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Slide 1: Identifying and Managing Hereditary
Colorectal Cancer
This slide set is designed for educational presentations about hereditary
colorectal cancer to audiences of healthcare professionals as well as the
community. These materials are provided as an educational service by
Myriad Genetic Laboratories, Inc. of Salt Lake City, Utah.
These slides and the corresponding text were updated in March of 2005. We
welcome your comments on these slides and the accompanying notes. You can
contact us by email:
helpmed@myriad.com. ¡
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Slide 12: HNPCC Increases Risk of Second Cancer
Colon cancer patients with HNPCC are at high risk of developing a second
primary cancer, especially of the colon or endometrium. For these
individuals, the risk of a second HNPCC-associated cancer is estimated to
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colorectal cancer. In addition, women with HNPCC who develop endometrial
cancer are at greatly increased risk of subsequent colorectal cancer.
Knowledge of these significant risks for second cancers can be useful in
planning appropriate interventions for individuals with HNPCC.
References:
1Lynch HT, Harris RE, Lynch PM, et al. Role of heredity in multiple
primary cancer. Cancer 1977;40:1849-54.
2Mecklin JP, Jarvinen HJ. Clinical features of colorectal carcinoma in
cancer family syndrome. Diseases of the Colon and Rectum 1986;29:160-4.
3Cali RL, Pitsch RM, Thorson AG, et al. Cumulative incidence of
metachronous colorectal cancer. Diseases of the Colon and Rectum
1993;36:388-93. ¡ ¬
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Slide 4: A BRCA Mutation Increases Breast and Ovarian Cancer Risks
Without intervention, the majority of women with inherited
mutations in BRCA1 and BRCA2 will develop breast and/or ovarian cancer.
The range of risks of breast and ovarian cancer associated with mutations
in these genes has been characterized through numerous studies. The lower
estimates of risk are derived from analysis of mutations in an unselected
general population of individuals, whereas higher estimates of mutationassociated cancer risk are derived from families with a strong history of
cancer.
Generally, mutations in BRCA1 and BRCA2 are associated with a 45%
to 87% risk of breast cancer by age 70. 1-3 Most importantly, hereditary
breast cancer occurs at a far earlier age than the nonhereditary
(sporadic) form. Women in the general population have only a 2% chance of
developing breast cancer before age 50. However, a woman with a mutation
in BRCA1 or BRCA2 has a 33% to 50% likelihood of developing breast cancer
before reaching 50 years of age. 2,4
The risk of ovarian cancer due to inherited BRCA1 mutations is 28%7
to 44%1 by age 70, compared to the general population risk of <1%.
Mutations in BRCA2 confer a risk of ovarian cancer of 11%9 to 27%8 by
age 70, which represents up to a 15-fold increase compared to the general
population.
References:
1.
Ford D, et al. Breast Cancer Linkage Consortium: Risks of cancer in
BRCA1-mutation carriers.
Lancet 1994;343:692-695.
2.
Struewing JP, et al. The risk of cancer associated with specific
mutations of BRCA1 and BRCA2
among Ashkenazi Jews. NEJM 1997;336:1401-1408.
3.
Antoniou A, et al. Average risks of breast and ovarian cancer
associated with BRCA1 or BRCA2
mutations detected in case series unselected for family history: a
combined analysis of 22 studies.
AJHG 2003;72:1117-1130.
4.
Easton DF, et al. Breast and ovarian cancer incidence in BRCA1mutation carriers. AJHG
1995;56:265-271.
King MC, et al. Breast and Ovarian Cancer Risks Due to Inherited
Mutations in BRCA1 and BRCA2.
Science Oct 24 2003:643-646.
Narod SA, Offit K. Prevention and Management of Hereditary Breast
Cancer. J Clin Oncol. 2005
Mar 10;23(8):1656-63.
7.
Whittemore AS, Gong G, Itnyre J. Prevalence and contribution of
BRCA1 mutations in breast cancer and
ovarian cancer: results from three U.S. population-based casecontrol studies of ovarian cancer.
Am J Hum Genet 1997;60:496-504.
8.
Ford D, et al. Genetic heterogeneity and penetrance analysis of the
BRCA1 and BRCA2 genes
in breast cancer families. Am J Hum Genet 1998;62:676-689.
9.
Antoniou A, et al. Average Risks of Breast and Ovarian Cancer
Associated with BRCA1 or BRCA2 Mutations
Detected in Case Series Unselected for Family History: A Combined
Analysis of 22 Studies.
Am J Hum Genet. 2003 May; 72(5):1117-30.
10.
DevCan: Probability of Developing or Dying of Cancer Software,
Version 6.0. Statistical Research
and Applications Branch, National Cancer Institute, 2005.
http://srab.cancer.gov/devcan
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Slide 5 : A BRCA Mutation Increases the Risk
of a Second Cancer
Women who have developed breast cancer are at greatly increased
risk of a second cancer if they carry a mutation in BRCA1 or BRCA2.2,4,5
The risk of a contralateral breast cancer is increased up to 64% by age
702, or 27.1% within five years of the initial diagnosis5 in women with
BRCA1 mutations. Mutations in BRCA2 increase these risks to about 50% by
age 70,3 or 23.5% within five years of the first breast cancer.5
References:
1.
Frank TS, et al. Sequence analysis of BRCA1 and BRCA2: correlation
of mutations with family
history and ovarian cancer risk. JCO 1998;16:2417-2425.
