SURGICAL ONCOLOGY

James Taclin C. Banez, MD, FPSGS, FPCS

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.

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.

2. Benign: Composed of normal appearing cells

that do not invade locally or metastasize to other sites

EPIDEMIOLOGY:

Overall cancer death rates shows slow steady increase

Lower death rates during past 50yrs:

1. Stomach2. Uterus

Increase death ratea:1. Lung2. pancreas

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%

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 & Uterus4%

each

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%

ETIOLOGY:1. Chemical carcinogens:

a. Hydrocarbons from coal tar = skin, larynx & bronchial CA

b. Aromatic amines = urinary tract CAc. Benzene = leukemiad. Asbestos = mesothelioma

2. Physical carcinogens:a. Ionizing radiations = bone cancerb. Multiple x-rays = skin/thyroid CAc. Atomic bomb (Japan) = leukemia

ETIOLOGY:3. Mechanical (chronic irritation):

Marjolin’s ulcer = burn scar cancer

4. Infection: Parasitic:

Schistosomas – Liver & bladder CA Viruses:

Hepatitis B – hepatocellular CA Epstein-Barr virus – Burkitts lymphoma Herpes simplex virus 2 – cervical CA Aids

ETIOLOGY:4. Hereditary factors:

Familial polyposis – colonic CA Breast CA – 2-3x in daughters and in younger age

5. 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

ETIOLOGY:6. Precancerous conditions:

a. Leuplakiab. Actinic keratosisc. Polyps of colon & rectumd. Neurofibromase. Dysplasia of cervix, bronchialf. Chronic ulcerative colitis

ETIOLOGY:6. Oncogenes & Growth Factors:

RNA tumor viruses cause: 1. Carcinomas2. Sarcoma3. Leukemia4. Lymphomas

Retrovirus have an enzyme that alters the viral genomic RNA resulting to abnormal growth and differentiation of the cell.

7. Multi-factorial: Lung / breast CA

CANCER BIOLOGY1. 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

CANCER BIOLOGY2. 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)

CANCER BIOLOGY

3. Growth rates of neoplasm: Doubling time is doubled Takes 30 doubling time to produce

1cm nodule

CANCER BIOLOGY4. Effector mechanism in tumor

immunity: Host provides a number of effector

mechs. That destroys the tumor:a. Tumor-antigen-specific antibodiesb. Mononuclear phagocytesc. Natural killer cellsd. Cytotoxic T lymphocytese. Neutrophilsf. K cells

CANCER BIOLOGY4. 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 cellsb. Stimulation of procoagulant activity by

vascular endothelial cellsc. Induction of fever by direct effect on the

hypothalamic thermoregulatory center

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).

CANCER PATHOLOGYB. Grading of malignancy:

Broders classified carcinoma into 4 grades according to:1. Degree of differentiation2. Appearance of cells, their nuclei and the

number of mitotic figures

Grade I – least malignantGrade 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

ROUTES OF SPREAD: Metastasis may entirely dominate the

clinical picture, while the primary tumor remains latent and asymptomatic

1. Direct extension2. Lymphatic spread

Common in epithelial neoplasms of all types (except for basal cell CA)

3. 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

4. Spread through serous cavities Peritoneal seedings (gastrointestinal CA)

CLINICAL MANIFESTATION: The onset of neoplastic state is

difficult to date (asymptomatic).Seven Danger Signals of Cancer

(Direct manifestation):1. Change in bowel or bladder habits2. A sore that does not heal3. Unusual bleeding or discharge4. Thickening or lump in breast or

elsewhere5. Indigestion or difficult in swallowing6. Obvious change in wart or mole7. Nagging cough or hoarseness

CLINICAL MANIFESTATION:Indirect or Systemic Manifestation:

1. Secondary to metastasis Cachexia

2. Secondary to none metastatic:a. Ectopic production of known hormonesb. Secretion of unidentified, hormone like

substancesc. Toxic substances secreted from the

tumord. Autoimmune – host is sensitized to an

antigen from the tumor

CLINICAL MANIFESTATION:Signs of Expansile growth:1. Obstruction2. Destruction

Signs of Infiltrative Growth: Tumor infiltrates the nerves

1. Pain2. Numbness3. paralysis

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

DIAGNOSIS OF CANCER:

A. Clinical History: Warning signs for Cancer:1. Weight loss2. Loss of Appetite3. Bleeding or a discharge from any body orifice

or nipple4. Sore that is slow to heal5. Persistent cough or wheeze6. Change in voice7. Difficulty of swallowing8. Change in bowel habit9. Growing lump in the skin, breast, abdomen or

muscle

DIAGNOSIS OF CANCER:

B. Physical Examination: Palpable masses (movable, non-

movable) LN enlargement

C. Laboratory Examination: Blood examination Radiological procedure:

X-ray, esophagoram, Barium enema, mammography, thyroid scan, CT scan, MRI

DIAGNOSIS OF CANCER:

C. Laboratory Examination: Endoscopy:

Bronchoscopy, esophagoscopy, gastroscopy, proctosigmoidoscopy, colonoscopy, cystoscopy

Biopsy: To document presence of malignancy Types:

1. Needle biopsy (cytological)2. Incisional biopsy3. Excisional biopsy

o Rapid frozen biopsy / exfoliative cytology (Pap smear)

STAGING OF CANCER:

A. 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:

STAGING OF CANCER:

B. 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.

C. Re-treatment Staging: Restaging is necessary for additional or secondary

definitive treatment after a (disease-free) interval following 1st treatment.

D. Autopsy Staging; Used only when the cancer is 1st diagnosed at

autopsy.

CANCER TREATMENT:

Interdisciplinary Approach:1. 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.

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.

CANCER TREATMENT:

CRITERIA of Incurability:1. Distant metastasis (most common)2. 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.

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. To relieve symptoms2. To prolong a useful comfortable life3. Gastrojejunostomy, colostomy

CANCER TREATMENT:

RADIOTHERAPY: Destroy tumor with preservation of

anatomic structures Direct toxic effect to cells due to

ionization of water

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

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

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

PROGNOSIS:

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