This document summarizes hereditary cancer syndromes and BRCA mutations. It discusses that most cancers are sporadic, but 5-10% are hereditary due to germline mutations passed down from relatives. Hereditary cancers often occur earlier and increase risk for multiple cancer types. Specific cancer susceptibility genes are discussed, including BRCA1 and BRCA2 mutations which increase lifetime risks of breast and ovarian cancers. Diagnostic testing and management strategies for individuals with BRCA mutations are outlined, including increased cancer screening, risk-reducing surgeries, and lifestyle modifications. Genetic counseling plays an important role in assessing cancer risks and managing hereditary cancer syndromes in families.
It describes the prevalence of Breast Cancer among BRCA 1/2 mutations with special consideration to biological background, detection and screening, actions taken upon discovering mutation carriers and whether we have a different therapeutic algorithm than sporadic cases. Special emphasis on the role of PARP inhibitors in the management of metastatic disease.
Audio and slides for this presentation are also available on YouTube: http://youtu.be/ukXhuy5cXrE
Huma Q. Rana, MD, a cancer geneticist with Dana-Farber Cancer Institute, explains the cancer risk associated with BRCA1 and BRCA2 gene mutations. This presentation was originally given on July 23, 2013 as part of the "What Every Woman Should Know" event put on by Dana-Farber's Susan F. Smith Center for Women's Cancers.
It describes the prevalence of Breast Cancer among BRCA 1/2 mutations with special consideration to biological background, detection and screening, actions taken upon discovering mutation carriers and whether we have a different therapeutic algorithm than sporadic cases. Special emphasis on the role of PARP inhibitors in the management of metastatic disease.
Audio and slides for this presentation are also available on YouTube: http://youtu.be/ukXhuy5cXrE
Huma Q. Rana, MD, a cancer geneticist with Dana-Farber Cancer Institute, explains the cancer risk associated with BRCA1 and BRCA2 gene mutations. This presentation was originally given on July 23, 2013 as part of the "What Every Woman Should Know" event put on by Dana-Farber's Susan F. Smith Center for Women's Cancers.
Audio and slides for this presentation are available on YouTube: http://youtu.be/e_KVYJX2GTs
Have you ever wondered about your genetic predisposition to cancer? How cancer evolves in families? Or how cancer cells differ from normal cells in your body? Join Judy Garber, MD, MPH, director of the Center for Cancer Genetics and Prevention at Dana-Farber Cancer Institute, as she explores the basics of cancer genetics, DNA mutations, genetic screening, management, and more.
BRCA – Importance in Hereditary Breast & Ovarian CancerLifecare Centre
BRCA – Importance in Hereditary
Breast & Ovarian Cancer
DGF & WOW India
presentation was made by
Dr Sharda Jain
based on presentation made by
Dr Sunil Tadepalli
Audio and slides for this presentation are available on YouTube: http://youtu.be/e_KVYJX2GTs
Have you ever wondered about your genetic predisposition to cancer? How cancer evolves in families? Or how cancer cells differ from normal cells in your body? Join Judy Garber, MD, MPH, director of the Center for Cancer Genetics and Prevention at Dana-Farber Cancer Institute, as she explores the basics of cancer genetics, DNA mutations, genetic screening, management, and more.
BRCA – Importance in Hereditary Breast & Ovarian CancerLifecare Centre
BRCA – Importance in Hereditary
Breast & Ovarian Cancer
DGF & WOW India
presentation was made by
Dr Sharda Jain
based on presentation made by
Dr Sunil Tadepalli
This slide show that how GSTM1(Glutathione S-transeferase M1) initiate sporadic breast cancer.Also show what is breast cancer,their types and causes.This is a short case control study on breast cancer cases and healthy population.
Feature story from the Garvan Institute of Medical Research's April 2013 issue of Breakthrough newsletter. More at https://www.garvan.org.au/news-events/newsletters
MSUD is metabolic genetic error . It happens due to lack of an enzyem that degrades specific amino acids
Homocystinuria is also a metbolic genetic error due to an enzyme defficiency it leads to an accumulation of homocystein and related chemical in the blood
Have you or someone you love recently been diagnosed with stage III or stage IV colorectal cancer? Feeling overwhelmed? Learn where to go from here.
We’ll talk about every leg of the journey from understanding your diagnosis to tips on building your treatment team.
Join Dr. Edward Crane to better understand your options for treatment and know that you are not alone in your diagnosis.
Surviving and Thriving with Gynecologic Cancer - 9.7.19Summit Health
Join Gynecologic Oncology and wellness experts for a special "brunch and learn," event for ovarian, cervical and other gynecologic cancer survivors and champions. Speaker-led sessions will cover innovation in treatment and complementary medicine to help manage menopause and other symptoms. Moderated by Darlene Gibbon, MD. FACOG, Medical Director of Gynecologic Oncology.