2.
Ford D, et al. Risks of cancer in BRCA1-mutation carriers. Lancet
1994;343: 692-695.
3.
The Breast Cancer Linkage Consortium. Cancer Risks in BRCA2
Mutation Carriers. JNCI
1999;15:1310-1316.
4.
Verhoog LC, et al. Survival and tumour characteristics of breastcancer patients with germline
mutations of BRCA1. Lancet 1998;351:316-321.
5.
Metcalfe K, et al. Contralateral breast cancer in BRCA1 and BRCA2
mutation carriers. JCO
2004;22:2328-2335.
6.
Metcalfe KA, et al. The risk of ovarian cancer after breast
cancer in BRCA1 and BRCA2 carriers.
Gynecol Oncol. 2005 Jan;96(1):222-6.
7.
Chen Y, et al. Epidemiology of contralateral breast cancer. Cancer
Epidemiol Biomarkers Prev.
1999 Oct;8(10):855-61.
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Slide: Impact of Hereditary Gynecologic Cancers
Up to 15% of all ovarian cancer cases are hereditary.1
Up to 2% of all endometrial cancer2 and up to 10% of early onset
endometrial cancer cases are hereditary.3
As many as 1 in 500 people carry a mutation in either the BRCA1 or the
BRCA2 genes.4 One academic institution found that 22% of newly diagnosed
breast cancer patients referred to a multidisciplinary clinic had at
least a 10% likelihood of testing positive for a BRCA1/2 mutation.5
Another study found that 21% of women with a personal history of breast
and/or ovarian cancer had at least a 10% likelihood of testing positive
for a BRCA1/2 mutation.6 Many patients should receive a risk assessment
for hereditary breast and ovarian cancer syndrome.
While ten percent of all colorectal cancer cases are hereditary7,
approximately 20-25% of all colorectal cancer cases are considered to be
at high familial risk and therefore warrant genetic testing8.
References:
Pal, T, et al. BRCA1 and BRCA2 mutations account for a large proportion
of ovarian carcinoma cases. Cancer 2005 Dec 15;104(12):2807-16.
Hampel, H, et al. Screening for Lynch Syndrome (Hereditary Nonpolyposis
Colorectal Cancer) among Endometrial Cancer Patients. Cancer Res 2006;
66(15): 7810-7)
Berends, MJW, et al. Toward New Strategies to Select Young Endometrial
Cancer. Patients for Mismatch Repair Gene Mutation Analysis. J Clin
Oncol. 2003;21(23):4364-70.
Coughlin SS, et al. BRCA1 and BRCA2 gene mutations and risk of breast
cancer: public health perspectives. AM J Prev Med. 1999;16(2):91-98.
Shannon KM, et al. Model-based predictions of BRCA1/2 mutation status in
breast carcinoma patients treated at an academic medical center. Cancer.
2002 Jan 15;94(2):305-13.
Dominguez FJ, et al. Prevalence of hereditary breast/ovarian carcinoma
risk in patients with a personal history of breast or ovarian carcinoma
in a mammography population. Cancer. 2005 Nov 1;104(9):1849-53.
Burt R, Petersen G. Familial colorectal cancer: diagnosis and
management. In: Young G, Rosen P, Levin B, eds. Prevention and Early
Detection of Colorectal Cancer. Philadelphia: WB Saunders, 1996; 171194.
Kerber RA, et al. Frequency of familial colon cancer and hereditary
nonpolyposis colorectal cancer (Lynch syndrome) in a large population
database. Fam Cancer 2005; 4(3):239-44.
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Slide 6: Risk of Ovarian Cancer AFTER Breast Cancer
in BRCA Mutation Carriers
There have been epidemiologic studies conducted in the general
population investigating the risk of ovarian cancer after a breast cancer
diagnosis.1-4 These studies suggest that there may be a slightly
increased risk for ovarian cancer after a breast cancer diagnosis (SIR
1.7-2.3). However, none of these studies control for BRCA1/2 mutation
carriers in their cohort.
Recent data indicate that the 10- year risk for ovarian cancer
AFTER a breast cancer in BRCA1 and BRCA2 mutation carriers is 12.7% and
6.8%, respectively.5 Other studies have shown that the risk for ovarian
cancer AFTER a breast cancer diagnosis on BRCA2 mutation carriers is 16%6
and women with a BRCA1 or BRCA2 mutation have a 10-fold increased risk
compared to women who do not have a BRCA1/2 mutation.7 Due to the
ineffectiveness to screen for ovarian cancer, the National Comprehensive
Cancer Network (NCCN) has recommended that mutation positive women have a
prophylactic bilateral salpingo-oophorectomy after child-bearing.8
References:
1.
Levi F, et al. Cancer risk in women with previous breast cancer.
Ann Oncol. 2003 Jan;14(1):71-3.
2.
Rubino C, et al. Increased risk of second cancers following breast
cancer: role of the initial treatment.
Breast Cancer Res Treat. 2000 Jun;61(3):183-95.
3.
Soerjomataram I, et al. Risks of second primary breast and
urogenital cancer following female breast
cancer in the south of The Netherlands, 1972-2001. Eur J Cancer.
2005 Oct;41(15):2331-7.
4.
Volk N, Pompe-Kirn V. Second primary cancers in breast cancer
patients in Slovenia. Cancer Causes
Control. 1997 Sep;8(5):764-70.
