cancer

Course: [Link]. Zoology

Department: Applied
Aquaculture and
Zoology
Institution:
Barkatullah University
index
• Introduction
• cancerous cell and normal cell
• Types of tumor
• The development of cancer
• Properties of cancer cells
• Causes of cancer
Molecular basis of cancer
 cancer treatment
 Conclusion
 references
 introduction
 Cancer cell ,which grow and divide in an uncontrolled manner,
Ultimately spreading throughout the body and interfering with the
function of normal
 Tissue and organs
 Cancer cell results from defects in fundamental cell regulatory
mechanism


 It is a disease that ultimately has to be understood at the molecular and

cellular levels
Normal and Cancerous cell

NORMALCELL CANCER CELL

Controlled /regulated cell divisions Uncontrolled cell growth and divisions

Undergo programmed cell death /apoptosis They fail to undergo programmed cell death
/apoptosis-immortal
Density dependent inhibition –they inhibit their They do not show density dependent inhibition
divisions upon reaching a finite density

Contact inhibition-cells stop dividing They don’t show contact inhibition,

(proliferation) and moving once they physically They grow in multiple layer
touch neighboring cells
Angiogenesis absent Occur angiogenesis-The formation of new blood of such new
blood vessels for nutrients and oxygen to cancerous cell

Metastasis absent (mobility) Occur metastasis-the spread of cancer cells from their original
site to other parts of the body
Invasiveness absent –they do not invade their Invasiveness-they invade their surrounding cells
surrounding cells
Fig:-1
 TUMOR
 TUMOR IS AN OF ABNORMAL MASS TISSUE RESULTING FROM UNCONTROLLED
DIVISIONS .
 THERE IS TWO TYPES OF TUMOR
• BENIGN TUMOR
• MALIGNANT TUMOR
 BENIGN TUMOR :-a benign tumor ,such as a common skin wart ,remains
confined to its original location ,neither invading surroundings normal
tissue nor spreading to distant body sites .
• Cells that closely resemble, and function like normal cells.
• Easily to removed by surgery
 MALIGNANT TUMOR :-A malignant tumor however, is capable to both
invading surrounding normal tissue and spreading throughout the body
via the circulatory or lymphatic system.
• Spread by forming metastasis.
• Very difficult to diagnose.
Fig:2
CLASSIFICATION OF CANCER
(Based on their origin/acc. to the type of cell from
which they arise.)

• CARCINOMA;- malignancies of epithelial cell(skin

or organ lining) approx. 90% of cancer

• SARCOMA:-rare in human, tumor of connective

tissues,(bone cartilage and fibrous tissue)

• LEUKEMIA:- arise from the blood forming cells(

bone marrow, WBC)

• LYMPHOMAS:-Cells of immune system (lymph

nodes ,spleen)

• MELANOMA;-PIGMENT producing cell

• GERM LAYER TUMOR;- testis ,ovary

• MYELOMA :- PLASMA CELLS8 CENTRAL NERVOUS

SYSTEM cancers (brain &spinal cord) Fig:-3
Development of cancer

 The development of cancer is viewed as a multistep process

involving mutations and selection for cells with progressively
increasing capacity for proliferation,survival ,invasion,metastasis.
 Initiation: A normal cell experiences a genetic alternation leading
to abnormal proliferation of a single cell, making it
susceptible to becoming cancerous
 Promotion: These initiated cells begin to multiply abnormally,
often due to hormonal influences or chronic inflammation,
creating a population of abnormal cells (dysplasia)
 Malignant Conversion/Progression: Further mutations occur, giving cells
more aggressive traits like faster division, immortality (using telomerase),
and ability to invade surrounding tissues.
 Invasion & Metastasis: Cancer cells break away from the primary
tumor, enter the bloodstream or lymphatic system, and form new
tumors (metastases) in distant parts of the body.
Fig:-4
Properties of cancer:-

Fig:-5
[Link]:-Cancer cells fail to undergo apoptosis
therefore exhibit increase life span compared their normal
cells. Cancer cells can grow in the absence of growth
factors. Many cancer cells produce growth factor that
stimulates their own proliferation.

2:- LOSS OF CONTACT INHIBITION & DENSITY DEPENDENT

INHIBITION:-Cancer cells generally continue growing to high Fig:-6
cell densities in culture, cancer cells continue proliferating
under conditions that cause normal cells to cease
proliferation and enter GO.

3;-INVASIVENESS:-Cancerous cells are invasive i.e., they

have ability to invade other tissues. Cancer cells secrete
proteases that digest ECM components, allowing the cancer
cells to invade adjacent normal tissue.

Fig:-6
4 .ANGIOGENESIS:-Cancer cells secrete growth
factor that the promote the formation of new
blood vessels. New blood vessels are required to
supply oxygen and nutrients to the proliferating
cancerous cells. The formation of NEW BLOOD
VESSELS is important not only in supporting tumor
growth ,but also in metastasis .

5. DEFECTIVE DIFFERENTIATION:-Differentiation of
Fig:-7
cancer cell is usually blocked at early stage. Most fully
diferentiatied cells cease the cell the cell divison.

