benign:
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 ratea:
Lung
pancreas

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

6. EPIDEMIOLOGY: Cancer death by sites and sex: Male Female Lung 36% 20%
Colon & Rectum
11%
Breast
18%
Prostate
10%
14%
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, 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: Physical 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): Infection:
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: Hereditary factors: Geographic factors:
Familial polyposis – colonic CA
Breast CA – 2-3x in daughters and in younger age
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: Leuplakia Actinic keratosis
Polyps of colon & rectum
Neurofibromas
Dysplasia of cervix, bronchial
Chronic ulcerative colitis

12. ETIOLOGY: Oncogenes & Growth Factors: Multi-factorial:
RNA tumor viruses cause:
Carcinomas
Sarcoma
Leukemia
Lymphomas
Retrovirus have an enzyme that alters the viral 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 sturctures

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)
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)

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

20. 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)
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)

21. 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

22. 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

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

24. 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 prsenting as metastases

25. 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
Persistent cough or wheeze
Change in voice
Difficulty of swallowing
Change in bowel habit
Growing lump in the skin, breast, abdomen or muscle

26. DIAGNOSIS OF CANCER: Physical Examination: Laboratory 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

27. DIAGNOSIS OF CANCER: Laboratory Examination: Endoscopy: Biopsy:
Bronchoscopy, esophagoscopy, gastroscopy, proctosigmoidoscopy, colonoscopy, cystoscopy
Biopsy:
To document presence of malignancy
Types:
Needle biopsy (cytological)
Incisional biopsy
Excisional biopsy
Rapid frozen biopsy / exfoliative cytology (Pap smear)

28. 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 1st definitive treatment:

29. 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 1st treatment.
Autopsy Staging;
Used only when the cancer is 1st diagnosed at autopsy.

30. 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.

31. 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.

32. 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 coecisteing disease must be considered in planning therapy.
The PSYCHOLOGICAL makeup of the patient and the patient’s life situation must be considered.

33. 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

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

35. CANCER TREATMENT: CHEMOTHERAPY: Antimetabolites: Alkylating agents:
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

36. CANCER TREATMENT: CHEMOTHERAPY: Antibiotics: Vinca Alkaloids:
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

37. 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

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