5.
Metcalfe KA, et al. The risk of ovarian cancer after breast cancer
in BRCA1 and BRCA2 carriers.
Gynecol Oncol. 2005 Jan;96(1):222-6.
6.
The Breast Cancer Linkage Consortium: Cancer Risks in BRCA2
Mutation Carriers. JNCI.
1999;15:1310-1316.
7.
Frank TS, et al. Sequence analysis of BRCA1 and BRCA2: Correlation
of mutations with family
history and ovarian cancer risk. J Clin Oncol. 1998 16:2417-2425.
8.
The NCCN has developed recommendations for male BRCA1 and BRCA2
mutation positive
individuals
http://www.nccn.org/professionals/physician_gls/PDF/genetics_screening.pd
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Slide 7: Risks in Men with a BRCA Mutation
To date, fewer men than women have undergone genetic testing for
BRCA1 and BRCA2 mutations, in part because of misinformation about male
cancer risks.1 However, men who carry BRCA1 or BRCA2 mutations have a
significantly increased risk of cancer, with BRCA2 the more important
gene for cancer susceptibility in men. In a study of BRCA2 families, the
cumulative risk of all cancers in men was 32% by age 70, compared with
90% for women.2
For BRCA2 mutation carriers, the risk of male breast cancer by age
80 is approximately 7%.4 The risk of male breast cancer in BRCA1
families is less characterized, but is significantly higher than the
general population risk. Mutations in BRCA2 also are associated with an
increased risk of invasive prostate cancer (20% by age 80)2. In a recent
case-control study of Ashkenazi Jewish men, BRCA2 mutation carriers had a
nearly 5-fold increased risk of prostate cancer.3 A modestly increased
risk of prostate cancer was reported in men under age 65 with BRCA1
mutations.4
References:
1.
Liede A, et al. Cancer risks for male carriers of germline
mutations in BRCA1 or BRCA2: A review
of the literature. JCO 2004;22:735-42.
2.
The Breast Cancer Linkage Consortium: Cancer Risks in BRCA2
Mutation Carriers. Journal of the
National Cancer Institute 1999;15:1310-1316.
3.
Kirchhoff T, et al. BRCA mutations and risk of prostate cancer in
Ashkenazi Jews. Clinical Cancer
Research 2004;10:2918-2.
4.
Thompson D, Easton D; Breast Cancer Linkage Consortium. Variation
in cancer risks, by mutation
position, in BRCA2 mutation carriers. Am J
Hum Genet. 2001
Feb;68(2):410-9. Epub 2001 Jan 19.
5.
Thompson D, et al. Cancer Incidence in BRCA1 mutation carriers. J
Natl Cancer Inst. 2002 Sep
18;94 (18):1358-65.
6.
DevCan: Probability of Developing or Dying of Cancer Software,
Version 6.0. Statistical Research
and Applications Branch, National Cancer Institute, 2005.
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Slide 9: HNPCC Increases Colorectal and Endometrial Cancer Risks
The risk of colorectal cancer in the general population is about 0.2% by
the age of 50 and 2% by the age of 70. The risk of endometrial cancer in
the general population is about 0.2% by the age of 50 and less than 2% by
the age of 70.1
Without medical intervention, most people with inherited mutations in the
mismatch repair genes will develop colorectal cancer. The risk of
colorectal cancer in mutation carriers is at least 25% by age 50 and
about 80% by age 70.2,3 It must be emphasized that although adenomatous
polyps may form at a relatively early age in patients with HNPCC, a
profusion of polyps is not a feature of HNPCC.
Early onset of colorectal cancer is one hallmark of HNPCC but may not
always be present in these families. For example, while the average age
of diagnosis of colorectal cancer is 43-44 years in MLH1 and MSH2
mutation carriers, families with MSH6 mutations have an average age of
colorectal cancer onset of approximately 54-55 years.4
Additionally, women who inherit HNPCC-associated germline mutations also
have a greatly elevated risk of endometrial cancer. The risk of
endometrial cancer in MLH1 and MSH2 carriers is 20% by age 50 and up to
60% by age 70.2,3 Recent literature on MSH6 suggests that carriers of
mutations in MSH6 may have as high as a 71% chance to develop endometrial
cancer.3
As with colorectal cancer, endometrial cancer in patients with MLH1 and
MSH2 mutations occurs at a younger age, often before age 50. Again the
age of onset of endometrial cancer in those with MSH6 mutations is
slightly later with a mean age of 54 years.4 Some studies have reported
that if a woman carries an MLH1, MSH2, or MSH6 mutation, her risk of
endometrial cancer may be even higher than her risk of colorectal
cancer.3 Early onset of endometrial cancer should therefore raise
suspicion for HNPCC, especially in women with a family history of
colorectal cancer or endometrial cancer.
References:
1Fay MP, Pfeiffer R, Cronin KA, et al. Age-conditional probabilities of
developing cancer. Statistics in Medicine 2003;22:1837-48.
2Vasen HFA, Wijnen JT, Menko FH, et al. Cancer risk in families with
hereditary nonpolyposis colorectal cancer diagnosed by mutation analysis.
Gastroenterology 1996;110:1020-7.
3Aarnio M, Sankila R, Pukkala E, et al. Cancer risk in mutation carriers
of DNA-mismatch-repair genes. International Journal of Cancer
1999;81:214-8.
