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• a neoplasm is often referred to as a tumor
• the study of tumors is called oncology.
• based on their clinical behaviour there are two categories of
neoplasm.
1. benign
2.malignant ( ?????????? collectively referred to as cancers)
Nomenclature
a)Naming of Benign tumors
• In general, benign tumors are designated by attaching the suffix
-oma to the cell type from which the tumor arises.
Examples
• Fibroma-A benign tumor arising in fibrous tissue.
• Adenoma- A benign epithelial neoplasms producing gland
patterns
• Benign tumors sometimes named on the basis of their
microscopic or macroscopic pattern
• Papillomas – those which produce finger-like projections
• A polyp - is a mass that projects above a mucosal surface, as in the
gut, to form a macroscopically visible structure.
Colonic
polyp/adenoma
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b)Naming of Malignant tumors
mesenchymal
• sarcomas (sar = "flesh") : liposarcoma, fibrosarcoma,
osteosarcoma,chondrosarcoma, etc.
epithelial:
carcinoma (karkinos = "crab") : squamous cell carcinoma (pituitary
carcinoma
hepatocellular carcinoma
renal tubular carcinoma
adrenal cortical carcinoma
adeno carcinomas: bronchoalveolar adenocarcinoma
(if glandular patterns) mammary adenocarcinoma
c) Mixed Tumors
• the majority of neoplasms are composed of cells representative of a
single germ layer, and the neoplastic cells closely resemble each
other.
• mixed tumors contain more than one cell type, but these are all
derived from one germ layer.
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May occur whenever a malignant neoplasm penetrates into a
natural “open field”.
Most involved-peritoneal cavity, others pleura, subarachnoid spaces
& joint spaces
Characteristics 0f carcinoma arising from ovaries
Mucus secreting ovarian & appendicial carcinomas fill peritoneal
cavity with a gelatinous neoplastic mass pseudomyxoma
peritonei
2. Lymphatic spread
• Most common pathway for initial dissemination of carcinomas, but
sarcoma may also use this route.
a. Lymphatic embolism: malignant cells invade the wall of a lymph
vessel, detach as small groups and carried by the current of lymph as
tumor emboli
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b. Lymphatic permeation:
Tumor cells grow with in the lumen of the lymphatic vessels as solid
cords which extend to a variable distance from the primary tumor,
causes edema in the area
Usually Occurs in breast, prostate, and bronchial carcinoma as these
organs rich in lymphatics
The pattern of LN involvement follows the natural routes of drainage.
E.g –Breast Ca in UOQ Axillary LNs
Enlargement of LNs may be caused by:
-spread &growth of cancer cells or
-reactive hyperplasia
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3. Hematogenous spread
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Comparison between a benign tumor of the myometrium (leiomyoma) and a 30
Cancer Epidemiology
The only certain way to avoid cancer is not to be born, to live is to incur
the risk
due to the typically long delay between exposure to carcinogens and the
development of tumors, specific causes of neoplasms can be determined
accurately only through carefully designed epidemiological studies.
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CARCINOGENESIS
• One of the fundamental principles of carcinogenesis is Nonlethal genetic
damage .
• Such genetic damage (or mutation) may be acquired by the action of
environmental agents, such as chemicals, radiation, or viruses, or it may be
inherited in the germ line.
• The principal targets of genetic damage are the normal regulatory genes
• there are four classes of these regulatory genes.
1.growth-promoting proto-oncogenes
2. growth-inhibiting tumor suppressor genes,
3. genes that regulate programmed cell death (i.e., apoptosis),
4. genes involved in DNA repair
ETIOLOGY OF CANCER:
CARCINOGENIC AGENTS
• A large number of agents cause genetic damages and induce
neoplastic transformation of cells.
• There are three categories:
• (1) chemicals carcinogen
• (2) radiant energy, and
• (3) microbial agents.
• These agents may act alone , together or sequentially to produce the
multiple genetic abnormalities characteristic of neoplastic cells.
Chemical Carcinogens
• hundreds of chemicals have been shown to be carcinogenic.
Steps in chemical carcinogenesis:
• Cells exposed to chemical carcinogen formation of initiation –promotion
sequence cancer
• Initiation –
• causes permanent DNA damage (mutation) which, is rapid and irreversible
• Need promoters to cause tumor
• Promoters
• The transformed (initiated) cell can remain harmless, unless and until
it is stimulated to
undergo further proliferation, upsetting the cellular balance.
