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***Melanoma/Seminoma/Hepatoma
Teratoma
Teratoma
CHARACTERISTICS OF BENIGN
AND MALIGNANT NEOPLASMS
The distinction is based on morphology and
behaviour using four criteria
1. differentiation and anaplasia
2. rate of growth
3. local invasion
4. Metastases
Three Routes:
1. Spread into body cavities seeding of surfaces in
peritoneal, pleural, pericardial, subarachnoid
spaces
Eg. Ovarian Ca spreads transperitoneally to the
surfaces of the liver.
Pseudomyxoma peritonei mucus-secreting
appendiceal Ca fill the peritoneal cavity with gelatinous
neoplastic mass
2. Invasion of lymphatics followed by transport to
regional nodes, then other parts of the body.
*skip metastases
METASTASES
3. Hematogenous spread typical of sarcomas and
also renal Ca
veins (thinner) more frequently invaded than arteries
lung and liver are common sites of hematogenous
metastases because these receive both systemic and
venous outflow.
Age
most Ca occur in later life (>55)
under 15 yrs: 60% of cancer deaths due to
acute leukemia and neoplasms of CNS
eg. Neuroblastoma, Wilms tumor,
retinoblastoma, acute leukemia, rhabdomyosarc
PREDISPOSITION TO CANCER
Heredity
close relatives of cancer patients have higher than
normal incidence of same neoplasm
childhood retinoblastoma: 40 % are familial,
inherited as an autosomal dominant (AD) trait
susceptibility to multiple colonic polyposis is
inherited as an AD trait, and almost all patients
develop Ca in later life
chromosomal-DNA instability syndromes are
inherited as autosomal recessives, char. by some
defect in DNA repair, and greatly increased risk to
develop Ca
eg. Xeroderma pigmentosum
ACQUIRED PRENEOPLASTIC
SYNDROMES
regenerative hyperplastic and dysplastic
proliferations are fertile soil for the origin of
a malignant transformation
well defined asso. between certain forms of
endometrial hyperplasia and endometrial
Ca, between cervical dysplasia and cervical
Ca
ACQUIRED PRENEOPLASTIC
SYNDROMES
Non-neoplastic precancerous conditions:
cirrhosis of liver hepatocellular Ca
atrophic gastritis of pernicious anemia
stomach Ca
chronic ulcerative colitis Ca of the colon
H. pylori gastritis
Viral hepatitis
Chronic Pancreatitis
ACQUIRED PRENEOPLASTIC
SYNDROMES
Proposed mechanics:
increase cytokine production growth of
transformed cells
increase the pool of tissue stem cells,
susceptible to mutagens
ROS produced genomic instability
ACQUIRED PRENEOPLASTIC
SYNDROMES
Precancerous benign neoplasia:
Villous adenoma of colon 50% risk to
become AdenoCa
Longstanding leimyoma leimyosarcoma
(rarely)
Pleomorphic Adenoma rare malignant
transformation
most benign neoplasms do not become
cancerous, most malignant tumors arise de
novo.
GRADING AND STAGING OF
CANCER
grade and stage provide a semiquantitative
estimate of the clinical gravity of tumor
both valuable for prognostication and for
planning therapy, although staging has
proved to be of greater clinical value
GRADING AND STAGING OF
CANCER
Grading: based on the degree of
differentiation and the number of mitoses
grades I-IV, with increasing anaplasia
in general, high grade tumors are more
aggressive
imperfect:
(1). Different areas may show different degrees of
differentiation
(2). Grade of tumor may change as tumor grows
Staging:based on
anatomic extent of
tumor
TNM: tumor, node,
metastases
LABORATORY DIAGNOSIS OF
CANCER
Histologic and Cytologic Methods
histologic examination is the most
important, aided by:
availability of relevant clinical data
adequate tissue preservation and sampling
Alpha-fetoprotein (AFP)
normally produced by fetal yolk sac and
liver
elevations
marked: in liver Ca and testicular germ cells
less marked: cirrhosis, hepatitis
measurements useful in indicating presence
of liver or testicular Ca, assessing
recurrence and response to therapy
Tumor Markers