cystic teratoma

Soft tissue mass prob

Lipoma

fibroma
nevus

NEOPLASIA
Ma. Minda Luz M. Manuguid, M.D.
fibrosarcoma
 Definition of Terms
 APLASIA – absence of growth
 HYPOPLASIA – insufficient growth or development
 HYPERPLASIA – increase in number of cells;
increased growth
 METAPLASIA – change from one cell type to
another due to chronic irritation or trauma
 DYSPLASIA – disordered proliferation of cells;
atypical hyperplasia; malformation
 DESMOPLASIA – marked collagen formation in the
stroma
 ANAPLASIA – “backward development”
 ANAPLASIA
 failure to develop into mature,
differentiated cells
 tumor giant cells
 dyskaryosis – nuclear abnormalities
– chromatin clumping, anisokaryosis
hyperchromasia, multiple nuclei
multiple &/or prominent nucleoli
 ↑ number of mitoses; abnormal
mitotic figures; aneuploidy
 pleomorphism
 Definition of Terms
 NEOPLASIA – “new growth” – autonomous
proliferation of cells that is uncoordinated with the
growth of surrounding normal tissues, persistent even
when the stimulus for growth has been removed;
purposeless & preys on the host.
 NEOPLASM – an abnormal mass of tissue, the
growth of which exceeds, & is uncoordinated with,
that of normal tissues, & persists in the same
excessive manner after cessation of stimuli that
provoked the change.
 Definition of Terms
 ONCOLOGY – Gr. “oncos”= tumor – study of
neoplasms
 ONCOLOGIST – specialist physician in the
management of Neoplasia
 TUMOR – literally any swelling or mass; as used in
Neoplasia, it is equivalent to a neoplasm, which may
be benign or malignant
 CANCER – common term for a malignant neoplasm:
L. “crab”, with a tenacious hold on the surrounding
tissues
 Composition of a Neoplasm
 PARENCHYMA – main bulk/mass of the
neoplasm; main component cells – determines
the behavior of the neoplasm, invasiveness,
metastatic tendency, etc.
 STROMA – supporting framework to the
neoplasm; consists of connective tissues,
vasculature, innervation, etc. – modifies the
growth, nutrition, of the neoplasm
 Nomenclature
 type of parenchymal cell – root word –
describes the cell of origin of the neoplasm
 suffix “oma” – denotes benignity
 suffix “carcinoma” / “sarcoma” – malignant
neoplasms derived from epithelial /
mesenchymal elements
 gross/microscopic architectural features
 eponymic designations – based on actual
persons involved in the naming
 Nomenclature
Parenchymal cell type + suffix

 fibro- fibroma fibrosarcoma

 lipo- lipoma liposarcoma
 chondro- chondroma chondrosarcoma
 osteo- osteoma osteosarcoma
 rhabdomyo- rhabdomyoma rhabdomyosarcoma
 leiomyo- leiomyoma leiomyosarcoma
 angio- / angiosarcoma
hemangio- hemangioma
lymphangio- lymphangiomalymphangiosarcoma

 meningio- meningioma invasive meningioma

 Nomenclature
 synovium synovial sarcoma

 squamous cell- S C papilloma S C carcinoma

basal cell carcinoma

 neuroectoderm nevus malignant melanoma

 glandular adenoma adenocarcinoma

epithelium
 placenta H molechoriocarcinoma

 pluripotent mature teratoma immature teratoma

cells in gonads
 Nomenclature
 exceptions:
 teratoma, immature teratoma (teratocarcinoma)
 leukemia
 mixed mesenchymal tumor
 pleomorphic adenoma
 non-neoplastic lesions w/ suffix “oma”:
 hematoma,
 granuloma, amoeboma, tuberculoma
 hamartoma, choristoma
 malignant lesions w/ suffix “oma”
 hepatoma (hepatocellular CA), seminoma, mesothelioma
 glioma, glioblastoma, malignant lymphoma
 malignant melanoma, invasive meningioma
 Nomenclature
 gross / microscopic architectural features:
 cyst- ♦ pleiomorphic
 papillary ♦ scirrhous
 villous ♦ nodular
 follicular
 eponymic designations:
 Wilms tumor
 Krukenberg tumor
 Warthin’s tumor
Mucinous cystadenoma, Ovary
Papillary Villous