4Hendriks YM, Wagner A, Morreau H, et al. Cancer risk in hereditary
nonpolyposis colorectal cancer due to MSH6 mutations: Impact on
counseling and surveillance. Gastroenterology 2004;127:17-25. ¡ €
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Slide 5: Hereditary Colorectal Cancer (CRC)
Syndromes
The hereditary colorectal cancer syndromes can be categorized into two
groups: nonpolyposis, or those with few or no polyps; and adenomatous
polyposis, or those with multiple adenomas. Hereditary nonpolyposis
colorectal cancer (HNPCC) falls into the group of nonpolyposis syndromes,
while patients with multiple adenomatous polyps can be further delineated
into three syndromes. Classic familial adenomatous polyposis (FAP)
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with less severe colonic polyposis. MYH-associated polyposis (MAP) has
been seen in individuals with varying degrees of colonic polyposis and,
due to the relationship of MAP to multiple polyps, the colorectal cancer
risk is thought to be significantly elevated.
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HNPCC Surgical Guidelines
Approximately half of HNPCC patients with CRC will develop a second
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References:
1Church J, Simmang C. Practice parameters for the treatment of patients
with dominantly inherited colorectal cancer (familial adenomatous
polyposis and hereditary nonpolyposis colorectal cancer). Diseases of
the Colon & Rectum 2003;46:1001-12.
2Giardiello FM, Brensinger JD, Petersen GM. AGA technical review on
hereditary colorectal cancer and genetic testing. Gastroenterology
2001;121:198-213.
3Burke W, Petersen G, Lynch P, et al. Recommendations for follow-up care
of individuals with inherited predisposition to cancer. I. Hereditary
nonpolyposis colon cancer. Journal of the American Medical Association
1997;277:915-19.
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Slide 10 : Surveillance for Breast Cancer
The high survival rate of women diagnosed with early-stage breast
cancer warrants heightened surveillance for women who carry mutations in
BRCA1 and BRCA2, commencing at an early age in recognition of the earlier
age of onset of hereditary breast cancer. The National Comprehensive
Cancer Network, recommends the initiation of clinical breast
examinations, mammography, and MRI at age 25. In addition, some
clinicians suggest that breast imagining should occur once every 6 months
to maximize the chance to detect interval cancers. For example, a woman
would be offered a mammogram in January and an MRI 6 months later in July
to meet her annual imaging recommendation. Although, there currently is
no literature to provide support that this screening schedule is more
effective than performing mammography and MRI in unison.
Women with mutations in BRCA1 and BRCA2 may also benefit from
imaging methods not generally available for routine screening.1,2
Magnetic resonance imaging (MRI) has been shown to identify precancerous
and cancerous lesions that were missed by mammography.2,4,6
A recent
study compared the effectiveness of mammography, breast ultrasound, and
magnetic resonance imaging (MRI) for surveillance of women at increased
familial risk for breast cancer.5 The findings showed that mammography
alone, and mammography combined with breast ultrasound, appears to be
insufficient for early diagnosis of breast cancer in women who are at
increased familial risk. In terms of breast ultrasound, this technology
has a role in complementing diagnostic mammography.8 Furthermore, there
are data to support that exposure to ionizing radiation through routine
screening mammography does not increase the breast cancer risk in BRCA1
and BRCA2 mutation carriers.9
References:
1.
Stoutjesdijk MJ, et al. Magnetic resonance imaging and mammography
in women with a hereditary risk of
breast cancer. JNCI 2001;93:1095-1102.
2.
Hartman AR, et al. Breast magnetic resonance image screening and
ductal lavage in women at high genetic
risk for breast carcinoma. Cancer 2004;100:479-89.
3.
Kriege M, et al. Efficacy of MRI and mammography for breast-cancer
screening in women with a familial or
genetic predisposition. NEJM 2004;351:427-37.
4.
Leach MO, et al. Screening with magnetic resonance imaging and
mammography of a UK population at high
familial risk of breast cancer: a prospective multicentre cohort
study (MARIBS). Lancet. 2005 May 2127;365(9473):1769-78.
5.
Warner E, et al. Surveillance of BRCA1 and BRCA2 mutation carriers
with magnetic resonance imaging,
ultrasound, mammography, and clinical breast examination. JAMA.
2004 Sep 15;292(11):1317-25.
6.
BlueCross BlueShield Association. Magnetic Resonance Imaging of
the Breast in Screening Women
Considered to be at High Genetic Risk of Breast Cancer. 2003.
7.
The NCCN has developed recommendations for male BRCA1 and BRCA2
mutation positive individuals
http://www.nccn.org/professionals/physician_gls/PDF/genetics_screen
ing.pdf.
8.
Kuhl CK, et al. Mammography, breast ultrasound, and magnetic
resonance imaging for surveillance of women
at high familial risk for breast cancer. J Clin Oncol. 2005 Nov
20;23(33):8469-76.
9.
Narod, et al. Screening mammography and risk of breast cancer in
BRCA1 and BRCA2 mutation carriers: a
case-control study. Lancet Oncol. 2006 May;7(5):402-6.