6. TELOMERE:- Cancer cell effetively maintained the

end of chromosomes, which are lost as normal cell
devide telomere consist of repeated sequences that are
replicated by a special enzyme called telomerase .

Fig:-8
Fig:9
Molecular basis of cancer Oncogenes
The molecular basis of cancer
involves genetic mutations in
key regulatory genes, primarily
oncogenes (promoting growth)
and tumor suppressor genes
(inhibiting growth/repair), tumor
leading to uncontrolled cell suppressor
genes
division, altered cell death
(apoptosis)

GENES PLAYING ROLE IN CANCER

DEVELOPMENT
[Link]
[Link]
[Link] SUPRESSOR GENE
[Link] REPAIR GENE
Fig:-10
 Fig:-1
Fig:-1 1
1
Fig:-12
GENES PLAYING ROLE IN CANCER DEVELOPMENT
 [Link]

 [Link]
 [Link] SUPRESSOR GENE
 [Link] REPAIR GENE
Oncogenes and Proto-oncogenes oncogenes are
dominant
 Oncogenes are mutated
versions of normal genes
called proto-oncogenes
 Oncogenes can be
activated through
mutations, gene
amplification, or
chromosomal
translocations
 When a proto-oncogene is
mutated and becomes an
oncogene, it can lead to a
cascade of events that
promotes cancer.
Oncogenes can encode
proteins that act as:
 Growth factors
Fig:-13
 Growth factor receptors
 Intracellular signaling
molecules
 .
Examples of oncogenes and associated cancers
 BCR/ABL1: Associated with chronic myeloid leukemia (CML) and some types of acute
lymphocytic leukemia.
 CMYC: Associated with Burkitt lymphoma.
 EGFR: Mutations are frequent in non-small cell lung cancer.
 KRAS: A major oncogene in lung, colorectal, and pancreatic cancers.
 BRAF: Mutations are often found in colorectal and other cancers, such as melanoma.
Oncogenes and cancer treatment
 Many cancer therapies are designed to target the proteins produced by
oncogenes.
 For example, Gleevec (imatinib) blocks the BCR-ABL protein in CML, and
 HER2-targeted therapies are used for breast cancers with an overactive
HER2 oncogene.
TUMOR SUPPRESSOR GENES Fig:-15
 Tumor suppressor genes are genes that help protect
the body from cancer by regulating cell growth,
repairing DNA damage, and telling cells when to die.
 When these genes are mutated and stop working
correctly, cells can grow out of control, leading to
cancer
 Functions
• Regulate cell division
• Induce apoptosis
• Repair DNA
 What happens when they are mutated
• Loss of function
• Uncontrolled cell growth
• Increased cancer risk
• EX:-p53 (TP53), Rb (RB1), BRC
Tumor suppressor
genes (TSGs) are
typically recessive

Fig:-16
DNA REPAIR GENES
 These are genes that ensures each
strand of genetic information is
accurately copied during cell division
of the cell cycle.
 Mutations in DNA repair genes lead to
increase in the frequency of mutations
In other genes ,such as proto-
oncogenes and tumor suppressor
genes.
 i.e, Breast cancer susceptibility genes
(BRCA1 and BRCA2)
Hereditary non –polyposis colon cancer
susceptibility genes (MSH2,MLH1,PMS2)
have DNA repair functions .
There mutation will cause tumorigenesis.

Fig:-18
 cancer treatment
 Surgery: Removing tumors, often combined with
other treatments.

 Radiation Therapy: High-energy beams to kill

cancer cells (external beam, brachytherapy).

 Chemotherapy: Uses drugs to kill cancer and

other fast-growing cells. These drugs can be
taken orally (pills) or given through a vein.

 Targeted therapy: Uses drugs that specifically

target changes in cancer cells that help them
grow and spread.

 Immunotherapy: Helps the body's own immune

system fight cancer cells.

 Hormone therapy: Blocks or removes hormones

that certain cancers, such as some breast and
prostate cancers, need to grow.
 Stem Cell Transplant (HSCT): blood-forming
cells after intensive treatment, especially for Fig:-19
Fig:-20
Fig:-21
 conclusion
 Cancer is a complex, multifactorial disease marked by
uncontrolled cell growth and genetic instability.

 It develops due to genetic mutations, environmental factors,

lifestyle habits, and certain viral infections.

 Cancer cells evade apoptosis and can invade nearby tissues

and metastasize to distant organs.

 Early diagnosis and screening play a crucial role in improving

treatment outcomes.

 Advances in targeted therapy and immunotherapy have

significantly improved patient survival.

 Despite progress, challenges like drug resistance and late

detection remain.

 Continuous research, prevention, and public awareness are

essential to reduce the global burden of cancer.
 References
 Research Article Hanahan, D. (2022). Hallmarks of
cancer: New dimensions. Cancer Discovery, 12(1), 31–46.
 Immunotherapy Waldman, A. D., Fritz, J. M., & Lenardo,
M. J. (2020). A guide to cancer immunotherapy. Nature
Reviews Immunology, 20, 651–668.
 mRNA VaccineSahin, U., et al. (2017). Personalized RNA
mutanome vaccines mobilize therapeutic immunity.
Nature, 547, 222–226.
 Karp cell biology