Basics of Cancer, its aetiopathogenesis for Medical undergraduates

1. CANCER
Dr. V.P.Acharya

2. Definition
 A group of diseases in which cells grow
abnormally
 Malignant neoplasm
 Simply “Malignancy”

3. Tumour and cancer are not synonymous
Tumour– Abnormal, excessive,
uncoordinated, autonomous and
purposeless proliferation of cells
Benign– Doesn’t spread to distant sites and
destroy the tissue of origin
Malignant– Destroys the tissue of origin and
spreads to distant sites via blood stream
and lymphatic system

4. Properties of cancer cells
 Unrestrained growth
 Local invasion
 Distant metastasis

5. Aetiological factors
 Familial/ Genetic factors—5% of all CA
 Racial or geographical factors
 Environmental factors
 Age –Older age
 Gender—M>F

6. Carcinogenesis & Carcinogens
Carcinogenesis– Induction of cancer
Carcinogens– Agents that cause cancer
1.Chemical carcinogens
2. Physical carcinogens
3. Biological carcinogens
4. Hormonal carcinogens

7. 1. Chemical carcinogens
 Initiators– initiate the process
 Promoters– Lack carcinogenic potential but help
in proliferation of initiated cells
Initiating carcinogens
Direct acting Indirect acting (Procarcinogens)
Metabolic activation
Ultimate carcinogens
Reactive electrophiles
No metabolic activation
Interact with neutrophiles (DNA)
Mutation in DNA

8.  Direct acting carcinogens– Alkylating
agents e.g. anti- cancer drugs
Acylating agents e.g. acetyl imidazole
 Indirect acting carcinogens
(Procarcinogens)– Aromatic hydrocarbons,
aromatic amines

9. Promoters of carcinogenesis– Phenols,
hormones, Phenobarbital, artificial
sweeteners

10. 2. Physical carcinogens
 UV rays, ionizing radiations
 Non-radiation physical agents– various
injuries
 UV radiations– pyrimidine dimers in DNA,
elimination of bases or breaking or cross-
linking of single or double strands of DNA
 Ionizing radiations– directly alter cellular
DNA or generate free radicals

11. 3.Biologic carcinogens
 Viruses, bacteria & parasites
 Viruses are more important
 DNA and RNA viruses
 DNA viruses– HPV, EBV, HBV
 RNA viruses– Rous sarcoma virus, HTLV-I
& II

12. 4. Hormonal carcinogens
 Estrogens
 Contraceptive hormones
 Anabolic steroids

13. Antimutagens
 Vitamin A, E, C
 Turmeric– Curcumin
 Dietary fibers

15. Oncogenes
 Proto-oncogenes are normal versions of genes
which promote cell division.
 Expression at the wrong time or in the wrong
cell type leads to cell division and cancer.
 Proto-oncogenes are called oncogenes in their
mutated form.
 One copy of an oncogenic mutation is sufficient
to promote cell division.

16. Tumor suppressor genes
 Cancer can be caused by loss of genes that
inhibit cell division.
 Tumor suppressor genes normally stop a cell
from dividing.
 Mutations of both copies of a tumor suppressor
gene is usually required to allow cell division.
 RB gene and p53 gene are mostly studied

17. P53– Guardian of the genome
 suppresses progression through the cell
cycle in response to DNA damage
 initiates apoptosis if the damage to the
cell is severe
 acts as a tumour suppressor
 is a transcription factor and once
activated, it represses transcription of one
set of genes (several of which are involved
in stimulating cell growth) while
stimulating expression of other genes
involved in cell cycle control

18. Tumour markers
 Substances, usually proteins, that are produced
by the body in response to
cancer growth or by the cancer tissue itself
e.g. CEA (Carcinoembryonic antigen)
PSA (prostate specific antigen)
Importance of tumor marker detection for
• Screening
• Diagnosis
• Stage
• Prognosis
• Guide treatment
• Monitor treatment
• Determine recurrence

19. Tumour markers commonly used in clinical practice
Tumour markers Associated CA/ Tumours
Antigens
 CEA
 AFP
 PSA
GI Cancers
Hepatocellular CA, Teratoma of
testes
Prostatic CA
Hormones
HCG
Calcitonin
Choriocarcinoma
Medullary CA of thyroid
Enzyme
Prostatic acid phosphatase
Prostatic CA

20. For more ppts on Medical Biochemistry for undergraduates please visit my
website www.vpacharya.com