An oncogene is a gene that has the potential to cause cancer. In tumor cells, they are mutated or expressed at high levels. Most normal cells undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered.
An oncogene is a gene that has the potential to cause cancer. In tumor cells, they are mutated or expressed at high levels. Most normal cells undergo a programmed form of rapid cell death (apoptosis) when critical functions are altered.
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
INTRODUCTION
HISTORY
GENES INVOLVED IN CANCER
ONCOGENES
TUMOUR SUPPRESSOR GENES
ONCOGENE
INTRODUCTION
TYPES
ACTIVATION OF PROTO ONCOGENES
FUNCTION
TUMOUR SUPPRESSOR GENES
INTRODUCTION
EXAMPLE
RB GENE
TP53 GENE
CONCLUSION
REFERENCES
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.
Dna methylation ppt
definition of Dna methylation ppt
discovery of Dna methylation ppt
types of Dna methylation ppt
history of Dna methylation ppt
process of Dna methylation ppt
mechanism of Dna methylation ppt
methylation in cancer
cytosine methylation
genomic imprinting
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.
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
INTRODUCTION
HISTORY
GENES INVOLVED IN CANCER
ONCOGENES
TUMOUR SUPPRESSOR GENES
ONCOGENE
INTRODUCTION
TYPES
ACTIVATION OF PROTO ONCOGENES
FUNCTION
TUMOUR SUPPRESSOR GENES
INTRODUCTION
EXAMPLE
RB GENE
TP53 GENE
CONCLUSION
REFERENCES
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.
Dna methylation ppt
definition of Dna methylation ppt
discovery of Dna methylation ppt
types of Dna methylation ppt
history of Dna methylation ppt
process of Dna methylation ppt
mechanism of Dna methylation ppt
methylation in cancer
cytosine methylation
genomic imprinting
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 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.
describe the tumor suppressor genes and examples for downloading the presentation, more presentations , infographics and blogs visit :
studyscienceblog.wordpress.com
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
1. S P E A K E R :
D R . M D . S H A I F U L H A S S A N S H A M E E M
A S S I S T A N T R E G I S T R A R
D E P T . O F R A D I O T H E R A P Y
D H A K A M E D I C A L C O L L E G E H O S P I T A L
INTRODUCTION
TO
CANCER GENETICS
2. The genetic nature of Cancer
Cancer is a complex disease that result from the basic
process of uncontrolled growth. Cell proliferation results in
a mass that invades neighboring tissues and may
metastasize to more distant sites.
In order for a normal cell to transform into a cancer
cell, genes which regulate cell growth and
differentiation must be altered. When normal regulation
is altered, uncontrolled growth is initiated and a malignant
tumor develop.
Genetic changes can occur at many levels, from gain or
loss of entire chromosomes to a mutation affecting a single
DNA nucleotide.
3. Carcinogenesis
Carcinogenesis is a multistep
process at both the phenotypic &
genetic levels, resulting from the
accumulation of multiple mutation.
4. A tumor is formed by the
clonal expansion of a
precursor cell that has
incured genetic damage.
Even though most
malignant tumors are
monoclonal in origin, by the
time they become clinically
evident their constituent
cells are heterogenous.
5. Cancer arises from the accumulation of genetic aberrations
in somatic cells
These aberrations consist of mutations and chromosome
defects
Epigenetic aberrations are also present
Together, they lead to altered gene expression
Over 500 genes are now known to be involved in cancer
development
6. Controls or check points of Cell cycle
The orderly progression of cells through the various phases of
cell cycle is regulated by cyclins & their cyclin-dependent
kinases (CDKs).mutation of genes that encode these cell
cycle regulators have been found in several human cancer.
7. Mutation
The basic mechanism in all cancer is mutation. Mutation is change in
DNA sequence.
Rate in humans ~5x10-9 /nucleotide / generation = 25 mutations /cell
/generation
Carcinogenic agents are involved through causing mutation. It may be-
Germline mutations are responsible for 5% to 10% of cancer cases.
This is also called familial cancer. These mutations are present in every
cell of the body and are passed from parent to child.
Sporadic cancer or somatic mutation are caused by tobacco,
over-exposure to UV radiation, and other toxins and chemicals. These
mutations are not in every cell of the body and are not passed from
parent to child.
8. Chromosome defects
STRUCTURAL
translocation
inversion
insertion
duplication
amplification
Deletion
NUMERICAL
loss or gain of whole chromosome
loss of gain of whole chromosome set
9. Genes & cancer
Four classes of normal regulatory genes are the principle target of
genetic damage.
-The growth promoting Proto-oncogenes
-The growth inhibiting tumor suppressor genes
-Genes that regulate programmed cell death(Apoptosis)
- DNA repair genes
10. Proto-oncogene
Have multiple roles, participating in cellular functions
related to growth & proliferation.
Proteins encoded may function as growth factors or their
receptors, signal transducers, transcription factors or cell
cycle components.
Mutations convert proto-oncogene into constitutively active
cellular oncogene that are involved in tumor
development.