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Slide 14: Chemoprevention of Ovarian Cancer
It has been shown in the general population that oral
contraceptives reduce the risk of ovarian carcinoma by 50%. A
retrospective, multicenter, case-control study of 207 women with
mutations in BRCA1 or BRCA2 demonstrated that the use of oralcontraceptives for six or more years was associated with a 60 percent
reduction in the hereditary risk of ovarian cancer.1 The authors found no
difference in the history of oral contraceptive use between women who
developed breast cancer and those who had not, suggesting that in this
population of oral contraceptives do not significantly increase the risk
of breast cancer.
However, the role of oral contraceptives in the chemoprevention of
hereditary cancer remains controversial. Another study found a modest
increase in breast cancer risk among some women with BRCA1 mutations,
such as those who used oral contraceptives for 5 years or more or before
1975 (prior to the introduction of current low-dose formulations ).2 This
study found no increased risk of breast cancer among women with BRCA2
mutations who used oral contraceptives.
In addition, the efficacy of oral contraceptives in reducing the
risk of ovarian cancer in mutation carriers was confirmed in a separate
study by different investigators.3, 4
References:
1.
Narod SA, et al. Oral contraceptives and the risk of hereditary
ovarian cancer. NEJM
1998;339:424-428.
2.
Narod SA, et al. Oral contraceptives and the risk of breast cancer
in BRCA1 and BRCA2 mutation
carriers. JNCI 2002;94:1773-9.
3.
Modan B, et al. Parity, Oral contraceptives, and the risk of
ovarian cancer among carriers and
noncarriers of a BRCA1 or BRCA2 mutation. NEJM 2001;345:235-40.
4.
Milne RL, 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.
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Slide 12: Prophylactic Mastectomy
Previously, prophylactic mastectomy was shown to reduce the risk of
breast cancer in high risk women by more than 90%,1 and recent studies
have demonstrated that prophylactic mastectomy specifically reduces the
risk of breast cancer in women with mutations in BRCA1 or BRCA2 by 89.5%
to 100%.1-5
With several studies confirming a significantly reduced risk in
women with BRCA mutations, prophylactic mastectomy is now considered an
effective option that should be discussed with BRCA mutation positive
individuals. A total (simple) mastectomy is more effective than a
subcutaneous mastectomy. These types of prophylactic surgeries removes
most but not all breast tissue.
References:
1.
Hartmann LC, et al. Efficacy of bilateral prophylactic mastectomy
in women with a family history
of breast cancer. NEJM 1999, 340:77-84.
2.
Meijers-Heijboer H, et al. Breast cancer after prophylactic
bilateral mastectomy in women with a
BRCA1 or BRCA2 mutation. NEJM 2001;345:159-164.
3.
Hartmann LC, et al. Efficacy of bilateral prophylactic mastectomy
in BRCA1 and BRCA2 gene
mutation carriers. JNCI 2001;93:1633-1637.
4.
Rebbeck TR, et al. Bilateral prophylactic mastectomy reduces breast
cancer risk in BRCA1 and
BRCA2 mutation carriers: The PROSE Study Group. JCO 2004;22:10551062.
Van Sprundel TC, et al. Risk reduction of contralateral breast
cancer and survival after
contralateral
prophylactic mastectomy in BRCA1 or BRCA2 mutation
carriers. Br J Cancer. 2005
Aug 8;93(3):287-92.
Additional Reference:
Anderson, K. et
women with a BRCA1 or
BRCA2 mutation.
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Slide 15: Prophylactic Oophorectomy
It is currently estimated that prophylactic oophorectomy reduces
the risk of ovarian cancer by up to 96% in women with BRCA mutations.1
Prophylactic oophorectomy has also been shown to reduce the risk of
breast cancer by up to 68% in women with BRCA1 and BRCA2 mutations.2
A recent study found that for breast cancer risk reduction, a BSO that is
performed before age 40 versus a later age, appears to have had the most
significant outcome in terms of cancer risk reduction.8 Therefore,
breast cancer reduction after BSO is based personal health history; age,
cancer diagnosis versus no cancer diagnosis, parity, oral contraceptive
and hormone replacement use, etc. Significantly, the protective effect of
prophylactic oophorectomy with regard to breast cancer was also seen in
women taking hormone replacement therapy.3 The most important concern
regarding prophylactic oophorectomy is the possibility of subsequent
peritoneal carcinomatosis, which has been documented in 2% to 11% of high
risk women who have undergone this procedure.4,5 Most studies of this
phenomenon were conducted before direct genetic testing for BRCA1 and
BRCA2 was available, and consequently there are few data regarding the
specific risk of peritoneal carcinoma following prophylactic oophorectomy
for carriers of mutations in BRCA1 and BRCA2. This remains an area of
ongoing investigation.
Two studies published in the New England Journal of Medicine in
2002 demonstrated such significant risk reduction for both ovarian and
breast cancer that the authors concluded prophylactic oophorectomy should
be considered as soon as possible after childbearing is complete.1,2
More recently, the Society of Gynecologic Oncologists developed a
committee statement regarding prophylactic salpingo-oophorectomy.
Specifically relating to technical procedure, the society recommends that
as much of the ovaries and fallopian tubes be removed to maximize the
efficacy of the procedure. There are currently no recommendations for or
against removal of the uterus. If the surgical procedure does not
include a hysterectomy, the recommendation is for the fallopian tubes to
be excised as close as possible to the uterine coruna.7
References:
1.
Rebbeck TR, et al: Prophylactic oophorectomy in carriers of BRCA1
or BRCA2 mutations. NEJM 2002;346:1616-1622.
