2. CANCER
DEFINATION
CHARACTERISTICS OF CANCEROUS CELLS
TUMOURS
TYPES OF TUMOURS
ETIOLOGY
PATHOGENESIS OF CANCER
DIAGNOSIS
TREATEMENT OF CANCER
3. DEFINATION:
o CANCER IS UNCONTROLLED PROLIFERATION OF CELLS WITHOUT DIFFERENTIATION
AND WHICH ARE INVASIVE IN NATURE.
o CANCER IS A GROUP OF DISEASE INVOLVING ABNORMAL AND EXCESSIVE CELL
GROWTH WITH THE POTENTIAL TO INVADE OR SPREAD TO OTHER PARTS OF THE
BODY.
o TOBACCO USE IS THE CAUSE OF ABOUT 2% OF CANCER DEATHS.
5. UNCONTROLLED PROLIFERATION-
GENERALLY CELL DIVISION AND TISSUE GROWTH IS CONTROLLED BY THE
BODY.
IN SOME CONDITION , BODY FAILS TO CONTROL THE PROLIFERATION
(MULTIPLICATION OF CELLS) LEADING TO UNCONTROLLED CELL DIVISION.
THE RATE OF PROLIFERATION MAY VARY TYPE TO TYPE, SOME CANCER
CELLS PROLIFERATE FASTER AND SOME AT SLOWER RATE.
LOSS OF FUNCTION (UNDIFFERENTIATION)-
• EACH TYPE OF CELLS (NORMAL) IN THE BODY PERFORMS SEPARATE
FUNCTIONS ACCORDING TO THEIR TYPE (DIFFERENTIATED CELLS).
• THE CANCEREOUS CELLS REMAIN UNDIFFERENTIATED, i.e THEY CANNOT
PERFORM ANY FUNCTION.
6. INVASIVENESS-
• IT IS THE ABILITY OF CANCER CELLS TO INVADE OTHER TISSUES.
MALIGNANT CELLS GENERALLY SECRETE PROTEASES THAT DIGEST
EXTRACELLULAR MATRIX COMPONENTS ALLOWING THE CANCER
CELLS TO INVADE ADJACENT NORMAL CELLS.
METASTASIS-
• THE MIGRATION OF PRIMARY TUMOURS TO ANOTHER LOCATION
THROUGH BLOOD VESSELS ORLYMPHATIS OR AS A RESULT OF BEING
SHED INTO BODY CAVITIES RESULT IN FORMATION OF SECONDARY
TUMOR KNOWN AS METASTASIS.
7. TUMOURS-
• AN ABNORMAL MASS OF TISSUE THAT FORMS WHEN CELLS GROWS
AND DIVIDE MORE THAN THEY SHOULD OR DO NOT DIE WHEN THEY
SHOULD.
TYPES OF Tumours-
• BENIGN TUMOURS
• MALIGNANT TUMOURS
8. BENIGN TUMOUR-
• IT IS DESIGNATED BY ATTACHING THE SUFFIX “oma” TO THE CELL TYPE
FROM WHICH THE TUMOUR ARISES.
• BENIGN TUMOUR GROWS SLOWLY AND IT IS CONFINED TO ITS SITE
OF ORIGIN AND THEY ARE SIMILAR TO THE ORIGINAL CELLS.
• EXAMPLE- FIBROMA, A BENIGN EPITHELIAL TUMOUR ARISING IN
FIBROUS TISSUE.
9. MALIGNANT TUMOUR-
• MALIGNANT TUMOUR GROWS FASTER AND THEY ARE INVASIVE AND
METASTATIC IN NATURE. THESE CELLS ARE UNDIFFERENTIATED.
• MALIGNANT TUMOURS ARE CANCEROUS. THEY SPREAD TO DISTANT
SITES via BLOODSTREAM, THE LYMPHATIC SYSTEM. THIS SPREAD IS
CALLED “METASTASIS”.
11. CARCINOMA-
• IT INCLUDES ABOUT 90% OF CANCER IN HUMAN BEING. THIS TYPE IS
PRINCIPALLY DERIVED FROM EPITHELIAL CELLS OF ECTODERM &
ENDODERM.
• EXAMPLE- TUMOURS OF NERVOUS TISSUE, CERVICAL OR BREAST
CANCER.
• NOTE- ECTODERM IS THE OUTERMOST LAYER OF THE EMBRYO TISSUE
AND ENDODERM IS THE INNERMOST LAYER OF EMBRYO TISSUE.
12. SARCOMA-
• SARCOMAS ARE SOLID TUMOURS OF CONNECTIVE TISSUE ( MUSCLE,
BONE, CARTILAGE ETC.)
• IT OCCURS RARELY IN HUMAN ONLY 2% OF CASES ARE FOUND OUT
OF CELL TYPES OF CANCERS.
LYMPHOMAS-
• THIS IS THE TYPE OF CANCER IN WHICH THERE IS EXCESSIVE
PRODUCTION OF LYMPHOCYTES BY THE LYMPH NODES AND SPLEEN.
