It is all about to the causes and effects of cancer ,how it proliferate and damage the DNA. It also includes the cancer ratio of males and females in the year 2020. Later it discusses the 3 steps of carcinogenesis and at the end there is a portion of suppressor genes that play key role in protecting our DNA to get mutated and especially protect our cell from developing any cancerous symptoms . There are 2 types of tumor Benign Malignant The benign being not much virulent and dangerous as compared to malignant one as the later can be fatal in most cases . Metastasis can lead to the increase in risk of losing a person's life as it continues to grow unchecked and the size increases vigorously damaging the surrounding cells

1. CANCER, ONCOGENES
AND TUMOUR
SUPPRESSOR GENES
PRESENTED BY:ALI RIZWAN

2. CANCER
• CANCER IS THE UNCONTROLLED GROWTH OF CELLS DUE TO DAMAGE TO DNA
(MUTATIONS).
• CELL DIVISION (PROLIFERATION) IS A PHYSIOLOGICAL PROCESS THAT OCCURS IN ALMOST
ALL TISSUES AND UNDER MANY CIRCUMSTANCES. NORMALLY HOMEOSTASIS, THE
BALANCE BETWEEN PROLIFERATION AND PROGRAMMED CELL DEATH (APOPTOSIS) IS
MAINTAINED BY TIGHTLY REGULATING BOTH PROCESSES TO ENSURE THE INTEGRITY OF
ORGANS AND TISSUES.
• MUTATIONS IN DNA THAT LEAD TO CANCER DISRUPT THESE ORDERLY PROCESSES BY
DISRUPTING THE PROGRAMMING REGULATING THE PROCESSES. IN FACT, A SERIES OF
SEVERAL MUTATIONS TO CERTAIN CLASSES OF GENES IS USUALLY REQUIRED BEFORE A
NORMAL CELL WILL TRANSFORM INTO A CANCER CELL. ONLY MUTATIONS IN THOSE
CERTAIN TYPES OF GENES WHICH PLAY VITAL ROLES IN CELL DIVISION, CELL DEATH, AND
DNA REPAIR WILL CAUSE A CELL TO LOSE CONTROL OF ITS PROLIFERATION.

3. SOLID TUMORS
• ANAL CARCINOMA
• BILLARY TRACT CARCINOMA
• BRAIN TUMOURS (GLIOMAS)
• BREAST CANCER
• CERVICAL CARCINOMA
• COLORECTAL CARCINOMA
• ENDOMETRIAL CARCINOMA
• ESOPHAGEAL CARCINOMA
• GASTRIC CARCINOMA
• GERM CELL CARCINOMAS
• HEAD AND NECK CARCINOMAOMA
• HEPATOCELLULAR CARCINOMA

4. HEMATOLOGIC TUMORS
• ACUTE LYMPHOBLASTIC LEUKEMIA (ALL)
• ACUTE MYELOID LEUKEMIA (AML)
• CHRONIC LYMPHOCYTIC LEUKEMIA (CLL)
• CHRONIC MYELOID LEUKEMIA (CML)
• HAIRY CELL LEUKEMIA (HCL)
• HODGKIN’S LYMPHOMA (HL)
• NON-HODGKIN’S LYMPHOMA (NHL)

6. CHARACTERISTICS OF CANCER CELLS
1- THEY ARE RESISTANT TO APOPTOSIS ("PROGRAMMED" CELL DEATH).
2- THEY HAVE AN UNCONTROLLED ABILITY TO DIVIDE (OR, THEY ARE IMMORTAL),
AND THEY OFTEN DIVIDE AT AN INCREASED RATE.
3- THESE CELLS ARE SELF-SUFFICIENT WITH RESPECT TO GROWTH FACTORS.
4- THEY ARE INSENSITIVE TO ANTIGROWTH FACTORS.
5- THEY HAVE THE ABILITY TO INVADE NEIGHBORING TISSUES, USUALLY THROUGH
THE SECRETION OF METALLOPROTEINASES THAT CAN DIGEST EXTRACELLULAR
MATRIX MATERIAL. THEY CAN FORM NEW TUMORS (METASTASES) AT DISTANT
SITES.
6- THEY SECRETE CHEMICAL SIGNALS THAT STIMULATE THE GROWTH OF NEW
BLOOD VESSELS (ANGIOGENESIS).