2.
Kauff ND, et al. Risk-reducing salpingo-oophorectomy in women with
a BRCA1 or BRCA2 mutation. NEJM
2002;346:1609-1615.
3.
Rebbeck TR, et al. Breast cancer risk after bilateral prophylactic
oophorectomy in BRCA1 mutation carriers. JNCI
1999;91:1475-9.
4.
Piver MS, et al. Primary peritoneal carcinoma after prophylactic
oophorectomy in women with a family history of
ovarian cancer. Cancer 1993;71:2751-2755.
5.
Tobacman JK, et al. Intra-abdominal carcinomatosis after
prophylactic oophorectomy in ovarian-cancer-prone
famillies. Lancet 1982;2:795-797.
6.
Narod SA, Offit K. Prevention and Management of Hereditary Breast
Cancer. J Clin Oncol. 2005 Mar 10;23(8):1656-63.
7.
Society of Gynecologic Oncologists Clinical Practice Committee
Statement on Prophylactic Salpingo-oophorectomy.
Gynecol Oncol. 2005 Aug;98(2):179-81.
8.
Eisen A, et al. Breast cancer risk following bilateral oophorectomy
in BRCA1 and BRCA2 mutation carriers: an
international case-control study. J Clin Oncol. 2005 Oct
20;23(30):7491-6.
9.
Finch A, et al. Salpingo-oophorectomy and the risk of ovarian,
fallopian tube, and peritoneal cancers in women
with a BRCA1 or BRCA2 Mutation. JAMA. 2006 Jul 12;296(2):185-92.
Additional Reference:
Anderson, K. et al. Cost-effectiveness of preventive strategies for
women with a BRCA1 or a BRCA2 mutation.
Ann Intern Med. 2006 Mar 21;144(6):397-406.
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Slide 15: Rationale for Frequent Colonoscopy
In individuals with HNPCC, the progression from colorectal adenoma to
cancer takes 1-3 years compared to 5-10 years in the general population.
Therefore, colonoscopy in individuals with HNPCC must be more frequent.1
Additionally, the majority of colon cancers and adenomas within HNPCC are
proximal or right-sided.2 As a result, it is necessary to perform a
complete colonoscopy rather than a sigmoidoscopy. The intent of this
procedure is to remove any adenomas throughout the entire colon, thus
reducing the risk for colon cancer.
Without colonoscopy and polypectomy, the lifetime risk for developing
colorectal cancer is 80% for HNPCC patients. However, at least one study
has shown that colonoscopic surveillance every 3 years has the potential
to reduce the risk of colorectal cancer in HNPCC by more than 50% as well
as decrease overall mortality by about 65% in HNPCC families.3
References:
1Ivanovich JL, Read TE, Ciske DJ. A practical approach to familial and
hereditary colorectal cancer. American Journal of Medicine 1999;107:6877.
2Lynch HT, Smyrk TC, Watson P, et al. Genetics, natural history, tumor
spectrum, and pathology of hereditary nonpolyposis colorectal cancer.
Gastroenterology 1993;104:1535-49.
3Jarvinen HJ, Aarnio M, Mustonen H, et al. Controlled 15-year trial on
screening for colorectal cancer in families with hereditary nonpolyposis
colorectal cancer. Gastroenterology 2000;118:829-34.
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Slide 4: Epidemiology of Colorectal Cancer
All cancer is genetic, because it results from mutations in genes that
normally control cell functions. Most of these mutations are acquired
during a person's lifetime, but in a minority of people mutations in
critical genes are inherited.
Colorectal cancer (CRC) is the second leading cause of cancer death in
the United States, with more than 145,000 cases diagnosed annually.1 In
general, CRC is classified into three categories, based on increasing
hereditary influence and cancer risk:
Sporadic CRC comprises about 60% of cases. Patients with sporadic CRC do
not have a notable family history of CRC nor do they have, by definition,
an identifiable inherited gene mutation that accelerates cancer
development.2
Familial CRC comprises up to 30% of cases and refers to patients who have
at least one blood relative with CRC or an adenoma. However, no specific
germline mutation or clear pattern of inheritance is identifiable.2
Familial CRC probably has multiple causes, such as shared exposure to
carcinogens or interactions between the environment and multiple or
moderately penetrant genes.3
Hereditary CRC syndromes account for up to 10% of CRC.3 The majority of
hereditary colorectal cancer syndromes are inherited in an autosomal
dominant pattern, resulting in the inheritance of single gene mutations
in highly penetrant cancer susceptibility genes.2 Hereditary nonpolyposis
colorectal cancer (HNPCC) is the most common hereditary CRC syndrome,
comprising about 3% to 5% of all CRCs.3,4 Familial adenomatous polyposis
(FAP) is responsible for approximately 1% of all CRC, while several rare
disorders, such as Peutz-Jeghers syndrome and juvenile polyposis, make up
approximately 4%.5 An evolving hereditary colorectal cancer syndrome
called MYH-associated polyposis (MAP) is inherited in an autosomal
recessive pattern and, by definition, requires the inheritance of two
mutations (one from each parent). MAP is responsible for approximately
1% of all CRC.6
References:
1American Cancer Society. Cancer Facts and Figures 2004. Available at
http://www.cancer.org/downloads/STT/CAFF_finalPWSecured.pdf. Accessed
December 16, 2004.
