The term ‘neoplasia’ means the new growth . And the new growth present is called “neoplasm” or “tumor”.

However every new growth is not neoplasm as the new growth is also present in repairs and regenration, embryogenesis , hyperplasia and hormonal stimulation.

So we can define as “a mass of tissue formed as a result of abnormal ,excessive uncordinated,autonomous and purposeless proliferation of the cells.

COMPARISION OF THE BENIGN AND MALIGNANAT TUMORSfeatures Benign malignant

1. CLINICAL AND GROSS FEATURES

A.Boundries Encapsulated and well circumscribed

Poorly circumscribed and irregular.

B. Surrounding tissues Often compressed Usually invaded

C. Size Usually small Large

D. Secondary changes Less often More often

2.MICROSCOPIC FEATURES

A. Pattern Usually resembel the tissue of origin

Do not resembel

B. Basal polarity Retained Lost

C. N/C ratio Normal Increased

D. Mitosis Maybe present but allways typical

Mitotic figures increased and generally atypical

E. Tumor giant cells Maybe present but without nuclear atypia

Present with nuclear atypia

F. Chromosomal abnormalities

Infrequent Frequently present

G. Function Usually well maintained Retained ,lost or maybe abnormal

3.GROWTH RATE slow fast

4.LOCAL INVASION Often compress the surrounding tissue without compressing or invading them

Usually invade and infiltrate the surrounding tissue

5.METASTASIS Absent Present

6. PEOGNOSIS Local complication Death by local and metastatic complications.

(1)-RATE OF GROWTHThe tumor cells grows rapidly as

compare to the normal cells the rate of growth is depand on the 2 main factors.

1-Rate of division and destruction of the tumor cells

2-degree of diffrentiation3- growth factors

Epidermal growth factors (EGF)Fibroblast growth factor(FGF)Platelet derived growth factor(PDGF)Colony stimulating factor(CSF)Transforming growth factorβ(TGF- β) Interleukins(IL)

DIFFERENTIATION It is defined as the extent of

morphological and functional resemblance of the parenchymal tumor to the corresponding normal cell.

Well differentiated-most of benign and low grade malignant tumors

Poorly differentiated-most of the malignant tumors

ANAPLASIAAnaplasia is the lack of

differentiation and is characteristic feature of most of the malignant tumors.

Poorly diffrentiated tumors have high degree of anaplasia.

TUMOR ANGIOGENESIS In order to provide nourishment to the

growing tumor ,new blood vessels are formed from pre-existing ones.

Micro vascular density Central necrosis

TUMOR STROMA It is the presence of the fibroblastic

tissues in the tumor stroma . In primary stage the tumor remain soft . But later it converts in hard tumor. bFGF(basic fibroblastic growth

factor )controls the growth of fibrous cells.

BENIGN TUMORS- Most of the benign tumors are

encapsulated they expand and push the surrounding tissues without actually invading them.

MALIGNANAT TUMORS- Malignant tumor also enlarges by

expansion ,invasion ,infilttration and metastasis.

Metastasis is define as the spread of tumor by invasion in such a way that discontinuous secondary tumor are form at the site of lodgement.

ROUTES OF METASTASIS-1-lymphatic spread- Carcinoma is

spread by the lymphatic routes.

2-Hematogenous spread- Blood-borne metastasis is the

common routes for the sarcoma but certain carcinoma also frequently use this route.

Tumor of lung, breast , thyroid, kidney , prostate , liver and ovary are mostly metastasize by this route.

Systemic veins drains blood into vena cava from limbs ,head and neck , pelvis . Therefore cancers from these sites can be spread to lungs.

Portal veins drain blood from the bowel spleen and pancreas into the liver .therefore tumor of these organ have secondaries in the liver.

Arterial spread of tumor is less likely because they are thick walled and contain elastic tissue which is resistant to invasion.