Pleiomorphic Scirrhous
 Etiologic Factors
• age – the elderly are more susceptible to developing
neoplasms because of diminished anti-oxidant
production & declining immunocompetence/ tumor
surveillance; infants & young children appear to be
susceptible to specific neoplasms e.g. germ cell tumors
like teratomas, genetically linked tumors like
retinoblastoma, neuroblastomas,
• diet – regional / ethnic dietary preferences show trends
in the development of certain neoplasms: consumption of
large amounts of very hot beverages like tea throughout
the day, every day, predisposes to esophageal cancer;
low fiber, high animal fat diets predispose to colorectal
cancer; the “Japanese” diet predisposes to gastric cancer;
nitrites & nitrates in processed meats predispose to
gastric cancer; smoked foods—esophageal CA;
 Etiologic factors
• occupation – exposure to: carcinogenic agents in
mining, working in factories that manufacture
processors, insulators, batteries, & plastics,
shipbuilding; radiation; infections that predispose to
cancer (health care workers); insecticides;
• other lifestyle factors – sexual practices- genital warts;
urban dwellers; exposure to environmental
pollutants/toxins; cigarette smokers
• infections – viral: EBV (nasopharyngealCA, Burkitt’s
lymphoma); HIV (lymphoma, Kaposi’s sarcoma); HBV
(hepatocellular CA); HTLV (leukemia); HPV (genital
CA); helminthic: Schistosoma haematobium (urinary
bladder)
 Etiologic factors
• ionizing radiation – nuclear facilities, nuclear
accidents like leaks/explosions; diagnostic &
therapeutic radiation; solar UV rays; ambient
radiation
• genetic – defective/ absent “anti-cancer” gene P53:
Li-Fraumeni syndrome – familial clustering of
neoplasms due to inadequacy/loss of DNA repair
systems; presence of oncogenes – DNA sequences
that predispose to certain forms of cancer:
 Oncogenes
def. : Nucleotide sequences capable of inducing
malignant transformation
 v-oncs: viral oncogenes (retrovirus / RNA
viruses)
 c-oncs: cellular oncogenes in human DNA:
(also called “proto-oncogenes”)
 erb-B: squamous cell CA;
 res: bladder, lung, colon CA;
 myc: Burkitt’s lymphoma;
 met: osteosarcoma
 Pre-neoplastic
syndromes/conditions
 Leukoplakia
 Barrett’s esophagus
 Atrophic gastritis (Pernicious anemia)
 Paget’s disease of Bone
 CIN (Cervical intraepithelial neoplasia)
Pre-neoplastic
Conditions
Cervix: Dysplasia & Carcinoma
 Carcinogenesis
acquired changes in the genetic
environmental genome of factors
factors somatic cells

activation of alteration of inactivation of

growth-promoting apoptosis-regulating cancer-
suppressor
oncogenes genes genes

expression of altered gene products

& loss of regulatory gene products
CLONAL EXPANSION ADDITIONAL MUTATIONS ( PROGRESSION )

MALIGNANT NEOPLASM
 Signs & Symptoms
 lump / mass
 pain
 bleeding
 obstructive Sx
 abnormal function / loss of function
 paraneoplastic syndromes: DI/SIADH;
Cushing’s syndrome;
 Cachexia : anemia; anorexia; malnutrition;
 Hypercoagulability (DIC)
 Metastasis
*** spread of the neoplasm to tissues distinct, & maybe
distant, from the primary site
 DIRECT SEEDING OF BODY CAVITIES – e.g.
Pseudomyxoma peritonei
 LYMPHATIC – favored by carcinomas – follows the
drainage sequence
 HEMATOGENOUS – favored by sarcomas – tumor
emboli in the vascular system
 IATROGENIC – thru inanimate objects – caused by the
surgeon
 Diagnosis
 CLINICAL ASSESSMENT – symptomatology
& physical examination
 RADIOGRAPHY – X-rays; Nuclear imaging;
Ultrasonography; Computerized tomography
scanning; Magnetic resonance imaging
 LABORATORY – serology- tumor markers;
indirect indices of overall systemic effects of
cancer, e.g. blood counts, blood in the stools,
 Tumor Markers
• Tumor (oncofetal) antigens
– AFP (liver, testicular germ cell tumors) ;
– CEA (colon, pancreas, lung, stomach, breast)
• Hormones
– HCG, ACTH, ADH, Calcitonin, Catecholamines
• Specific Proteins:
- Immunoglobulins (Multiple Myeloma),
- Prostate-Specific Antigen
• Glycoproteins, Mucin, CA 15-3(breast), CA 125(ovary),
CA 19-9 (colon, pancreas)
• Enzymes
– Acid phosphatase, neuron-specific enolase, galactosyl
transferase II,
 Diagnosis
 BIOPSY – histopathologic examination of living
tissue/ neoplasm:
 Paraffin sections
 Excision
 Incision
 Punch / endoscopic
 Frozen section
 EXFOLIATIVE CYTOPATHOLOGY – microscopic
examination of naturally/ artificially exfoliated cells
from body surfaces, usually stained with the
Papanicoulaou method of staining – the “Pap” smear
 Grading & Staging
 GRADING
 Grade I : well differentiated (75-100%)
 Grade II : moderately differentiated (50-74%)
 Grade III : poorly differentiated (25-49%)
 Grade IV: undifferentiated
 STAGING
 T1-T5 : tumor size
 N0-N3 : (lymph) nodal involvement
 M0-M2 : metastasis
 NEOPLASMS
 BENIGN NEOPLASM –
non-invasive, non-
metastasizing; incapable of
spreading to other sites
-slow, expansile growth
 MALIGNANT
NEOPLASM – “CANCER”
- invasive/infiltrative;
always has the capacity to
metastasize= spread to other
tissues of the body, even
distant ones, from the
primary site
 Benign vs Malignant
 Differentiation • good/well * variable
 nucleus:cytoplasm • 1:4 to 1:6 * 1:1 (nucleus
ratio normal enlarged)
 anaplasia • none * present
 encapsulation • may be (+) * none
 growth • slow, expansile * infiltrative
 desmoplasia • none * may be (+)
 angiogenesis • none * present (TAF)
 metastasis • none * capacity
always present
Squamous cell papilloma- Squamous cell carcinoma

Adenoma Adenocarcinoma
Fibroma Fibrosarcoma

Fibrous Histiocytoma
Benign malignant
 Osteoma Osteosarcoma

Chondroma Chondrosarcoma
 Lipoma Liposarcoma

Hemangioma Angiosarcoma
Thank
You
Very
Much