Other event materials can be found under the Patient Tools tab on this page: https://www.summitmedicalgroup.com/service/gynecological-oncology/
Learning about health, family history and what information to collect is important! As we prepare for November as Health History Month, the holidays provide an excellent opportunity for families to share health history. This webinar will help you learn about colorectal cancer and cancer diagnosis, and what this means for you and your family. We’ll give you tools and resources that help you collect this important information.
http://fightcolorectalcancer.org/get-resources/webinar-series/
Presentation from Peter Hulick, MD, MMSc, to help nurses and nurse practitioners:
1) Understand the genetic consultation process
2) Examine genetic contribution to breast cancer
3) Identify suggestive family history patterns and risk estimation
4) Influence of genetic testing on management
Taken from a CNE-granting presentation given on 2/17/12 in Highland Park, IL, put together by the Chicago Center for Jewish Genetic Disorders and NorthShore University HealthSystem.
At our October webinar we spent time reviewing the importance of family history. In this webinar, we will discuss genetic and familial syndromes that are specific to colorectal cancer. We will discuss what you might look for in your family history and think about implications for prevention and management of the colorectal cancer syndromes based on this information!
About our Speakers:
Lisa Ku, MS, CGC | Certified Genetic Counselor at the University of Colorado.
Lisen Axell, MS, CGC | Certified Genetic Counselor at the University of Colorado.
Genetic counselor, Heather Herrmann, will dive in to the topic of Lynch Syndrome & CRC. Heather has enjoyed working in both pediatric genetics and cancer genetics throughout her career. She has focused the last eight years in the area of hereditary cancer syndromes and hereditary cancer risk assessment.
In this webinar, Fight CRC Medical Advisory Board member, Heather Hampel, MS, LGC, will discuss the major sub-types of hereditary colon cancer, the types of genetic tests that by be useful for you and your family, and what to do with your test results.
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.
Dr Sujoy Dasgupta was invited to deliver a lecture on "Male Infertility, Antioxidants and Beyond" on 3 February in Yuvacon 2024 organized by the Bengal Obstetric and Gynaecological Society (BOGS). The session was supported by UNS.
"Radical excision of DIE in subferile women with deep infiltrating endometrio...Sujoy Dasgupta
Dr Sujoy Dasgupta participated in an invited debate FOR the motion "Radical excision of DIE in subferile women with deep infiltrating endometriosis is not recommended" in ENDOGYN 2024, organized by the IAGE (Indian Association of Gynaecological Endoscopists) and the BOGS (Bengal Obstetric and Gynaecological Society) on 10 February 2024.
Adenomyosis or Fibroid- making right diagnosisSujoy Dasgupta
Invited lecture by Dr Sujoy Dasgupta in the Ultrasound Workshop of the Annual National Conference of Indian Association of Gynaecological Endoscopists (IAGE) held on 15 March 2024 at the Taj Ganges, Varanasi
Invited lecture by Dr Sujoy Dasgupta on "Azoospermia - Evaluation and Management" in a CME on "Standardising Male Factor Evaluation" organised by Indian Fertility Society (IFS) on 20 January 2024.
Are we giving much importance to AMH in infertility practice?Sujoy Dasgupta
Dr Sujoy Dasgupta delivered "Kamini Rao Oration" on "Are we giving much importance to AMH in infertility practice?" in East Zone Yuva FOGSI Conference organized by Imphal Obstetric and Gynaecological Society (IOGS) on 24 December, 2023
Male Infertility-How a Gynaecologist can Manage?Sujoy Dasgupta
Dr Sujoy dasgupta delivered an invited lecture on "Male Infertility-How a Gynaecologist can Manage?" in a CME on "New Frontiers in Infertility" organized by Genome Fertility Centre and Bhagirathi Neotia Woman and Child Care Centre, Kolkata held on 15 December 2023
Endometriosis and Subfertility, Primium non nocereSujoy Dasgupta
Dr Sujoy dasgupta and Dr Arun Madhab Barua were invited to moderate a panel discussion on "Endometriosis and Subfertility, Primium non nocere" in the International Congress on Endometriosis (ICE) on 10 December 2023 at Dhana Dhanya Auditorium, Kolkata
Dr Sujoy Dasgupta delivered an invited talk on "Embryo Transfer" in "Ultrasound Workshop" on 8 December 2023 at Milan, 2023, the conference of all the Obstetric and Gynaecological Societies of West Bengal. This conference was organized by Kalyani Obstetric and Gynaecological Society (KOGS).
Rational Investigations and Management of Male InfertilitySujoy Dasgupta
Dr Sujoy Dasgupta delivered an invited lecture in the annual conference of WMOGS (West Midnapore Obstetric and Gynaecological Society) held on 16 September, 2023
Endometriosis and Subfertility - What to do?Sujoy Dasgupta
Lecture delivered by Dr Sujoy Dasgupta in IPCON 2823, the Mid term conference of ISOPARB (Indian Society of Perinatology and Reproductive Biology) held at Kolkata on 10 September
IVF- How it changed the perspective of Male InfertilitySujoy Dasgupta
Dr Sujoy Dasgupta was invited to deliver a talk in a CME held on the World IVF Day (25 July, 2023) organized by Burdwan Obst Gynae Society and Corona Remedies.
Male Infertility- How Gynaecologists can manage?Sujoy Dasgupta
Dr Sujoy Dasgupta delivered an invited lecture in a CME organised by JB Pharma with the support from West Midnapore Obst and Gynae Society and Genome Fertility Centre held at Medinipur on 22 July, 2023.
