Neoplasia

Neoplasia Dr. Mehzabin Ahmed

Neoplasia •

Neo = new

•

Neoplasm= new growth – Syn: tumor, denoted by suffixing “OMA” to the tissue

Plasia = growth

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 breastIrregular margin & invades into surrounding normal

Clinical effects of tumors Benign (a) They exert pressure on the adjacent tissues (b) Obstruction of the flow of fluid (c) Production of hormones (d) Transformation into malignant tumors

Malignant Malignant tumors encroach and destroy the adjacent structures thus enabling the neoplastic cells to penetrate the walls of the blood vessels and lymphatic channels thereby disseminate 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 disorderabnormal DNA repair genes

risk of developing Skin cancer -

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