• induce rapid proliferation in initiated cells
• non-tumourogenic (do not affect cellular DNA) by themselves
• e.g., phorbol esters, hormones, phenols, and drugs
• Chemical carcinogenic agents fall into two categories:
• 1. Direct-Acting Agents
• 2. Indirect-Acting Agents
Direct-acting agents
• They require no metabolic conversion to become carcinogenic.
• few alkylating and acylating agents are directly acting carcinogens
• They are in general weak carcinogens and some of them are cancer
chemotherapeutic drugs.
Indirect-Acting Agents
• require metabolic conversion to be an ultimate carcinogen
• Most known carcinogens are metabolized by cytochrome p-450 dependent
mono-oxygenase.
• Examples:
• polycyclic hydrocarbons , aromatic amines, amides, azo dyes
• Natural Plant and Microbial Products
• aflatoxin
• Vinyl chloride, nickel, chromium
• Insecticides, fungicides
Radiation Carcinogenesis
Radiation can transform and induce neoplasm
• Two types of radiation injuries are recognized
• I. non-ionizing radiation –
• cause vibration and rotation of atoms in biologic
molecules
• Cause damage and impaired DNA repair
• Example UV radiation from the sun cause skin cancers
• II. Ionizing radiation
• can ionize biologic target molecules and eject electrons
• Examples –
• Therapeutic irradiations --Thyroid cancer
• Radioactive elements -- lung cancer
• Atomic bombs -- leukaemia's and later solid
tumours
Viral and Microbial Oncogenesis
• Many DNA and RNA viruses have proved to be oncogenic
• Oncogenic RNA Viruses
• HTLV-1
• T-cell leukemia
• Oncogenic DNA Viruses
• human papillomavirus (HPV)
• warts) and SCC of the cervix.
• Epstein-Barr virus (EBV)
• Burkitt lymphoma,Hodgkin lymphoma, NK-cell lymphomas
• human herpes virus 8 Kaposi sarcoma
• hepatitis B and C viruses (HBV and C
• hepatocellular carcinoma
Oncogenic bacteria
• Helicobacter pylori
• implicated in the genesis of both gastric adenocarcinomas and gastric
lymphomas.
Clinical Effects of tumours
• Although malignant tumors are more threatening than benign
tumors, any tumor, may cause morbidity and mortality.
• tumors may cause problems because of :
1. location and impingement on adjacent structures
2. functional activity such as hormone synthesis or the development
of paraneoplastic syndromes,
3. bleeding and infections when the tumor ulcerates through
adjacent surfaces
4. symptoms that result from rupture or infarction
Location is crucial in both benign and malignant tumors.
• A small (1-cm) pituitary adenoma can compress surrounding
gland tissue leading to hypopituitarism.
• A 0.5-cm leiomyoma in the wall of the renal artery may be
enough to cause renal ischemia
• small carcinoma within the common bile duct may induce
fatal biliary tract obstruction.
• Hormone production
• seen with neoplasms arising in endocrine glands.
• hormonal activity is a character of well-differentiated benign tumor than a
corresponding carcinoma
• Eg. Neoplasms arising in the β-cells of the islets of the pancreas can produce
hyper insulinism
Paraneoplastic Syndromes
• Symptom complexes that cannot be explained
i. By local or distant spread of the tumor and
ii. By the elaboration of hormones indigenous to the tissue of origin of the
tumor.
• They appear in 10% to 15% of patients with cancer.
Mechanism of Hypercalcemia in cancer patients:
• synthesis of a parathyroid hormone-related protein (PTHrP) by tumor cells
• Tumor produces TGF-α, a polypeptide factor that activates osteoclasts
• NB. Hypercalcemia following a widespread osteolytic metastatic
disease of bone is not a paraneoplastic syndrome
Mechanism for Cushing syndrome:
• Ectopic production of ACTH or ACTH-like polypeptides by cancer cells.
Cancer Cachexia
• It is a progressive loss of body fat and lean body mass
accompanied by profound weakness, anorexia and anemia.
• Its severity correlates with the size and extent of spread of the
cancer
• Causes of cancer cachexia
• the action of cytokines such as TNFα (cachectin) produced by the
tumor – principal cause
• reduced food intake by the patients
• Increased calorie expenditure and basal metabolic rate
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