Some cancers may spread by “seeding” in another surfaces.the routes are

(1)-Transcoelomic spread –Certain cancer invade through the serosal wall of the coelomic cavity. So that the tumor fragments or clusters of the tumor cells may be implanted into the other part of the body.

Ca stomach seeding to ovaries Ca ovary ca of bronchioles and breast seeding to the

pleura and pericardium.

(2)-Spread along epithelium lined surface- it is usuall for the malignant tumor to spread through the epithelium lined surface because intact epithelium and mucus coat are resisitant to penetration by tumor cells.

(3)Spread through CSF- malignant tumor of ependyma may spread by release of tumor fragmaents and tumor cells into the CSF and produce metastasis and the other sites of the central nervous system.

(4) Implantation- rarely a tumor may spread by implantation by surgeon’s needle ,sutures or may be implanted by direct contact such as transfer of the cancer of the upper lip to the lower lip.

Parenchyma – Comprised by proliferating tumor cells:,it determine the and evolution of tumor cells.

“Supportive stroma” – composed of fibrous tissue and blood vessels :it provide the framework on which the parenchymal cell tumor grows.

GRADING –

It is largely base on two important histologic feature.The degree of anaplasia and the rate of growth.

GRADE I-well diffrentiated(less than 25% anaplastic)

GRADE II-moderately diff (25-50% anaplastic )GRADE III-moderately diff (50-75% anaplastic

cells)GRADE IV-poorly diff (more than 75%

anaplastic)

STAGING-The spread of the cancer is assessed

by three way –by clinical examination ,by examination.And by pathologic examination of

the tissue.

When the cytologic feature of the malignancy are present but the malignant cells are confined to epithelium without invasion across the basement membrane . It is called carcinoma in situ. the common sites are

Uterine cervix at the junction of the ecto and endo junction.

Bowen’s disease of the skin Oral leukoplakia Intralobular and intraductal carcinoma

of breast.

20% of all death are cancer related. (A)- Predisposing factors-1.Family and genetic factors- family

history increases the three fold risk in development of cancer.example- Retinoblastoma,familial polyposis coli(autosomal dominant ).

2.Racial and genetic factors- some factors such as climate, soil, water, diet etc can contribute to the cancer development eg:-1.white europians and amaricans—develop breast ,lung, colon cancer commonly.

2.Black Africans- they have more commonly cancer of skin ,penis , cervix and liver.

3. Japnese – 5 time higher risk for cancer of stomach.

1. Cigarette smoking.2. Alcohal abuse3. Alcohal and tobacco together4. Cancer of cervix

1. Carcinaoma in situ2. Some benign tomors( multiple villus

adenomas of large intestine have high incidence of adenocarcinoma )

3. Miscellaneus conditions-certain inflammatory and hyperplastic conditions are prone to develop cancers.

- Prolong ulcerative colitis can develop Ca colon.

- liver chirrosis develop hepatocellular carcinoma .

- Chronic iritation from ill fitteed dentures can develop cancer of oral cavity

1. Oestrogen high level of oestrogen can develop breast cancer,endometrial carcinoma and adenocarcinoma of vagina .

2. Contraceptives the sequenteal type of oral contraceptive increases the risk for breast cancer.

3. Anabolic steroidsit can develop the risk for benign and malignanat cancer of liver.

A large number of the cancer is associated with the genes . As the genes are related with every specific function of the body .

So these are the “Hallmarks of cancer”1.Excessive growth :- Growth promoting

oncogene.2.Growth inhibition:- growth supressing

antioncogenes.3.Escaping cell death by apoptosis:-genes

regulating apoptosis and cancer.

4. Avoiding cellular aging:-telomere and telomerase in cancer.

5. Continued perfusion of cancer:- cancer angiogenesis.

6. Invasion and distant metastasis:- cancer dessimination .

7. DNA damage and repair system:- mutator genes and cancer.

8.Cancer progression and tumor hetrogenicity:-clonal aggresiveness.