Types of Proto-oncogenes:
1)Cellular oncogenes(c- oncogenes): proto-oncogene
which have been to mutate in any individual.
2)Normal oncogene(n-oncogene): proto-oncogenes that
have not been found to mutate.
11. Proto-Oncogenes and Normal Cell Growth
Oncogenes are related to normal genes called proto-oncogenes that
encode components of the cell’s normal growth-control pathway.
Some of these components
are growth factors, receptors,
signaling enzymes, and
transcription factors. Growth
factors bind to receptors on the
cell surface,which activate
signaling Enzymes inside the
Cell that, in turn, activate special
proteins called transcription
factors inside the cell’s nucleus.
The activated transcription
factors “turn on” the genes
required for cell growth and
proliferation.
12. Oncogene
Act by gain of function. a "gain of function" mutation
because the cells with the mutant form of the protein
have gained a new function not present in cells with
the normal gene.
Dominant(activation of one allele is sufficient).
Activated by
- mutation
- chromosome translocation
- gene amplification
-retroviral insertion
14. When a proto-oncogene becomes activated it is called an
oncogene.
Proto-oncogene>>>>> >>>>>Oncogene
When an oncogene becomes activated it might
cause cancer.
Proto-oncogene -> oncogene -> other steps -> cancer
15.
16. Tumor suppressor gene
Normal genes implicated in the control of cell cycle,
repair DNA mistakes, and tell cells when to die
(apoptosis or programmed cell death). The product of
tumor suppressor genes normally block abnormal
growth and malignant transformation and lead to
malignancy when the function of both alleles is lost.
When tumor suppressor genes don’t work properly,
cells can grow out of control, which can lead to cancer.
In contrast to mutations in proto-oncogene, which are
dominant in their action, most mutation in tumor
suppressor genes are recessive.
17. Tumor Suppressor Genes
Act Like a Brake Pedal
Tumor suppressor
genes are a family of
normal genes that
instruct cells to
produce proteins that
restrain cell growth
and division. Since
tumor suppressor
genes code for
proteins that slow
down cell growth and
division, the loss of
such proteins allows
a cell to grow and
divide in an
uncontrolled fashion.
18. Tumor Suppressor Genes
Act Like a Brake Pedal
Tumor suppressor genes are
like the brake pedal of an
automobile. The loss of a
tumor suppressor gene
function is like having a
brake pedal that does not
function properly, thereby
allowing the cell to grow and
divide continually.
19. Genes that control cell division: Some tumor
suppressor genes help control cell growth and
reproduction. e.g. retinoblastoma gene (RB1).
Abnormalities of the RB1 gene can lead to a type of eye
cancer (retinoblastoma) in infants, as well as to other
cancers.
DNA repair genes:These are genes that fix any mistakes
made when DNA is replicated(copied). Mistakes that aren't
fixed become mutations, which may eventually lead cancer.
e.g. Genes responsible for HNPCC (hereditary
nonpolyposiscolon cancer). When these genes do not repair
the errors in DNA, HNPCC can result.
Cell "suicide" genes e.g. p53.
21. DNA repair genes
Each cell loses more than 10000 bases per day from
spontaneous breakdown of DNA at body temperature.
Fortunately, the DNA repair genes code for enzymes that
fix crack in DNA.
Genetics disorders in which DNA repair process is defective
exhibit risk for certain type of cancers-
- Xeroderma pigmentosa
- Ataxia telangiectasia.
- Bloom syndrome.
- Fanconi’s anaemia
22. P53 gene(TP53) : Guardian of genome
Located in 17p13,1 & most common target for genetic alteration
in human cancer. A little over 50% of human tumors contain
mutations in this gene.
Homozygous loss(deletion or mutation) of p53 occurs virtually
every type of cancer, including carcinoma of lung, colon and
breast.
Assist in DNA repair by inducing DNA repair genes & direct the
cells to undergo apoptosis.If damaged, DNA cannot be repaired.
so p53 is called guardian of genome.
The malignant tumors that retain normal p53 genes respond well
to chemotherapy & radiotherapy.
Inheritance of one mutant p53 allele predisposes malignancy.
These individuals said to have Li-Fraumeni syndrome.
23. RB gene
Located in 13q14 position.
RB protein inactivates E2F(transcription factor) & thereby
inhibit cell cycle at G1 phase.usually cyclin D rise in late G1
phase & later inactivates RB to maintain the usual process
of cell kinetics.
Certain tumor antigen(derived from viruses) may combine
with RB protein& results in uncontrollable & continuous
cell division leads to cancer.(Retinoblastoma)
Associated neoplasm: osteosarcoma, carcinoma of breast
colon & lung.
24. Inherited Abnormalities of Tumor Suppressor Genes have
been found in several cancers that tend to run in families.
Mutations in p53, RB1, and the genes involved in HNPCC, .
A defective APC gene causes familial polyposis, a condition in
which people develop hundreds or thousands of colon polyps,
some of which may eventually acquire several sporadic
mutations and turn into colon cancer.
Abnormalities of the BRCA genes account for 5% to 10% of breast
cancers.
