ANTINEOPLASTIC AGENTS LECTURE 9 PATHOLOGY PHARMACOLOGY.

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ANTINEOPLASTIC AGENTSLECTURE 9

PATHOLOGYPHARMACOLOGY

Neoplasia

• New growth• Abnormal mass of tissue the growth of which

exceeds and is uncoordinated in comparison to that of the normal tissue and continues even in the absence of the stimulus that initiated the growth of the tissue in this manner.

• Clinically divided into benign and malignant types

Malignant Neoplasia

• Innocent• Localized• Small, demarcated, well

differentiated• Surgical removal• Can progress to

malignancy• Nomenclature:suffix –oma• Examples: Fibroma,

lipoma, osteoma, meningioma, papilloma (glands), hepatoma, etc

Benign Neoplasia

• Common terms-cancer or crab-due to their strong adherence properties

• Can affect neighboring and far away tissues (metastasis)

• Large, poor demarcation, faster growth, invasive

• Drug treatment plus surgery• No specific nomenclature: • Suffix –sarcoma/ carcinoma for

mesenchymal tissue like fibrosarcoma, squamous cell carcinoma, adenocarcinoma, HCC, etc• Leukemia, lymphoma, etc

Clinical Characteristics- To decide the candidature of cancer chemotherapy

1. Differentiation and Anaplasia - Benign tumors are well differentiated to perform the normal functions of the tissue. Malignancies are anaplastic (anaplasia-dedifferentiated) and pleomorphic. (Not to be confused with dysplasia – abnormal but non-malignant malfunctioning)

2. Rate of growth

Low risk: Low grade, well differentiated tumour, Gleason score 2–6

Intermediate risk: Intermediate grade, moderately differentiated, Gleason score 7

High risk: High grade, poorly differentiated, Gleason score 8–10

3-10

3. Local invasion (staging)

2-4

4. Metastasis

ETIOLOGY

• Geographical – sun, UV, oxygen deficiency• Environmental – asbestos, benzene, phenol• Age – breast, prostrate• Hereditary – protooncogenes, tumour

suppressor genes, DNA repair• Acquired – hyperplastic, dysplastic, gastritis

induced, leukoplakia (betel leaf)

CELL CYCLE AND CANCER

Apoptosis

Oncogenes

Tumor Suppressor

Inv. and Mets

Angiogenesis

Cell cycle

CURRENT TARGETS

12

MOLECULAR BASIS OF CANCER

POSSIBLE CHECKPOINTS FOR RETARDING CANCER

GROWTH

PHARMACOLOGY OF ANTINEOPLASTIC AGENTS

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