Role of Multivitamins & Antioxidants in Managing Male Infertility Sujoy Dasgupta
Dr Sujoy Dasgupta was invited to deliver a talk on "Role of Multivitamins & Antioxidants in Managing Male Infertility " in a CME organized by Agartala Obstetric and Gynaecological Society and ArEx Laboratory held at Agartala on 8 July 2023
Panel discussion moderated by Dr Sujoy Dasgupta and Dr Sudip Basu on "Troubleshooting in Male Subfertility" in the Andrology Workshop organized by Special Interest Group (SIG) Andrology and Indian Fertility Society (IFS) West Bengal Chapter held on 11 June 2023 at Kolkata
Fertility Management: Synergy between Endoscopists and Fertility SpecialistsSujoy Dasgupta
Dr Sujoy Dasgupta was invited to moderate a panel discussion on "Fertility Management: Synergy between Endoscopists and Fertility Specialists " in a CME by Torrent held on 27 May 2023.
ESHRE Guideline on Recurrent Pregnancy Loss (RPL)Sujoy Dasgupta
Dr Sujoy Dasgupta invited to deliver a lecture on "RPL- ESHRE Guideline" in the Annual Conference of RCOG (Royal College of Obstetricians and Gynaecologists) IRC (International Representative Committee) India East held on 20-21 May, 2023
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!
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
3. HEREDITARY CANCER
SYNDROMES (HCS)
• Changes (or mutations) in specific genes are
passed from one blood relative to another.
• Individuals who inherit one of these gene
changes will have a higher likelihood of
developing cancer within their lifetime
4. Characteristics
Cancer is a common disease, so some families will
have some members who having the same cancer
but that does not mean the cancer in that family is
hereditary.
• Hereditary cancers often occur earlier than the sporadic
form of the same cancer, so SCREENING from younger
age is recommended
• Individuals having the inherited gene may be at a higher
risk for more than one type of cancer. For cancer
survivors, this may affect cancer treatment options or
follow-up care
• Usually produce site-specific cancers
• Two or more relatives affected
5. MOLECULAR BIOLOGY
• Cancer- Accumulation of series of mutations at various cancer-
susceptibility genes
• Most solid adult Tx requires 5-10 rate limiting mutations to
acquire malignant phenotype
• Uncontrolled cell growth, invasion and metastasis
GATE-KEEPER GENES
• Oncogenes-
c-ras, k-ras
• Tumour Suppressor genes
(Anti-oncogenes)
p53, p21
CARE-TAKER GENES
• Stability genes/ DNA
mismatch repair genes
(DNA MMR)
MLH1, MSH2, MSH6
6. • Everyone has two copies of each gene, one from each parent.
• Most people are born with two normal copies of each gene.
• In hereditary cancers a person is born with changes or mutations in
one copy of a cancer-susceptibility gene
• In the majority of these cases, the changes were inherited from the
mother or father.
• Knudson's "two-hit" hypothesis- two hits/ mutations within a
genome are necessary for a malignant phenotype to develop*
Hereditary cancer- One hit is already present in every cell (from
birth)- only one additional hit is necessary
Additional hit-
1.Gain in function- Proto-oncogene→ Oncogene
2.Loss of function- DNA Methylation- Inactivates
Tx Suppressor gene
Sporadic cancer- Both hit occurs within a single somatic cell (after
birth)
*
Carl O. Nordling in 1953, Alfred G. Knudson in 1971
7.
8. GENETIC SUSCEPTIBILITY
• To describe the high risk for cancer in people
with an inherited mutation
• People with an inherited gene change have a 50%
chance of passing the mutation to each of their
children
• Do not increase the risk for every type of cancer
• Not everyone who is born with a gene change
will develop cancer
9. WHY?
• Second hit may not take place
• Incomplete penetrance- the AD gene is
expressed at all or not
• Expressibility- Degree to which the
phenotypes are expressed
• Co-dominance- alleles of a gene pair are
different from each other but both are
expressed
10. HCS of GYNAECOLOGICAL SIGNIFICANCE
HCS Gene Mutation Tx phenotype Gynae Tx
Li-Fraumeni
Syndrome
TP53, CHEK2
Breast Ca
Soft tissue sarcoma
Adrenal cortical Ca
Brain Tx
Leukaemia
Ca Fallopian Tube
Cowden Syndrome
/Bannayan-Zonana
Syndrome/ PHTS
(PTEN Hamartmoa
Tx Syndrome)
PTEN
Breast Ca
Hamartoma
Glioma
Ca endometrium (Type
I)
Hereditary Breast
and Ovarian Cancer
(HBOC)
BRCA1,
BRCA2
Breast Ca
Male breast Ca
Male Prostate Ca
Ca Pancreas
Fanconi Anaemia
Brain Tx
Ca Ovary
Ca Fallopian Tube
Primary Peritoneal Ca
11. HCS of GYNAECOLOGICAL SIGNIFICANCE
(Contd.)