2Ivanovich JL, Read TE, Ciske DJ. A practical approach to familial and
hereditary colorectal cancer. American Journal of Medicine 1999;107:6877.
3Lynch H, Smyrk T. Hereditary nonpolyposis colorectal cancer: an updated
review. Cancer 1996;78:1149-67.
4Salovaara R, Loukola A, Kristo P, et al. Population-based molecular
detection of hereditary nonpolyposis colorectal cancer. Journal of
Clinical Oncology 2000;11:2193-200.
5 Burt R. Colon cancer screening. Gastroenterology 2000;119:837-53.
6Halford SE, Rowan AJ, Lipton L, et al. Germline mutations but not
somatic changes at the MYH locus contribute to the pathogenesis of
unselected colorectal cancers. American Journal of Pathology
2003;162:1545-8.
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Slide 6: Hereditary Nonpolyposis Colorectal
Cancer (HNPCC)
Approximately 3-5% of colorectal cancer results from mutations in the
mismatch repair genes, causing HNPCC.1,2 Germline mutations in MLH1 and
MSH2 account for the vast majority of detected mutations in families with
HNPCC.1,3 Germline mutations in MSH6 also have an important role in
HNPCC and may account for up to 15% of all mismatch repair gene
mutations.4 There are some families, however, whose family history is
highly suspicious for HNPCC who do not have an identifiable mutation.
Research studies continue to look for mutations within the known genes
that have thus far gone undetected as well as additional genes that may
cause HNPCC.
References:
1Salovaara R, Loukola A, Kristo P, et al. Population-based molecular
detection of hereditary nonpolyposis colorectal cancer. Journal of
Clinical Oncology 2000;11:2193-200.
2Lynch H, Smyrk T. Hereditary nonpolyposis colorectal cancer: an updated
review. Cancer 1996;78:1149-67.
3Peltomaki P. Role of DNA mismatch repair defects in the pathogenesis of
human cancer. Journal of Clinical Oncology 2003;21:1174-9.
4Plaschke J, Engel C, Kruger S, et al. Lower incidence of colorectal
cancer and later sge of disease onset in 27 families with pathogenic MSH6
germline mutations compared with families with MLH1 or MSH2 mutations:
The German Hereditary Nonpolyposis Colorectal Cancer Consortium. Journal
of Clinical Oncology 2004;22:4486-94.
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Slide 6: A p16 Mutation Increases Melanoma
The range of risks for melanoma and pancreatic cancer associated
with mutations in this gene has been characterized through numerous
studies. The lower estimates of risk are derived from analysis of
mutations in an unselected general population of individuals, whereas
higher estimates of mutation-associated cancer risk are derived from
families with a strong history of these cancers.
Generally, mutations in p16 are associated with a 28% to 76% risk
of melanoma by age 80.1,2 Studies have also shown that cancer rates
among mutation carriers vary greatly by geographic location.1 In the
United States, the incidence of melanoma in p16 mutation carriers by age
80 is greatly increased above the 1% risk in the general population.
Numerous studies have shown an increased risk for pancreatic cancer
in some families with p16 mutations. In one study, the risk was found to
be up to 17% by the age of 75.3 Another study has shown that the risk of
pancreatic cancer was increased by a factor of 13-22 in p16 mutation
positive families.4 In the United States, the incidence of pancreatic
cancer by age 75 in the general population is <1%.
References:
1.
Bishop DT, et al. Geographical variation in the penetrance of
CDKN2A mutations for melanoma.
J Natl Cancer Inst. 2002;94(12):894-903.
2.
Begg CB, et al. Lifetime risk of melanoma in CDKN2A mutation
carriers in a population-based
sample. J Natl Cancer Inst. 2005;97(20):1507-15.
3.
Vasen HF, et al. Risk of developing pancreatic cancer in families
with familial atypical multiple
mole melanoma associated with a specific 19 deletion of p16 (p16Leiden). Int J Cancer.
2000;87(6):809-11.
4.
Goldstein AM, et al. Increased risk of pancreatic cancer in
melanoma-prone kindreds with
p16INK4 mutations. N Engl J Med. 1995;333(15):9704. ¡ ü
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Slide 28: American Society of Clinical Oncology
Guidelines for Genetic Testing
For an individual whose personal or family history suggests the
possibility of a hereditary cancer syndrome, only a genetic test can
confirm whether he/she carries a mutation in one of the hereditary
colorectal cancer genes. The American Society of Clinical Oncology (ASCO)
has recommended that genetic testing be offered when 1) the individual
has personal or family history features suggestive of a genetic cancer
susceptibility condition, 2) the test can be adequately interpreted, and
3) the results will aid in diagnosis or influence the medical or surgical
management of the patient or family members at hereditary risk of
cancer.1 These criteria can be applied to identify appropriate candidates
for genetic testing for hereditary colorectal cancer.