• EXAMPLE- HODGKIN’S DISEASE.
13. LEUKEMIAS-
IT IS A CANCER OF BLOOD FORMING CELLS COMMONLY CALLED AS
BLOOD CANCER.
LEUKEMIAS ARE NEOPLASTIC GROWTH OF LEUKOCYTES OR WHITE
BLOOD CELLS. THIS IS CHARACTERIZED BY EXCESSIVE PRODUCTION OF
WBCs.
TYPE OF CANCER BASED ON-
TISSUE/ ORGAN AFFECTED: LUNG CANCER, BREAST CANCER
TYPE OF CELLS INVOLVED: FIBROSARCOMA, ARISES FROM FIBROBLAST.
14. ETIOLOGY
ENVIRONMENTAL FACTORS-
1) TOBACCO, SMOKES, DIETS, ENVIRONMENTAL POLLUTANTS
2) HEAVY SMOKING CAUSE LUNG, ORAL CAVITY AND OESOPHAGUS CANCER
3) EXCESSIVE INTAKE OF ALCOHOL CAUSE LIVER CANCER
CHEMICAL CARCINOGEN- NICKEL COMPOUND, CADMIUM, ARSENIC, NITROSAMINES, TRICHLOROETHYLENE, ARYLAMINE,
BENZOPYRENE, AFLATOXINS, REACTIVE OXYGEN RADICALS ETC.
PHYSICAL CARCINOGEN- UV RAYS, IONIZING RADIATION (X-RAYS AND GAMMA RAYS)
BIOLOGICAL CARCINOGEN-
1) VIRUS: ALSO BEEN ASSOCIATED WITH VARIOUS TYPES OF CANCER, THESE VIRUSES ARE CALLED ONCOVIRUSES
• Rous sarcoma virus (RSV) is the first discovered retro-virus causing cancer.
2)(Oncovirus); Human papilloma virus (HPV), Epstein-BarrVirus, (EBV), Hepatitis B virus, Herpes virus
• Hepatitis B and C virus is casually related with hepato-cellular carcinoma.
• Cytomegalovirus (CMV) is associated with kaposi’s sarcoma.
• Human papilloma virus (HPV) is a chief suspect of cervix cancer.
• Bacteria; Helicobacter pylori,
16. PATHOGENESIS OF CANCER
• Refers to change inone nucleotide of gene with abnormal nucleotide,
There may be deletions and insertion especially at the promoter region of the gene
This changes the protein production coded by that gene, this mutation may be due to integration of genomic material from a DNA
virus or retrovirus.
This may lead to formation of oncogenes
POINT MUTATION
• The process in which two separate chromosomalfragments become abnormally fused, leading to abnormalgene regulation.
TRANSLOCATION
• It involves the removal of genetic material from chromosome which significantly changes the normal functioning of cells. The
genetic material which is responsible for control of multiplication (tumour suppressor genes) if get suppressed then it may lead
to progression of cancer.
• During DNA damagerepair the fragments are tend to join but in the process any fragment of DNAmay remain to get attached at
DNA.This may lead to cancer initiation.
GENE DELETION
17. Mechanism of carcinogenesis
4 steps are involved-
Initiation- exposure of cell to carcinogen lead to damage in normal
DNA
Promotion- induces proliferation to initiated tissue and stimulates
tumour formation
Conversion- proliferated cells occurs, depending on chromosomal
changes, type of cancer can be identified
Progression- associated with spread of tumour cells (metastasis)
18. TREATMENT OF CANCER
The treatment of cancer mainly involves chemotherapy and radiotherapy.
A) CHEMOTHERAPY- Chemical- therapy; use of chemical compounds/ medicines to treat cancer.
i) antimetabolites- methotrexate
ii) alkylating agent- nitrogen mustard
iii) anticancer antibiotics- ebgleomycin
iv) vinca alkaloids -vinblastin
v) hormonal therapy –estrogen & antitestosterone
vi) enzyme inhibitors-irinotecan
vii) miscellaneous-cisplatin
B) RADIOTHERAPY- in radiotherapy the specific affected area exposed to ionizing radiation. These
radiation act on DNA and damages to it causing death of exposed cells also, it affect the reproduction of
that cells.
19. REFERENCE-
• Pathophysiology by Atish A. Salunkhe
• https://www.google.com/search?q=pathophysiology+of+cancer+slideshare&tbm=isch&hl=en&s
a=X&ved=2ahUKEwis97a57Z37AhUXi9gFHeTkDdwQrNwCKAB6BQgBEPMB&biw=1519&bih=714#
imgrc=9MzN1Z6NRiDgtM
• https://www.google.com/search?q=CANCER&sxsrf=ALiCzsZE_UrG9oi_I9VksnReGkppCKjjOA:1667
883660577&source=lnms&tbm=isch&sa=X&ved=2ahUKEwiG5_Xo5p37AhUMTWwGHWjFAd8Q_
AUoAXoECAEQAw&biw=1536&bih=714&dpr=1.25#imgrc=WbSS8Aap8y0_wM