introduction to neoplasia

2. 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.

4. COMPARISION OF THE BENIGN AND MALIGNANAT
TUMORS
features 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

5. 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.

6. (1)-RATE OF GROWTH
The 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 diffrentiation
3- growth factors

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

8. 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

9. ANAPLASIA
Anaplasia is the lack of differentiation and is
characteristic feature of most of the
malignant tumors.
Poorly diffrentiated tumors have high degree
of anaplasia.

10. 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.

11. 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.

12. 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.

13. 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.

14. 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.

15. 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.

16. (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.

17. (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.

18. 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.

19. 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)

20. STAGING-The
spread of the cancer is assessed by three
way –
by clinical examination ,
by examination.
And by pathologic examination of the tissue.

21. 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.

22. 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 ).

23. 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.

24. 1. Cigarette smoking.
2. Alcohal abuse
3. Alcohal and tobacco together
4. Cancer of cervix

25. 1. Carcinaoma in situ
2. 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

26. 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 steroids
it can develop the risk for benign and
malignanat cancer of liver.

27. 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.

28. 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.