HCS Gene Mutation Tx phenotype Gynae Tx
Lynch Syndrome/
Hereditary Non-
Polyposis Colon
Cancer (HNPCC)
MLH1, MSH2,
MSH3, MSH6,
PMS2
Colon Ca
Somach Ca
Small Bowel Ca
Bladder Ca
Ca Endometrium
Ca Ovary
Multiple Endocrine
Neoplasia type I
(MEN I)
Menin
Ca Thyroid
Ca/ adenoma of Pituitary
Ca pancreas
Ovarian Carcinoid
MEN II RET
Ca Thyroid
Ca Parathyroid
Pheochromocytoma
Ovarian Carcinoid
Peutz-Jeghers
Syndrome
STK11
GI hamartomatous polyps
Tx of colon/ small bowel/
stomach
Ca Breast
SCTAT (Sex Cord
Tx with Annular
Tubules) of Ovary
12. MANAGEMENT OF
FAMILY MEMBERS OF HCS
• Genetic Counseling
• Reproductiove options- PGD, AN testing,
Third Party Reproduction
• Screening
• Intervention
1.Life-style modification
2.Pharmacological (Chemoprevention)
3.Surgical
13. Genetic counseling (NCCN, 2014)
• Consulting with an expert in cancer genetics
• Reviewing the family medical history including family members who
never developed cancer
• Primary site of the cancers
• Age of onset for any cancers in the family
• Medical examination of all the family members
• Preventive strategies
• Assessing and explaining risk for hereditary cancers
• Discussing the benefits and limitations of genetic testing
• Outlining available medical management options
• Determining which family member is most appropriate to begin the genetic
testing process in a family
• Interpreting genetic test results and explaining what they mean for
• Providing referrals to experts for follow-up screening and risk management
• Addressing common concerns about the privacy and confidentiality of
personal genetic information
14. Pedigree Analysis (NCCN, 2014)
• First Degree Relatives
Shares 50% of genes
Parents, Siblings, Children
• Second Degree Relatives
Shares 25% of genes
Grand-Parents, Grand-Children, Uncles/Aunts,
Nephew/ Niece, Half-Siblings
• Third Degree Relatives
Shares 12.5% of genes
Great Grand-Parents, Great Grand-Children, Great
Uncles/ Great Aunts, 1st Cousins
15. PRE-IMPLANTATION GENETIC
DIAGNOSIS (PGD)
• For individuals who do not want the mutation to be transferred
to their offsprings
• Needs IVF→ screening of embryos for genetic mutations →
Only unaffected embryos are transferred
• In May 2006, the UK Human Fertilization and Embryology
Authority (HFEA) approved it
• Approved by NCCN, 2014
• Problems
1. Ethical issue- cancer risk may be only probable
2. Not a ''immediate life-threatening or disabling condition"
3. Costly
4. Large number of mutations
17. GENETICS
• BRCA1 (17q12-q21) and BRCA 2 (13q12-q13)
• Autosomal Dominance Inheritance
• Tx suppressor genes- encode proteins (1863 amino acid with zinc finger
domain) necessary for repair of damaged DNA and also in DNA transcription
• Mutation→ profoundly sensitizes cells to the inhibition of PARP enzymatic
activity→ uncontrolled cell proliferation in breast, ovary, tube, peritoneum
• Incomplete penetrance- depending on type of the mutation, phenotype of the
individual and exogeneous factors
• Prevalence- 0.24% in general population (Whittemore AS, Balise RR, Pharoah PD et al.
Br J Cancer 2004;91:1911-1915)
• Highest prevalence- Ashkenazi Jewsish population (2%) (Struewing JP,
Hartge P, Wacholder S et al. N Eng J Med 1997;336:1401-1408)
• Founder mutations- Similar mutations found in different ethnic groups
• Most prevalent mutations-
BRCA1- 85delAG, 5382insC
BRCA2- 6174delT
18. Cancer Risks with BRCA mutations
Breast Cancer
• Accounts for 5-10% of Ca Breast
• Life-time risk- 60-85%
(cf- general population- 13%)
• Fast growing Tx
• Prognosis same as non-BRCA
Ovarian Cancer
• Accounts for 5-10% of all Ca Ovary
(29-41% in Ashkenazi Jews)
• Prognosis better than BRCA -ve
Types
• 75%- Papillary Serous
• Less common- Endometrioid
• Rare- Mucinous, Clear cell
Other Cancers
• Fallopian Tube Ca- Life time risk 3%
(general population- 0.025%)
• Primary Peritoneal Ca- Life time
Risk 1.3%
• Both 10 yr earlier than general
population
• Pancreatic, prostate, male breast Ca
Life-time
Risk
Average
age at
diagnosis
Overall
(BRCA)
15-65%
5-10 years
ealrier (late
30, early
40)
BRCA-1 28-66% 50.8 years
BRCA-2 16-27% 59.2 years
General
population
1.7%
ER +ve PR +ve
BRCA1 10% 21%
BRCA2 65%
40-
60%
19. How to test for BRCA
• The first person in a family to have genetic testing will usually
have “full-sequencing” of the BRCA1 and BRCA2 genes, i.e., to
examine the entire DNA of both genes
• If a mutation has already been identified in a family, then often
(but not always) a “single-site” test can be ordered to look for the
specific mutation that was already found.