Non-inherited mutations of tumor suppressor genes :
Acquired mutations of the p53 gene appear to be involved in a
wide range of cancers, including lung, colorectal, and breast
cancer, as well as many others.
Acquired changes in many other tumor suppressor genes also
contribute to the development of sporadic (not inherited) cancers
25. Several close (first or second degree) relatives with a
common cancer.
Several close relatives with related cancers. e.g.
breast and ovary or bowel and endometrial cancer.
Two family members with the same rare cancer
An unusually early age of onset
Bilateral tumors in paired organs
Synchronous or successive tumors
Tumors in two different organ systems in one
individual
Feature Suggestive of
an Inherited Cancer Susceptibility Syndrome in Families
26. Inherited Susceptibility for the Common Cancers
The heritability of cancers are usually affected by complex
interactions between carcinogens and the host's genome.
The level of risk for persons with a family history of one of the
common cancers such as bowel or breast cancer depends on a
number of factors. These include the number of person at risk
to the affected individuals and the age at which the affected
family members develop cancers,…
The presence of an oncogene in a germ line cell (egg or sperm)
results in an inherited predisposition for tumors in the
offspring. However, a single oncogene is not usually sufficient
to cause cancer, so inheritance of an oncogene does not
necessarily result in cancer.
Persons at risk of an inherited cancer susceptibility can be
screened for associated features of a familial cancer
predisposing syndrome or for particular cancer
27.
28. Telomerase & cancer cells
Replication of DNA at the telomeres is regulated by the
enzyme telomerase.
In normal cells, telomeres being the mitotic clock shorten
at each cell division, and when they reduce below a critical
length, the cells die.
In cancer cells, however shortening of telomeres is
prevented by telomerase.
Telomerase inhibitors may have anti-cancer activity.
30. Genetic testing
Inherited cancer genes can significantly increase the lifetime risk
of developing cancer . Therefore, the identification of well-
characterized germline cancer genes can be used to predict both
the type and extent of cancer susceptibility.
Testing is done on a small sample of body fluid or tissue—usually
blood, but sometimes saliva, cells from inside the cheek, skin
cells, or amniotic fluid.
A “positive test result” means that the laboratory found a
specific genetic alteration (or mutation) that is associated with a
hereditary cancer syndrome.
A “negative test result” means that the laboratory did not find
the specific alteration that the test was designed to detect. This
result is most useful when working with a family in which the
specific, disease-causing genetic alteration is already known to be
present.
31. When a person has a strong family history of cancer but the
family has not been found to have a known mutation
associated with a hereditary cancer syndrome, a negative
test result is classified as an “uninformative negative”.
If genetic testing shows a change that has not been
previously associated with cancer in other people, the
person’s test result may report “variant of unknown
significance,” or VUS.
If the test reveals a genetic change that is common in the
general population among people without cancer, the
change is called a polymorphism.
32. Diagnosis and prognosis.
Many cancers have a course that is highly variable and
therefore difficult to predict. Because cancer genes dictate
the aberrant phenotype of cancer cells, genotypic analysis
can provide information on the capacity of a given tumor to
grow and spread.
This information can potentially be used to categorize
tumors and to predict their course and responses to
therapy.
Early detection. The most treatable cancers are those
that are diagnosed at an early stage.
33. Genetic counselling
Genetic counselling is a communication process to inform
the consultands about the recurrence risk of predisposing
familial cancer which might affect the offsprings of future
generations.
Three important steps in genetic sounselling are –
- The establishment of diagnosis.
- Estimation of recurrence risk.
- Communication of relavant information to the consultands
in a sympathetic manner so that latter can exercise their
own choices or options available for dealing with the risk.
34. As part of the process of genetic education and counseling,
genetic testing may be considered when the following
factors are present:
An individual's personal history (including ethnicity)and/or
family history is suspicious for a genetic predisposition to
cancer.
The genetic test has sufficient sensitivity and specificity to
be interpreted.
The test will impact the individual's diagnosis, cancer
management or cancer risk management, and/or help
clarify risk in family members
35. Gene therapy
Gene therapy envisages the replacement of a deficient gene
in the form of a protein or an enzyme or correction of
abnormal gene.
three different gene therapy treatment approaches:
1) Immunotherapy uses genetically modified cells and
viral particles to stimulate the immune system to destroy
cancer cells.
2) Oncolytic virotherapy, which uses viral particles that
replicate within the cancer cell to cause cell death, is an
emerging treatment modality that shows great promise,
particularly with metastatic cancers.
36. 3) Gene transfer is a new treatment modality that
introduces new genes into a cancerous cell or the
surrounding tissue to cause cell death or slow the growth of
the cancer.
No genetic disorders have been conclusively cured by gene
therapy, but some promising results are obtained from
ongoing clinical trials.
37. Conclusion
Cancer is a genetic disorder in which the normal control of
cell growth is lost. The basic mechanism in all cancer is
mutation, either in the germ line or much more frequently,
in somatic cells. Cancer is multi-factorial diseases, much
remains to be learned about the genetic processes of
carcinogenesis and about he environmental factors that
alter DNA and thus lead to malignancy.