References:
1American Society of Clinical Oncology policy statement update: genetic
testing for cancer susceptibility. Journal of Clinical Oncology
2003;21:2397-406. ¡ \
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Slide 2: Learning Objectives
The topic of hereditary breast and ovarian cancer risk has received
a great deal of attention in professional and community publications
alike. Many women are asking their healthcare professionals whether their
family history indicates an increased risk of breast or ovarian cancer,
whether medical management can effectively address these risks, and
whether they should be tested for alterations in the genes responsible
for most hereditary breast and ovarian cancer. This presentation is
designed to address these issues, providing the participants with an
understanding of the features of hereditary breast and ovarian cancer,
the cancer risks associated with BRCA1 and BRCA2 mutations, the clinical
management of hereditary breast and ovarian cancer syndrome, and the
relevant insurance issues. ¡ l
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Slide 17: Adenomatous Polyposis Syndromes
Among the hereditary colorectal cancer syndromes that are associated with
multiple adenomatous polyps are FAP, attenuated FAP and MYH-associated
polyposis (MAP). Classic familial adenomatous polyposis (FAP) increases
the risk for colorectal cancer to almost 100% without intervention and
exhibits severe colonic polyposis. Attenuated FAP (AFAP) also increases
the risk for colorectal cancer, but with less severe colonic polyposis.
MYH-associated polyposis (MAP) has been seen in individuals with varying
degrees of colonic polyposis and the colorectal cancer risk is thought to
be significantly elevated.
Up to 1% of colorectal cancer results from mutations in the APC gene,
causing FAP and AFAP.1,7 Germline mutations in APC account for up to 95%
of clinically diagnosed FAP,2 but only about 10% of clinically diagnosed
AFAP.3 An additional 1% of colorectal cancer (3% of early onset CRC) is
due to mutations in the MYH gene, causing MAP.4,5 MYH is responsible for
approximately 1.4% of all adenomatous polyposis and approximately 20% of
adenomatous polyposis without an identifiable APC mutation.8 There are
some individuals, however, who have multiple polyps but do not have an
identifiable mutation in either the MYH or the APC gene.
References:
1Burt R. Colon cancer screening. Gastroenterology 2000;119:837-53.
2Solomon C, Burt RW. APC-Associated Polyposis Conditions. Available at:
http://geneclinics.org/profiles/fap/details.html. Accessed June 1, 2007.
3Lamlum H, Al Tassan N, Jaeger E, et al. Germline APC variants in
patients with multiple colorectal adenomas, with evidence for the
particular importance of E1317Q. Human Molecular Genetics 2000;9:221521.
4Halford SE, Rowan AJ, Lipton L, et al. Germline mutations but not
somatic changes at the MYH locus contribute to the pathogenesis of
unselected colorectal cancers. American Journal of Pathology
2003;162:1545-8.
5Fleischmann C, Peto J, Cheadle J, et al. Comprehensive analysis of the
contribution of germline MYH variation to early-onset colorectal cancer.
International Journal of Cancer 2004;109:554-8.
6Nielsen M, Hes FJ, Nagengast FM, et al. Germline mutations in APC and
MYH are responsible for the majority of families with attenuated familial
adenomatous polyposis. Clin Genet 2007;71(5):427-33.
7Galiatsatos P, Foulkes WD. Familial Adenomatous Polyposis. Am J
Gastroenterol 2006;101(2):385-98.
8Lefevre JH, Rodrigue CM, Mourra N, et al. Implications of MYH in
colorectal polyposis. Ann Surg 006;244(6):879-9. ¡ ¬
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Chart 6
Identifying and Managing Hereditary Cancer
Syndromes k
Learning Objectives At the conclusion of this presentation
participants should understand the following: .
Impact of Hereditary
Cancer in Your Practice
Slide 4 %
Hereditary Breast and Ovarian
Cancer 5
“Red Flags” for Hereditary Breast and Ovarian Cancer ;
A
BRCA Mutation Increases Breast and Ovarian Cancer Risks 8
A BRCA
Mutation Increases Risk of Second Breast Cancer 4
Ovarian Cancer AFTER
Breast Cancer in BRCA carriers "
Risks in Men With a BRCA Mutation E
Medical Management Options for Hereditary Breast and Ovarian Cancer
Surveillance for Breast Cancer Chemoprevention of Breast Cancer
Tamoxifen 7
Chemoprevention of Ovarian Cancer Oral
Contraceptives X
Prophylactic Mastectomy Greater than 90% breast
cancer risk reduction in BRCA carriers y
Prophylactic Oophorectomy
Recommend bilateral salpingo-oophorectomy (BSO)
at age 35 or after
childbearing is complete ;
Managing Hereditary vs Sporadic Breast and
Ovarian Cancer
Interpreting Test Results
Interpreting Test
Results
Positive vs. Negative Result "
Epidemiology of Colorectal
Cancer .
Hereditary Colorectal Cancer (CRC) Syndromes 2
Hereditary
Nonpolyposis Colorectal Cancer (HNPCC) &
“Red Flags” for HNPCC/Lynch
Syndrome &
HNPCC Increases Lifetime Cancer Risk '
HNPCC Increases
Risk of Second Cancer *
Hereditary vs Sporadic Colorectal
Cancer #
Rationale for Frequent Colonoscopy
HNPCC Surgical
Guidelines >
Hereditary Colorectal Cancer Adenomatous Polyposis
Syndromes 9
Various Presentations of Adenomatous Polyposis
Syndromes
Hereditary Melanoma %
“Red Flags” for Hereditary
Melanoma (
A p16 Mutation Increases Melanoma Risk F
American Society
of Clinical Oncology Guidelines for Genetic Testing "
Societal
Standards and Guidelines
Genetic Testing '
Insurance Coverage of
Genetic Testing ,
Genetic Discrimination Myth versus Reality
In Summary:
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