• "Founder mutations" are tested in high risk populations
• BART (BracAnalysis Rearrangement Test) is a panel that looks
for specific rare genetic mutations known as "large
rearrangements" that cannot be detected on regular tests. BART
testing is usually recommended in families that have a suspicious
history of cancer but no identified mutation on comprehensive
BRCA testing.
• A positive BRCA test- “deleterious mutation” was found in either
the BRCA1 or BRCA2 gene
• A negative BRCA test- No such gene mutation was found
• “Variant of uncertain significance” (VUS)- a change was found
that may or may not increase the risk for cancer.
20. MANAGEMENT OF BRCA
CARRIERS
• Genetic Counseling
• Testing for BRCA- if elegible
• If BRCA +ve
1. Screening- Breast, Ovary,
Prostate
2. Life-style modification-
Pregnancy, Lactation, Tubal
Ligation
3. Chemoprevention- COC,
Tamoxifen
4. Prophylactic Surgery-
Mastectomy, BSO
21. HBOC Testing Criteria (NCCN, 2014)
• Individuals from a family with known BRCA1/2 mutation
• Personal H/O Breast Ca (invasive/ ductal Ca in situ) with any one
1. Diagnosed ≤45 yrs
2. Diagnosed ≤50 yrs with
Additional Primary (C/L breast or I/L with clear separation)
≥1 close blood relatives with Ca Breast at any age
Unknown/ limited family H/O
3. Diagnosed ≤60 yrs with triple negative Breast Ca (ER, PR, Her 2neu)
4. Diagnosed at any age with
≥1 close blood relative with Breast Ca ≤50 yrs
≥2 close blood relatives with Breast Ca at any age
≥1 close blood relatives with Epithelial Ca Ovary
≥1 close blood relative with Male Breast Ca
≥2 close blood relatives with Ca Pancreas &/or Ca Prostate (Gleason's Score ≥7)
High risk ethnicity (Ashkenazi Jewish)
• Personal H/O Epithelial Ovarian Tx (or tube/ peritoneal Ca)
• Personal H/O Male Breast Ca
• Personal H/O Pancreatic Ca/ Ca Prostate (Gleason's Score 7) at any age with 2≧ ≧
relatives on the same side affected with breast/ ovarian/ pancreatic/ prostate Ca
1. Family H/O only (Discuss limitations of genetic testing) with
2. First/ Second Degree Relative with Above-mentioned Criteria
• Third Degree Relative with Ca Breast/ Ca Ovary with ≥2 close blood relatives with Ca Breast
(at least one diagnosed ≤60 yrs)
22. If HBOC Testing Criteria Met
• Risk Assessment, Counseling, Psychological Support, Discuss
genetic testing, Informed Consent
Known BRCA1/2 mutation in family No known familial mutation
Test for specific familial mutation Comprehensive genetic testing
Positive Not done Negative Positive No mutation VUS
HBOC Management Routine screening HBOC Mx Test Other members
23. If HBOC Testing Criteria Not Met
Risk Assessment, Counseling, Psychological Support, Discuss genetic
testing, Informed Consent
Consider testing for other HCS (Li Fraumani, Cowden, HNPCC)
If all HCS excluded, routine screening- like general population
24. HBOC Syndrome Management
(Positive BRCA mutation Carriers)
