Neoplasia

Dr. Mehzabin Ahmed

 Neoplasia

• Neo = new Plasia = growth

• Neoplasm= new growth – Syn: tumor, denoted by suffixing “OMA” to the tissue
from which it arises.

• A neoplasm is an abnormal mass of tissue, that grows/ proliferates

excessively in a poorly regulated manner, after certain stimuli cause a
permanent alteration in its genetic structure resulting in an alteration in the
cellular growth pattern.

• It persists in the same excessive manner after the cessation of the stimuli
that has evoked the change.
 Basic terms

• Dysplasia (dys- disordered, plasia- growth) – the cells show

increased rate of proliferation ( mitosis) and incomplete
maturation.
• Preneoplastic diseases- diseases that increase the risk of cancer
formation, eg: chronic gastritis predisposes to cancer stomach,
cirrhosis of the liver predispose to liver cancer
• Insitu neoplasia- the neoplastic change in the cells is confined
to the epithelial lining without invasion into the deeper tissues.
• Differentiation- degree of similarity of the neoplastic cells to

the mature parent cell.

 Basic terms (contd.)
• Pleomorphism- degree of variation in the cytoplasm & the nucleus of the
malignant cells.

• Metastasis- distant spread of the malignant tumor cells to sites away from the
primary (original) tumor

• Carcinogenesis- process by which agents (carcinogens) cause cancer formation

(malignancy)

• Grading of a tumor is done by noting the degree of differentiation, pleomorphism

& the number of mitotic figures. It is done based on the cellular features.

• Staging is by noting the size of the tumor, its local invasion, and the distant
spread- TNM classification is employed(T- tumor size, N-lymph node
involvement, M- distant metastasis). Based on the gross features.
 Types of neoplasms
Based on behavior
– Benign
– Malignant
– Intermediate / Borderline
Based on histogenesis
• Epithelial tissue
Benign- Adenoma- glandular epithelium
Papilloma- squamous epithelium
Malignant- Carcinoma
• Mesenchymal or Connective tissue
Benign – ‘oma’ to the tissue
Bone- Osteoma,
Cartilage- Chondroma
Malignant- Sarcoma
 Differences between benign & malignant tumors
Benign
- Slow growth rate
- No invasion &
- No metastasis
- Encapsulated & well
circumscribed
- No necrosis
- No ulceration / rare
- Low mitotic activity
- Histologic resemblance to
normal cells of the parent
organ& normal nuclear
morphology
Malignant
- Rapidly growing
- Invasive into surrounding normal
tissue
- Metastasizes to distant organs
- Poorly circumscribed with
irregular margins
- Necrosis is common
- Ulcers are common especially
in the skin and GIT
- High mitotic activity
- Often poor resemblance but
can be variable. The nuclei are
abnormal & appear
hyperchromatic, irregular &
pleomorphic
Fibroadenoma – Benign tumor of the breast- Well circumscribed &
encapsulated

Ductal carcinoma – Malignant tumor of the breast-

Irregular margin & invades into surrounding normal
 Clinical effects of tumors

Benign Malignant
(a) They exert pressure on the Malignant tumors encroach and
adjacent tissues
destroy the adjacent structures
(b) Obstruction of the flow of
thus enabling the neoplastic
fluid
cells to penetrate the walls of
(c) Production of hormones
the blood vessels and lymphatic
(d) Transformation into malignant
channels thereby disseminate
tumors
into the distant sites.
 Structure of tumors

• Parenchyma
• Stroma

Parenchyma: represents the growing or the dividing component of

the tumors it determines the nature of the tumor. The cells
usually look similar to the cells in the organ where the tumor
arose, and cells will continue to perform some of the functions
of the parent organ.
Stroma: The neoplastic cell population or the parenchyma is embedded

in is supported by the connective tissue framework called the stroma

(mattress) which provided mechanical support and nutrition to the

neoplastic cells. Stroma contains blood vessels, which supply

nutrients to the tumor, and growth of the tumor is dependent upon

its ability to induce blood vessels to perfuse it. Stroma also contains

lymphocytic infiltrate, this reflects a host immune response to the

tumor, tumors, which have dense lymphocytic infiltration, have good

prognosis.
• A neoplasm must develop stromal support components if it is to grow

• The growth rate of the neoplasm depends on:

– The proportion of proliferating cells

– Rate of apoptosis

– Adequacy of blood suppply

 Metastasis

Spread of a tumor from its primary site is called metastasis

The invasiveness of cancer permits them to spread.

Metastatic spread strongly reduces the possibility of cure. 

 Pathways of spread
• Local invasion: direct spread into adjacent tissues is the most
common pattern of spread.
2) Lymphatic spread: via the draining lymphatics to local lymph nodes
are a common pathway for dissemination of carcinomas. The pattern
of lymph node involvement follows the natural routes of drainage.
E.g. Ca of breast arising in outer upper quadrant of breast involves
axillary lymph nodes; inner quadrant involves infraclavicular and
supraclavicular nodes. Carcinoma lung involves perihilar,
trachiobronchial and mediastinal nodes.
• Haematogenous spread: via draining veins. Tumors of the GI tract
spread via portal circulation to the liver while tumors that are carried
by systemic circulation spread to lungs, bones, brain & adrenal
glands. It is typical of sarcomas.
E.g. Carcinoma of thyroid& prostate.
4)   Direct seedling of body cavities or surfaces: peritoneal cavity,
pleural, pericardial, Subarachnoid, joint space may be affected.Direct
seeding spreads tumors to other organs in the cavity E.g. Ovarian
carcinoma 
Metastatic tumors in the liver
 Carcinogenesis

• Carcino- cancer, Genesis- formation

Agents that cause cancer- Carcinogens:

• Chemical agents: Polycyclic hydrocarbons, Alkylating agents, Aromatic

amines, Nitrosamines.

• Biological agents: Viruses (Ebstein barr virus, human papilloma virus),

Bacteria (H.pylori)

• Physical agents: Radiation, Asbestos

 Carcinogen

Damage to the DNA of the cell

Mutation in the genes (activaton of oncogenes or inactivation of cancer

suppressor genes)

Failure of the DNA repair mechanism

Produce abnormal cells that cannot be controlled

Proliferate rapidly under the influence of growth factors, hormones, diet etc
 Inheritable cancers

• Genetic abnormality that predisposes or increases risk of cancer

development is carried from generation to generation
• Patients from such families have an increased risk of developing cancers at
an early age
• Regular screening of such patients to detect the tumors early can help in
timely treatment.
Eg, Familial adenosis coli- multiple benign adenomata in the colon- risk of
developing Colon carcinoma – genetic defect is the absence of tumor
suppressor gene
Xeroderma pigmentosum- skin disorder- risk of developing Skin cancer -
abnormal DNA repair genes
 Diagnosis
• Imaging techniques- X-rays, MRI, CT scan

• Cytological examination by :
Studying cells in the body fluids,
Obtaining the cells by scraping or brushing the surface- exfoilative cytology
Aspirating cells from the mass by a needle-aspiration cytology

• Biopsy: histologic study of a piece of the tissue obtained by

Needle biopsy, Endoscopic biopsy, Incision biopsy, Excision biopsy

• Tumor markers- products (hormones, proteins, enzymes) secreted by the tumors

which can be detected in the blood samples and in the biopsy tisues
eg, alpha fetoprotein- in cancer of the liver,
human chorionic gonadotrophin- in large amounts in choriocarcinoma
acid phosphatase- in prostatic carcinomas