This document discusses neoplasia and cancer. It defines a neoplasm as abnormal tissue growth that exceeds normal limits. Cancer is the term for malignant tumors. The molecular basis of cancer involves genetic damage to proto-oncogenes, tumor suppressor genes, apoptosis genes, and DNA repair genes. Essential alterations for cancer include self-sufficiency in growth signals, insensitivity to growth inhibitory signals, evasion of apoptosis, defects in DNA repair, limitless replicative potential, sustained angiogenesis, and ability to invade and metastasize. Cancer development is a multistep process involving genetic alterations that affect cell cycle regulation, growth signals, tumor suppressor pathways, apoptosis, and DNA repair.
It starts with brief introduction about angiogenesis, history of angiogenesis, types and various stages of angiogenesis, followed by its clinical usage.
It starts with brief introduction about angiogenesis, history of angiogenesis, types and various stages of angiogenesis, followed by its clinical usage.
A detailed ppt about cancer immunotherapy.
includes:-
Immunosurveillance and Immunoediting
Dentritic cell vaccines
Antibody therapy
Combined therapy
immune blockades
Cytokine therapy
T cell therapy
Include latest research finding about therapy.
The presentation outlines aspects of immunity against cancer, evasion strategies by cells, immunotherapy in cancer, cancer vaccines etc. Download and view the slideshow for better experience.
Prepared in Sept 2014
IMMUNE RESPONSE TO TUMORS-Humoral immunity
-Cellular Immunity- Failure of Host Defenses
- Evasion of Immune Responses by Tumors
- Cancer Immunosurveillance vs Immunoediting- Immunotherapy
Cancer is mainly caused by the conversion of proto-oncogenes into oncogenes. The process is known as oncogenesis.
This slide will help to get an idea about oncogenesis and also the proto-oncogenes which get converted.
A detailed ppt about cancer immunotherapy.
includes:-
Immunosurveillance and Immunoediting
Dentritic cell vaccines
Antibody therapy
Combined therapy
immune blockades
Cytokine therapy
T cell therapy
Include latest research finding about therapy.
The presentation outlines aspects of immunity against cancer, evasion strategies by cells, immunotherapy in cancer, cancer vaccines etc. Download and view the slideshow for better experience.
Prepared in Sept 2014
IMMUNE RESPONSE TO TUMORS-Humoral immunity
-Cellular Immunity- Failure of Host Defenses
- Evasion of Immune Responses by Tumors
- Cancer Immunosurveillance vs Immunoediting- Immunotherapy
Cancer is mainly caused by the conversion of proto-oncogenes into oncogenes. The process is known as oncogenesis.
This slide will help to get an idea about oncogenesis and also the proto-oncogenes which get converted.
ONCOGENE AND PROTOONCOGENE
P53 GENE AND ITS APPLICATION IN CANCER ETIOLOGY
TUMOUR SUPPRESSOR GENE AND BCA AND BAC GENE AND ITS APPLICATION ON THE APOPTOSIS AND DEATH RECEPTORS
The p53 gene like the Rb gene, is a tumor suppressor gene, i.e., its activity stops the formation of tumors. If a person inherits only one functional copy
Introduction to Cancer
Stem cells and cancer cells
major pathways that lead to formation of tumors.
Tumor Supressors
Colon cancer to prove Knudson hypothesis.
The modern treatments available to treat cancer.
Cancer (Concept of oncogenes and tumor suppressor genes with special referenc...RubinSahu5
Cancer (Concept of oncogenes and tumor suppressor genes with special referencetop53, Retinoblastoma and Ras and APC)
Cancer is a non-infectious disease. It starts at the molecular level of the cell and, ultimately affects the cellular behavior.
It can be defined as uncontrolled proliferation of cells without any differentiation.
Cancer is a genetic disease because it can be traced to alterations within specific genes.
Most cancer cells experience a breakdown in all of these regulatory influences that protect the body from chaos and self‐destruction.
Cancer cells proliferate uncontrollably, producing Malignant tumors that invade surrounding healthy tissue.
Malignant tumors tend to metastasize, that is, to spawn renegade cells that break away from the parent mass, enter the lymphatic or vascular circulation, and spread to distant sites in the body where they establish lethal secondary tumors that are no longer amenable to surgical removal.
