SURGICAL ONCOLOGY
James Taclin C. Banez, MD, FPSGS, FPCS, DPBS, DPSA
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 rates: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, 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%
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 cancer
Multiple x-rays = skin/thyroid CA
b. 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: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. Leucoplakiab. Actinic keratosisc. Polyps of colon & rectumd. Neurofibromase. Dysplasia of cervix, bronchialf. Chronic ulcerative colitis
7. Hereditary factors: Familial polyposis – colonic CA6. Breast CA – 2-3x in daughters and in
younger age
ETIOLOGY:8. Oncogenes & Growth Factors:
RNA tumor viruses cause: 1. Carcinomas2. Sarcoma3. Leukemia4. Lymphomas
Retrovirus have an enzyme that alters genomic RNA resulting to abnormal growth and differentiation of the cell.
9. 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 structures
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)
CANCER BIOLOGY
2. 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)
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
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
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)
ROUTES OF SPREAD:
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 presenting 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 heal
DIAGNOSIS OF CANCER:
A. Clinical History: Warning signs for Cancer:5. 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
DIAGNOSIS OF CANCER:
C. Laboratory Examination: 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 PATIENT2. 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 co-existing 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:1. Site of origin of primary tumor2. Stage of the disease3. Histologic features of the cancer4. Host immune factors5. Age of the patients
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