For Women
• Breast Awareness- Starting at 18 years- Monthly SBE
• Clinical breast examination- from 25 yrs- every 6-12 mth
• Breast Screening
1. Age 25-29 yrs - Annual breast MRI (preferably D7-D14)
or mammography (if MRI not available)1
2. Age 30-75 yrs - Annual Mammography/ MRI
3. Age >75 yrs- Individualised management
1
Sensitivity of MRI 100% but Mammography 33%
25. HBOC Syndrome Management (Contd.)
For Women
• Discuss chemopreventive options
• Offer risk-reducing prophylactic mastectomy
Based on earliest age of onset of Breast Ca in the family
Discuss protection, risks, reconstructive options
• Offer risk reducing prophylactic BSO- 35-40 yrs, after family
is completed
• Psychological, social and medical support after mastectomy/
BSO
• If does not opt for BSO- 6 monthly screening from 30 yrs or 5-
10 yrs before earliest onset of familial Ca Ovary
1. CA-125- after D5 of the cycle
2. TVS- D1-D10 of the cycle
26. HBOC Syndrome Management (Contd.)
For men
• From 35 yrs- Monthly SBE
• From 35 yrs- 6-12 monthly clinical breast exam
• 40 yrs- Baseline Mammogram/ MRI
• Annual breast imaging from 40 yrs- if gynaecomastia or abnormal
initial imaging
• From 40 yrs- Annual DRE and TRUS (Prostate Screening)
For men and women
• No definite guidelines for pancreatic cancers
• Education regarding s/s of Cancers associated with BRCA
• Discuss reproductive options- PGD, AN diagnosis, childhood Tx
and Fanconi's anaemia in BRCA2
For relatives
• Risk Assessment and Genetic Counseling
27. Life-Style Modification
PREGNANCY
• General population- Early pregnancy (<40 yrs) increases risk of very early onset Ca Breast
but protects against late onset (>40 yrs) Ca Breast
• BRCA- Full Term Pregnancy <40 yrs increases risk of early onset Ca Breast (OR 1.6 for
BRCA1, 2.1 for BRCA2) but protects from late onset Ca Breast1
1
Nadine A, David EG, Douglas FE. Pregnancies, Breast-Feeding, and Breast Cancer Risk in the International BRCA1/2
Carrier Cohort Study (IBCCS). J Natl Cancer Inst (19 April 2006) 98 (8): 535-544
• By delaying first childbirth- Timing of BSO is prolonged- protection of BSO may be lost
• Two induced abortions- may protect against Ca Breast2
2
Eitan FL, Joanne K, Jan L, et al. Spontaneous and therapeutic abortions and the risk of breast cancer among BRCA
mutation carriers. Breast Cancer Research 2006, 8:R15
• Effect on Ca Ovary is uncertain- one study showed that parity protects against Ca Ovary in
BRCA1 but increases risk in BRCA23
3
John RM, Harvey A R, Jan L, et al. Reproductive risk factors for ovarian cancer in carriers of BRCA1 or BRCA2
mutations: a case-control study. The Lancet Oncology, Volume 8, Issue 1, Pages 26 - 34, January 2007
• Another study- Each FT pregnancy reduces risk by 12%4
4
Modan B, Hartge P, Hirsh YG, et al. Parity, oral contraceptives, and the risk of ovarian cancer among carriers and
noncarriers of a BRCA1 or BRCA2 mutation N Engl J Med. 2001 Jul 26;345(4):235-40
28. Life-Style Modification (Contd.)
BREAST-FEEDING
• Breast feeding reduces risk of Ca Breast in BRCA significantly by
suppressing ovulation, reducing estrogen and directly acting on mammary tissue1
1
Jernström, Lerman C, P Ghadirian, et al. Pregnancy and risk of early breast cancer in carriers of
BRCA1 and BRCA2.The Lancet, Volume 354, Issue 9193; 1846 - 1850
TUBAL LIGATION
• General population- TL protects against Ca Ovary
• BRCA carriers- protective in BRCA1, notnot in BRCA2 2
2
Narod SA, Sun P, et al. Tubal ligation and risk of ovarian cancer in carriers of BRCA1 or BRCA2 mutations: a
case-control study. Lancet 2001;357:1467-1470
• So, if BRCA1 carriers do not opt for BSO- Lap B/L TL can be done along with
evaluation of ovaries and peritoneal washing to detect occult primaries
29. CHEMO-PREVENTION
ORAL CONTRACEPTIVE PILLS (COC)
• Ca Ovary
General Population- Protective (50% reduced risk after 5 yrs, 80% after 10 yrs)
BRCA- Protective in both BRCA1 and BRCA2
Modan et al, 2001- No added protection as typically seen in general population1
1
Modan B, Hartge P, Hirsh YG, et al. Parity, oral contraceptives, and the risk of ovarian cancer among carriers and
noncarriers of a BRCA1 or BRCA2 mutation N Engl J Med. 2001 Jul 26;345(4):235-40
• Ca Breast
General population- Early start of OCP increases (slighly) risk of early Ca Breast but
protects from late onset Ca Breast
Earlier studies- Small increase in Ca breast, mainly in BRCA1
Recent studies- Low dose COC does not increase the risk2
2
Milne RL, Knight JA, John EM, Dite GS, et al. Oral contraceptive use and risk of early-onset breast cancer in carriers
and noncarriers of BRCA1 and BRCA2 mutations.Cancer Epidemiol Biomarkers Prev. 2005 Feb;14(2):350-6.
• Conclusion-
Newer forms of COC possibly protects against ca Ovary in BRCA
but role in Ca Breast is UNCERTAIN (probably no increased risk)
30. CHEMO-PREVENTION (Contd.)
TAMOXIFEN
• SERM use can protect against Ca Breast in BRCA2, but not in
BRCA11
• BRCA1 is mostly ER/PR -ve, while BRCA2 is mostly ER/PR +ve
1
King MC, Wieand S, Hale K, Lee M, Walsh T, Owens K, et al. Tamoxifen and breast cancer incidence among women with inherited
mutations in BRCA1 and BRCA2: National Surgical Adjuvant Breast and Bowel Project (NSABP-P1) Breast Cancer Prevention
Trial. JAMA 2001;286:2251-6
• A Decision Analysis- a BRCA carrier at 30 yrs- Tamoxifen
increases survival by 1.8 years and quality-adjusted survival by
2.7 years2
2
Grann VR1, Jacobson JS, Thomason D, Hershman D, Heitjan DF, Neugut AI. Effect of prevention strategies on
survival and quality-adjusted survival of women with BRCA1/2 mutations: an updated decision analysis.J Clin
Oncol. 2002 May 15;20(10):2520-9
INNOVATIVE METHODS
• PARP Sensitizers3
3Hannah F, Nuala M, Christopher JL. Targeting the DNA repair defect in BRCA mutant
cells as a therapeutic strategy. Nature 434, 917-921 (14 April 2005)
31. PROPHYLACTIC
OOPHORECTOMY
• NCCN 2014, NIH 1995, SGO 2005- all
recommend prophylactic BSO
• Reduces risk of Ca Ovary and Ca Tube
• Reduces risk of Ca Breast from 42% to 21%-
by removing the source of estrogen
• Benefit extends for even those with already
diagnosed Ca Breast
• Role in Primary Ca Peritoneum- Uncertain
32. PROPHYLACTIC OOPHORECTOMY
(Contd.)