All types of cancer can result from uncontrolled Cell Growth And Division of any of the different kinds of cells in the body.
The uncontrolled cell growth produces a mass of cells which are called tumors or neoplasm tumors may be Benign or Malignant.
Oncogenes encode proteins that promote the loss of growth control and the conversion of a cell to a malignant state and Cell Proliferation.
Oncogenes may lead to genetic instability, prevent a cell from becoming a victim of apoptosis, or promote metastasis.
Tumor‐suppressor genes act as a cell’s brakes; they encode proteins that restrain cell growth and prevent cells from becoming malignant.
The first tumor suppressor gene to be studied and eventually cloned is associated with a rare childhood cancer of the retina of the eye, called Retinoblastoma.
The gene responsible for this disorder is named RB .
RAS refers to a family of genes that encode proteins involved in cell signaling pathways regulating cell growth and differentiation.
APC stands for Adenomatous Polyposis Coli.
It's a tumor suppressor gene that plays a critical role in regulating cell proliferation and maintaining the integrity of the epithelial lining of the colon and rectum.
Mutations in the APC gene are associated with familial adenomatous polyposis (FAP), an inherited condition characterized by the development of numerous polyps in the colon and rectum, leading to a significantly increased risk of colorectal cancer.
The cells of patients with this condition were found to contain a deletion of a small portion of chromosome 5, which was subsequently identified as the site of a tumor‐suppressor gene called Adenomatous Polyposis Coli, or APC .
APC is known to suppress the Wnt pathway, which activates the transcription of genes, that promote cell proliferation.
Loss of APC function could therefore lead directly to abnormal chromosome segregation and aneuploidy.
Introduction
Definition
History
Two hit hypothesis
Functions
Mutation in tumor suppressor genes
What is mutation
Inherited mutation of TSGs
Acquired mutation of TSGs
What is Oncogenes?
TSGs and Oncogenes : Brakes and accelerators
Stop and go signal
Examples of TSGs:
RB-The retinoblastoma gene
P53 protein
TSGs &cell suicide
Conclusion
References
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2. Neoplasia
Neoplasia literally means the process of "new
growth," and a new growth is called a neoplasm.
The term tumor was originally applied to the
swelling caused by inflammation.
Cancer is the common term for all malignant tumors.
3. Definition
"A neoplasm is an abnormal mass of tissue, the growth
of which exceeds and is uncoordinated with that of the
normal tissues and persists in the same excessive
manner after cessation of the stimuli which evoked the
change."
4. Molecular Basis of Cancer
DNA repair genes affect cell proliferation or survival
indirectly by influencing the ability of the organism to
repair nonlethal damage in other genes, including
proto-oncogenes, tumor suppressor genes, and genes
that regulate apoptosis
5. Principal Targets of Genetic Damage:
4 Classes of Normal Regulatory Genes
Growth-promoting proto-oncogenes
Growth-inhibiting tumor suppressor genes
Apoptosis-regulating genes; genes that regulate the
programmed cell death
DNA repair genes
6. Essential Alterations
for Malignant Transformation
Self-sufficiency in growth signals
Insensitivity to growth-inhibitory signals
Evasion of apoptosis
Defects in DNA repair
Limitless replicative potential
Sustained angiogenesis
Ability to invade and metastasize
7.
8. Regulation of
cell cycle:
The orderly
progression of
cells through the
various phases of
cell cycle is
orchestrated by
cyclins and cyclin-
dependent kinases
(CDKs), and
by their inhibitors.
9. Cell-Cycle Inhibitors
The activity of cyclin-CDK complexes is tightly
regulated by inhibitors, called CDK inhibitors.
Two main classes of CDK inhibitors: the Cip/Kip.
These inhibitors function as tumor suppressors
Cip/Kip-p21 p27 p57
10. Self-Sufficiency in Growth Signals
Oncogenes - genes that promote autonomous cell
growth in cancer cells. Oncogenes are characterized by
the ability to promote cell growth in the absence of
normal mitogenic.
