9/2/2010
Introduction:
Pathology of
Neoplasia
Controls of Growth:
 Cytokines: Cyclins, Cyclin dependent
kinases (CDK).
 Growth factors – PDGF, FGF
 Growth Inhibitors.
 Cancer suppressor genes – p53
 Oncogenes – c-onc, p-onc, v-onc etc.
Neoplastic Proliferation:
Uncontrolled & Irreversible*
 Benign
– Localized, non-invasive.
 Malignant (Cancer)
–Spreading, Invasive.
 Inflammatory, Degenerative &
Neoplastic
 Growth – Increase in size due to
synthesis of tissue components.
 Proliferatation- Cell division.
 Differentiation: functional and
structural maturity of cells.
 Tumor – Swelling / new growth / mass
Non-Neoplastic Proliferation:
*Controlled & Reversible
 Hypertrophy – Size
 Hyperplasia – Number
 Metaplasia – Change
 Dysplasia – Disordered
Neoplasia:
 Progressive, Purposeless,
Pathologic, Proliferation of cells
characterized by loss of control over
cell division.
 DNA damage at growth control genes
is central to development of
neoplasm.
 Carcinogens – Chemical, physical &
genetic  DNA damage  Neoplasm.
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Willis Definition:
 Neoplasm is an abnormal mass of
tissue the growth of which exceeds
and is uncoordinated with that of
normal tissue and persists in the same
excessive manner after cessation of
the stimuli which evoked the change
Pathogenesis of Neoplasia:
 Normal  Hyperplasia  Metaplasia (DNA
damage)  Dysplasia  (DNA damage)  (DNA damage)
Anaplasia (DNA damage) Infiltration  (DNA
damage)  Metastasis….
 Progressive DNA Damage – features of
neoplasia.

Pathogenesis of Neoplasia: Mechanism of Neoplams

Normal Adaptation Benign Malignant
 Non lethal DNA Damage leading to
uncontrolled cell division.

Non-Neoplastic Neoplastic
(Polyclonal) (Monoclonal)

Structure of Neoplasm: Biology of Neoplasm:

 Cell of origin  Lung cancer
Neoplasticcells parenchyma.  Rate of growth  Grade - low, high
Non-neoplastic - stroma  Differentiation  Well, Mod, P, Un.
(Connective tissue & BV)  Local Invasion  Staging

 Metastasis  Staging

Fast growth  less stroma

Lung cancer:
Less stroma  more necrosis, Squamus cell carcinoma.
Poorly differentiated, high grade, stage 4, Liver+

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Benign Malignant:
 Slow growing,  Fast growing,
 capsulated,  non capsulated,
 Non-invasive  Invasive &

 do not Infiltrate
metastasize,  Metastasize.

 well  poorly
differentiated, differentiated,
 suffix “oma”  Suffix
eg. Fibroma. “Carcinoma” or
“Sarcoma”

Nomenclature: Cell of origin + Suffix Grading & Staging of Tumor

Suffix - oma Carcinoma / Sarcoma  Grading – Cellular Differentiation
 Fibroma  Fibrosarcoma (Microscopic)
 Osteoma  Osteosarcoma  Staging – Progression or Spread
 Adenoma  Adencarcinoma (clinical)
 Papilloma  Squamous cell carcinoma

 Chondroma  Chondrosarcoma

Exceptions: Leukemia, Lymphoma, Glioma,

TNM: Staging of tumor: Pathways of Spread:

 DirectSpread
 Body cavities
 Blood vessels
 Lymphatic vessels

 Lungs – Systemic Venous blood

 Liver– GIT venous return, nutrition.
 Brain – End arteries.

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Tumor Diagnosis:
Bilateral Cystadenoma Ovary:
 History and Clinical examination
 Imaging - X-Ray, US, CT, MRI

 Tumor markers Laboratory analysis

 Cytology –Pap smear, FNAB

 Biopsy - Histopathology, markers.

 Molecular Tech – Gene detection.

Lipoma Intestine: meningioma

Lung carcinoma
Hepatic Adenoma:

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Carcinoma Lung:
Carcinoma Breast:

Osteo - sarcoma: CT: metastatic adenocarcinoma

Biopsy – Slide preparation staining

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Colon Polyp: Hepatic Adenoma:

Normal Adenoma

Anaplasia in Sarcoma: Anaplasia:

Hepatic Adenocarcinoma: Hepatic Adenocarcinoma:

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Clinical Features.
Liver Metastasis:
 Tumor Impingement on nearby
structures
– Pancreatic ca on bile duct  Obst. Jaund.
 Ulceration/bleeding
– Colon, Gastric, and Renal cell carcinomas
 Infection (often due to obstruction)
– Pneumonia, Urinary inf.
 Rupture or Infarction
– Ovarian, Bladder, colon,

Cancer Cachexia Paraneoplastic Syndromes

 Due to Products released by tumor
 Progressive weakness, loss of  Cushing’s Syndrome
appetite, anemia and profound
 Adrenal, Lung Ca – ACTH
weight loss (>20%)
 Inappropriate ADH syndrome
 Often correlates with tumor mass &
(Hyponatremia) – lung ca
spread
 Hypothalamic tumors (vasopressin)
 Etiology includes a generalized
 Hypercalcemia – Ca is the common cause.
increase in metabolism and central
– lung.
effects of tumor on hypothalamus
 Hypoglycemia - insulin or insulin like
 Probably related to macrophage
activities Fibrosarcoma, Cerebellar
production of TNF-a hemangioma.

Skull in Myeloma: summary

 neoplasia- uncontrolled cell division
non responsive to growth controls.
 Benign and Malignant

 Naming – Cell of origin + Suffix

 Oma, Carcinoma, Sarcoma

 benign  slow-growing, well-

differentiated, localized, do not
metastasize, amenable to surgery.

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summary
 malignant neoplasms tend to be fast-
growing lesions which invade normal
structures
 malignant neoplasms vary in the
degree of differentiation and some
show anaplasia.
 malignant neoplasms are capable of
infiltration, invasion & metastasis.
NEOPLASM
Uncontrolled cell Division
(DNA abnormality)
Self Assessment Questions:
 What is carcinoma-in-situ?
 What is grading? And staging?
 How are neoplasms named?
 What is CIN? Classify
 What are the common routes of
cancer spread?
 How do we diagnose cancer?
 Brief note of tumor markers?
9/2/2010
summary
 The prognosis of a patient with any
type of neoplasm depends on a
number of factors including: the rate
of growth of the tumor, the size of
the tumor, the tumor site, the cell
type and degree of differentiation,
the presence of metastasis,
responsiveness to therapy, and the
general health of the patient.
Self Assessment Questions:
 What is a neoplasm? Write two special
characters?
 What is a papilloma, adenoma
 What is dysplasia, Metaplasia, Anaplasia
Hyperplasia? Mention examples?
 Mention major classes of neoplasms with
five differentiating features?
 Mention three features of malignant
tumor?
“Don’t fight a battle if you
don’t gain anything by
winning.”
–George S. Patton