7. NORMAL CELL
Growth factor
Growth factor receptor
Signal transduction
Activation of
transcription
cytoplasm
nucleus

8. NEOPLASTIC CELLS
Increased
In growth
factor
Increased
In growth
factor
receptors
Increased in
signal
transduction
Increase in
activation of
transcription

9. CAUSES OF NEOPLASIA
ENVIRONMENTAL CAUSES: (CARCINOGENS)
CHEMICALS
VIRUSES
RADIATION
HEREDITARY CAUSES- GENETIC DEFECTS.
COMBINATION – COMMON.
ALL CANCER IS GENETIC, NOT ALL CANCER IS HEREDITARY

11. Acquired environmental factors
chemicals ,radiation ,viruses
Changes in genome
of somatic cells
Activation of growth
promoting oncogenes
Inactivation of tumour
supressor genes
Expression all altered gene products
and loss of regular gene products
MALIGNANT NEOPLSM
Genetic factors
1/1/2015

12. CHEMICAL CARCINOGENESIS
• INITIATION
• DNA DAMAGE EG.
DENA (DIETHYLNITROSAMINE)
BENZYLPYRENE(LUNG CANCER)
• PROMOTION
• HISTOLOGIC CHANGE
CCL4
TURPENTINE (CO-CARCINOGENS)
• DENA + CCL4 (LIVER CANCER)
• MALIGNANT TRANSFORMATION:
• VISIBLE TUMOR FORMATION 1/1/2015

13. INITIATION
Initiation is an irreversible genetic alteration which
result from the interaction of the ultimate carcinogen
with the DNA in the target cell.
(1) Is an irreversible process
(2) Caused only by carcinogenic compounds
(3) Occurs after carcinogen exposure
(4) Initiator alone does not result in tumor formation

14. PROMOTION
Promotion refers to a phenomenon of gene activation in
which the latent altered phenotype of the initiated
cells becomes expressed through selection and clonal
expansion.
1- Is a reversible process
2- Acts only after exposure to an initiator
3- Requires repeated administration
4- Promotor is not carcinogenic in itself
5- promotor alone does not result in tumor formation

15. MOLECULAR BASIS OF
CARCINOGENESIS
FOUR CLASSES OF REGULATORY GENES.
1- TUMOUR PROMOTORS: PROTO-ONCOGENES
2- TUMOUR INHIBITORS:TUMOUR-SUPPRESSOR
GENES
3- GENES REGULATING APOPTOSIS
4- DNA REPAIR GENES.

16. TUMOR SUPPRESSOR GENES
• A TUMOR SUPPRESSOR GENE IS A GENE THAT REDUCES THE
PROBABILITY THAT A CELL IN A MULTICELLULAR ORGANISM
WILL TURN INTO A TUMOR CELL. A MUTATION OR DELETION
OF SUCH A GENE WILL INCREASE THE PROBABILITY OF THE
FORMATION OF A TUMOR.
• UNLIKE ONCOGENES, TUMOR SUPPRESSOR GENES GENERALLY
FOLLOW THE 'TWO-HIT HYPOTHESIS,' WHICH IMPLIES THAT
BOTH ALLELES THAT CODE FOR A PARTICULAR GENE MUST BE
AFFECTED BEFORE AN EFFECT IS MANIFESTED. THIS IS DUE TO
THE FACT THAT IF ONLY ONE ALLELE FOR THE GENE IS
DAMAGED, THE SECOND CAN STILL PRODUCE THE CORRECT
PROTEIN. HOWEVER, THERE ARE CASES WHERE MUTATIONS
IN ONLY ONE ALLELE WILL CAUSE AN EFFECT. A NOTABLE
EXAMPLE IS THE GENE THAT CODES FOR P53.

17. Tumor suppressor genes, or more precisely, the proteins for which they code, either
have a dampening or repressive effect on the regulation of the cell cycle or promote
apoptosis, and sometimes do both.
Examples of tumour suppressor Genes Includes:
P53, Rb, BRCA-1 and BRCA-2
The first tumor suppressor protein discovered was the pRB protein in
human retinoblastoma; however, recent evidence has also implicated pRb as a
tumor survival factor. Another important tumor suppressor is the p53 tumor
suppressor protein produced by the TP53 gene.
Families in which there is a high breast cancer frequency have mutations
affecting the tumor suppressor gene BRCA-1 and BRCA-2.