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
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
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