Evidences
• If done at 30 yrs- prophylactic oophorectomy improved
survival by 0.4 to 2.6 years; mastectomy, by 2.8 to 3.4 years;
and mastectomy and oophorectomy, by 3.3 to 6.0 years over
surveillance1
1
Grann VR1, Panageas KS, Whang W, Antman KH, Neugut AI. Decision analysis of prophylactic
mastectomy and oophorectomy in BRCA1-positive or BRCA2-positive patients.J Clin Oncol. 1998
Mar;16(3):979-85.
• Kauff et al, 2002 (NEJM, 2002;346:1609-1615)- BSO reduces risk of Ca
Ovary, compared to screening.
• 5 yr cancer-free survival was 94% (BSO) vs 69% (Screening)
• Moller et al, 2002 (Int J Cancer 2002;101:555-559)- 5 yr disease free
survival was 100% for Ca Breast
33. PROPHYLACTIC OOPHORECTOMY
(Contd.)
Timing of Surgery
• Recommendation- 35-40 yrs, after family is
completed (NCCN, 2014)
• BRCA1- Ca Ovary starts from late 30 and early 40-
54% before 50 yrs of age
• Modern trend of delay in child bearing- poses
problem
• BRCA2- Ca Ovary occurs 10 yrs later than BRCA1
BSO can be perfomred near natural menopause
Decreases protection against Ca Breast (at 50 yr- 26-
34% risk)
34. PROPHYLACTIC OOPHORECTOMY (Contd.)
Surgical Technique
• Laparotomy/ Laparoscopy- ?
• Bilateral Oophorectomy/ Bilateral Salpingo-
Oophorectomy (BSO)-
B/L OOphorectomy is minimum
SGO and NCCN recommends BSO
Risk of CA Tube is 120 fold higher
• Peritoneal washing (or laparoscopic culdocentesis)
Routine- ?
Agoff et al (Am J Surg Pathol 2002;26:171-178) and Colgan et al (Am J
Surg Pathol 2001;25:1283-1289)- detects some cases of Ca Ovary in
BRCA Carriers only after positive Peritoneal Cytology
• Routine random peritoneal/ omental biopsies
No clear consensus
35. PROPHYLACTIC OOPHORECTOMY
(Contd.)
Hysterectomy
• Points in favour
Reduces the risk of leaving behind a residual tube at the time of BSO
Theoretically malignant transformation in interstitial part of the tube
possible
Eliminates risk of Ca Endometrium in women receiving HRT/ Tamoxifen
Higher incidence of UPSC in Ashkenazy Jewish women carrying BRCA
mutation (Goldman NA et al. ASCO Proc 2002;21. Lavie O et al. Gynecol Oncol 2004;92:521-524)
• Points against
Ca tube occurs most commonly in the distal portion
No report of Ca tube in interstitial part in BRCA
Goshen et al (Gynecol Oncol 2000;79:477-481) did not find any
correlation between UPSC and BRCA
36. PROPHYLACTIC OOPHORECTOMY
(Contd.)
Pathological Examination
• No clear Consensus for examination of specimens of
apparently unaffected BRCA Carriers
• Occult Ca can be found in tubes/ ovaries/ peritoneal washings
(2-8%)
• Majority are normal on gross inspection
• Powell et al (J Clin Oncol 2005;23:127-132) suggested serial
sectioning of tubes and ovaries (2 mm interval) and
examination of all sections, exam of peritoneal washings and
random Bx from peritoneum/ omentum- discovered 17% cases
of occult Ca with grossly normal specimens
37. PROPHYLACTIC OOPHORECTOMY
(Contd.)