Proto-oncogenes - they are normal cellular
counterparts; genes in normal cells which encode
proteins that have normal function in cell. Proto-
oncogenes are physiologic regulators of cell
proliferation and differentiation
11. RAS Oncogene
15-20% of all human cancers have a RAS mutation
Normally, RAS is activated by receptors to exchange GDP
for GTP
Activated RAS returns to ground state by its intrinsic
GTPase activity
GTPase activating proteins (GAPs) augment this
process[1000 fold]
Mutant forms of RAS bind GAP but their GTPase activity is
not augmented.
K-ras-colon, pancreatic,
H-ras-bladder ca
N-ras –haematological
12. Insensitivity to Growth Inhibitory Signals:
Tumor Suppressor Genes
Failure of growth inhibition is one of the fundamental
alterations in the process of carcinogenesis.
The proteins that apply brakes to cell proliferation are
the products of tumor suppressor genes
13. Tumor suppressor genes: P53
Major function: Cell-cycle arrest and initiation of apoptosis
in response to DNA damage.
p53-induced cell-cycle arrest occurs late in the G1 phase
and is caused by the p53-dependent transcription of the
CDK inhibitor p21.
If the DNA damage can not be successfully repaired,
normal p53, as a last effort, sends the cell to the graveyard
by inducing the activation of apoptosis-inducing genes,
such as BAX
Loss of p53 results in DNA damage unrepaired, mutations
fixe in dividing cells, and eventually malignant
transformation
14. Role of p53 in Maintaining the
Integrity of Genome
15. Apoptosis associated genes
BCL2 increased expression inhibits apoptosis
P53 decreased expression decreases BAX protein (BAX
promotes apoptosis)
PTEN decreased expression decreases apoptosis.
Mutation of any of these genes causes a condition of
no cell death thus uncontrolled cell proliferation and
thus resulting in cancer.
16. DNA Repair Genes
DNA replication mistakes i.e. wrong base pairing (A-G
and T-C)
These mismatches are checked & corrected by
Mismatch repair proteins.
Defective repair by these proteins bring about
accumulation of DNA changes, resulting in mutations
of the proto-oncogenes & tumor suppressor genes
17. Microsatellites are the tandem repeats of 1-6
nucleotides in the genome.
Due to accumulation of the DNA mistakes the
microsatellites vary in length markedly (microsatellite
instability) which is marker for the defective mismatch
repair genes.
18. Pyrimidine dimers formation due to UV-B rays (280-
320nm) repaired by the Nucleotide excision repair
NER proteins
In xeroderma pigmentosum NER genes are defective
DNA changes accumulate causing skin degenerative
changes, cancers resulting from the accumulation of
the mutated protooncogenes & tumor suppressor
genes
19. Replicative Senescence
Normal cells, after a fixed number of divisions, become
arrested in a terminally non dividing state known as
replicative senescence.
With each cell division there is some shortening of
specialized structures, called telomeres, at the ends of
chromosomes
Once the telomeres are shortened beyond a certain point,
the loss of telomere function leads to activation of p53-
dependent cell-cycle checkpoints, causing proliferative
arrest or apoptosis.
Telomere shortening functions as a clock that counts cell
divisions.
23. Viral Carcinogenesis
Human papilloma virus (HPV)
Epstein-Barr virus (EBV)
Hepatitis B virus (HBV)
Human T-cell leukemia virus type 1(HTLV-1)
These viruses have the potential to induce the
carcinogenesis, by causing the mutation of various
genes regulating normal cellular function
24. References:
http://www.mdconsult.com/das/book/body/111818921-
4/0/1249/64.html?tocnode=51154820&fromURL
M. S. Greenblatt, W. P. Bennett, M. Hollstein, and C. C. Harris;
Mutations in the p53 Tumor Suppressor Gene: Clues to Cancer Etiology
and Molecular Pathogenesis; [CANCERRESEARCH54, 4855-4878,
Septemberi5, 1994J
John F. R. Kerr, Clay M. Winterford,and Brian V. Harmon, Apoptosis-Its
Significance in Cancer and Cancer Therapy
Lodish molecular biology, 5th edition, pg no.-935
Robbins and Cotran PATHOLOGIC BASIS OF DISEASE Seventh
Edition, pg no. -270