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 Inflammatory, Degenerative &
Pathology of  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

Controls of Growth: Non-Neoplastic Proliferation:

 Cytokines: Cyclins, Cyclin dependent *Controlled & Reversible
kinases (CDK).  Hypertrophy – Size
 Growth factors – PDGF, FGF  Hyperplasia – Number

 Metaplasia – Change
 Growth Inhibitors.
 Dysplasia – Disordered
 Cancer suppressor genes – p53

 Oncogenes – c-onc, p-onc, v-onc etc.

Neoplastic Proliferation:
Uncontrolled & Irreversible*  Progressive, Purposeless,
 Benign
Pathologic, Proliferation of cells
characterized by loss of control over
– Localized, non-invasive.
cell division.
 Malignant (Cancer)
 DNA damage at growth control genes
–Spreading, Invasive.
is central to development of
 Carcinogens – Chemical, physical &
genetic  DNA damage  Neoplasm.


Pathogenesis of Neoplasia:
Willis Definition:
 Normal  Hyperplasia  Metaplasia (DNA
 Neoplasm is an abnormal mass of damage)  Dysplasia  (DNA damage)  (DNA damage)
Anaplasia (DNA damage) Infiltration  (DNA
tissue the growth of which exceeds damage)  Metastasis….
and is uncoordinated with that of  Progressive DNA Damage – features of
normal tissue and persists in the same neoplasia.
excessive manner after cessation of
the stimuli which evoked the change

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+


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

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.


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:


Carcinoma Lung:
Carcinoma Breast:

Osteo - sarcoma: CT: metastatic adenocarcinoma

Biopsy – Slide preparation staining


Colon Polyp: Hepatic Adenoma:

Normal Adenoma

Anaplasia in Sarcoma: Anaplasia:

Hepatic Adenocarcinoma: Hepatic Adenocarcinoma:


Clinical Features.
Liver Metastasis:
 Tumor Impingement on nearby
– 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
 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.


summary summary
 malignant neoplasms tend to be fast-  The prognosis of a patient with any
growing lesions which invade normal type of neoplasm depends on a
structures number of factors including: the rate
 malignant neoplasms vary in the of growth of the tumor, the size of
degree of differentiation and some the tumor, the tumor site, the cell
show anaplasia. type and degree of differentiation,
 malignant neoplasms are capable of
the presence of metastasis,
infiltration, invasion & metastasis. responsiveness to therapy, and the
general health of the patient.

Self Assessment Questions:

 What is a neoplasm? Write two special
Uncontrolled cell Division  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
(DNA abnormality)

Self Assessment Questions:

 What is carcinoma-in-situ? “Don’t fight a battle if you
 What is grading? And staging? don’t gain anything by
 How are neoplasms named?
 What is CIN? Classify
 What are the common routes of –George S. Patton
cancer spread?
 How do we diagnose cancer?
 Brief note of tumor markers?