Disadvantages
• Surgical Complications- Surgeon's skills, patient
herself, type of Sx (laparoscopy/ laparotomy, more
with hysterectomy)
• Primary peritoneal Ca still possible (<1%)
• Premature menopause- if BSO done at 35 yrs- 16 yrs
earlier than natural menopause
More risk than general population- osteoporosis, vasomotor
symptoms, CVS ds, decreased sex drive, dyslipidaemia
HRT very much controversial
Theoretically- BRCA1 is ER/PR -ve, so can use HRT, but not
in BRCA2
Recent study (average 5 yr follow up)- HRT does not increase
risk of Ca Breast, rather small decline in Ca Breast
39. GENETICS
• Germline mutations of one of the six genes involved in DNA
MMR (Mis-Match Repair), i.e., encoding enzymes involved
in repair of errors that occur during normal DNA replication
• MSH2, MSH6, MLH1, MLH3, PMS1, PMS2
• After mutation→ replication errors accumulate → unstable
genome (MSI- micro-satellite instability) → Inactivates anti-
apoptotic genes (TGF-β and BAX) →Multiple somatic
mutations → Malignant phenotype
Types of LS
1. Lynch Syndrome I- Site specific CRC (more in Rt colon)
2. Lynch Syndrome II- CRC, Endometrial, Ovarian, Stomach,
Small Bowel, Renal pelvis/ Ureteric, Pancreatic, Breast,
Hepatobiliary, CNS, Sebaceous gland Ca
A variant of HNPCC- called Muir Torre Syndrome- increased
risk for certain skin tumors
A second variant, called Turcot Syndrome, is associated with
certain brain tumors (different than in FAP)
41. CLINICAL DEFINITION of LS
Minimum Criteria
(Amsterdam I)
• At least 3 relatives with
CRC. With all of the
followings-
1. One should be a 1st degree relative
of the other two
2. At least 2 succesive generations
should be affected
3. At least one relative having CRC
diagnosed <50 yrs
4. Tx verified by pathological
examination
5. FAP must be excluded
Revised Minimum Criteria
(Amsterdam II)
• At least 3 relatives with any of the
cancers of LS (Colorectal,
endometrial, small bowel, ureter, renal
pelvis)- With all of the followings-
1. One should be a 1st degree relative of the
other two
2. At least 2 succesive generations should
be affected
3. At least one relative having anay cancer
in LS diagnosed <50 yrs
4. Tx verified by pathological examination
5. FAP must be excluded in case of CRC (if
any)
42. Bethesda Criteria
For testing of CRC for Lynch Syndrome by
IHC or MSI (Microsatellite Instability)
• CRC diagnosed <50 yrs of age
• Synchronous/ metachronous/ other CRC or any other Ca* associated with
LS regardless of age
*Endometrial, ovarian, gastric, pancreatic, small bowel, ureter, renal pelvis, biliary
tree, brain- glioblastoma (Turcot syndrome), sebaceous gland adenoma and
keratocanthoma (Muir Tore Syndrome)
• CRC with MSI-H histology** in any patient <60 yrs of age
**Tx infiltrating lymphocytes, Crohn's like lymphocyte reactions, Medullary pattern,
Mucinous/ Signet ring
• CRC in a patient with ≥1 1st degree relative with any Ca of LS, at least one
of whom diagnosed <50 yrs
• CRC in a patient with ≥2 1st/ 2nd degre relatives with any Ca of LS,
regardless of age
43. LS Testing Criteria (NCCN, 2014)
• Satisfies clinical definition of LS (Amsterdam I or II Criteria)
• Bethesda Criteria for testing of CRC by IHC/ MSI
• Endometrial Ca <50 yrs
• Known LS in the family
Known LS mutation No known LS mutation Testing criteria not satisfied
Test for familial mutation Tx available for testing No Tx available Routine screening for CRC
Positive Not done Negative Test for IHC/ MSI Positive for Not tested/
mutation mutation Negative
LS Management Routine Screening LS MAnagement Routine Screening
44. Manamegement of known LS
(NCCN, 2014)
COLONIC CANCER
MLH1, MSH2, EPCAM
Mutation
• Colonoscopy from 20-25 yrs-
every 1-2 yearly
• If H/O Colon Ca <25 yrs, start
colonoscopy- 2-5 yrs earlier
than that age
• Aspirin may be considered as
chemoprevention
MSH6, PMS2
Mutation
• Colonoscopy from 25-30 yrs-
every 1-2 yearly
• If H/O Colon Ca <30 yrs, start
colonoscopy- 2-5 yrs earlier
than that age
45. Manamegement of known LS (Contd.)
EXTRA-COLONIC CANCER
MLH1, MSH2, EPCAM Mutation
Endometrium and Ovary
• Risk-reducing Surgery- Prophylactic
TAH+BSO after family is completed
• Education- any DUB needs consultation
• Annual Office Hysteroscopic Sampling
• Annual TVS and CA-125- data limited
Stomach and Small Bowel
• For Asian Ethnicity- UGI endoscopy with
duodenoscopy (upto jejunum) from 30-35 yrs, every
3-5 yrs
Urothelial
• Annual urine analysis from 25-30 yrs
CNS
• Annual clinical. imaging from 25-30 yrs
Pancreas, Breast
• No clear recommendation
MSH6, PMS2
Mutation
Endometrium and
Ovary
• Like MLH1, MSH2,
EPCAM
Other Ca
• Very low risk
• No screening needed
46. Manamegement of known LS
FURTHER MANAGEMENT
No Pathological Findings
• Continue surveillance
• Consider subtotal colectomy
• Consider TAH+BSO- if family completed/ post-menopausal
AdenoCarcinoma
• Manage Accordingly
Adenoma
• Endoscopic resection- with colonoscopy every 1-2 yr
Adenoma, not amenable to endoscopic resection
• Total colectomy with Ileo-Rectal anastomosis
• Consider TAH-BSO at that time (if family completed/ post-menopausal)
• Rectal endoscopy every 1-2 yr