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Kenneth Offit, MD, MPH is the Director of the Clinical Genetics Service of the Memorial Sloan Kettering Cancer Center

 

 

     

 RESEARCH OF KENNETH OFFIT, MD and his colleagues supported in part with Lymphoma Foundation research grants
 

Research by Kenneth Offit, MD MPH Chief, Clinical Genetics Service, Memorial Sloan Kettering Cancer Center and his colleagues… submitted to the Lymphoma Foundation...

A major publication in Nature Medicine in 2011… by Drs. Best, Onel... Offit, et al, …described a genomic change on chromosome 6 … that was highly correlated with therapy induced secondary malignances after Hodgkins lymphoma treatment. … This study assembled DNA samples of individuals who developed breast cancer following radiation therapy as part of treatment for Hodgkins Disease. In the study it was possible to identify a gene variant predictive of second cancer occurrence and that was strongly associated with the biology of radiation sensitivity (PRDM1). The issue of breast cancer developing  after Hodgkins treatment has been a topic of special interest particularly… to the Lymphoma Foundation… as… they were among the early forces to draw attention to the increased risk of Hodgkins survivors developing breast cancer and urged efforts to develop preventive action as well as early diagnosis of the breast cancer.

Utilizing statistical as well as functional genetic experiments… it was possible to demonstrate that individuals carrying a variant on Chromosome 6q21 were at an up to 3 fold increased risk for the development of secondary malignancies following treatment for Hodgkins  Disease. This study marked one of the first uses of genome wide association study methodology as a discovery tool for genetic markers linked to secondary cancers. While it is premature to suggest clinical testing for this marker, it is possible in the future that patients may be screened for this as well as other genomic markers.

 

Another publication of genetic research by Dr. Offit, et al, … in the Journal of Cancer Epidemiology Biomarkers and Prevention… acknowledged the partial grant support of the Lymphoma Foundation. This research included two large consortium studies analyzing genomic risk factors for breast and ovarian cancer. The first of these studies involved a group of international consortia worldwide and over 10,000 BRCA2 and 15,000  BRCA1  mutation carriers. This study further evaluated a novel locus at ZNF365 that Dr. Offit’s laboratory had associated with modifying the risk of breast cancer in the setting of the BRCA2 mutation.  Another  paper published in Human Mutation focused on the risk of ovarian cancer susceptibility in individuals carrying BRCA1 and BRCA2 mutations.

 

An additional publication in 2011 was a detailed encyclopedic review of the current status of genetics genomics and cancer risk assessments. This paper reviewed all of the commonly known mechanisms for cancer susceptibility... and was published in the Journal CA… and was distributed by the American Cancer Society to a large audience of cancer care providers worldwide.

2010
On
August 25, 2010 Dr. Offit wrote to the Lymphoma Foundation…During 2010, we cite three significant papers, which bear support of The Lymphoma Foundation…

The first of these is a major publication appearing in the high impact journal, PLoS Genetics.

This paper was recently accepted for publication. It is the result of three years of work, bringing together DNA samples from thousands of women around the world who provided these samples to our international consortia. The goal of the project was to identify genetic factors associating with resistance to breast cancer among the elderly. This project had initial early support from The Lymphoma Foundation. The aim of the project was to look at the genetic profiles of older individuals who did not experience a diagnosis of breast cancer over the course of their lifetime, despite having a very high risk genetic profile. These women were compared to younger women who did develop breast cancer at a very early age, and who also carried the same predisposing genetic mutations of BRCA genes. The result of a whole genome analysis conducted in collaboration with colleagues at Harvard and MIT, at The Broad Institute, revealed one particular marker, which was associated with a breast cancer risk or, inversely, with a resistance to breast cancer, in this population. This marker was comprised of single-nucleotide polymorphisms around the gene ZNF365. ZNF365 is a zinc finger gene, a member of the class of tyrosine kinase signaling pathways that have been found to be over expressed in breast cancers, as well as a number of other cancers, including solid tumors and lymphomas. Interestingly, genetic variants in this same gene were independently found to be associated with sporadic breast cancer risk in a study published at about the same time by colleagues at the University of Cambridge, and very recently (March 2012) this same gene has been implicated in breast density on mammography. While these findings are of interest, the relative protective effect of these variants was quite small, as in other genome-wide variants discovered to date. This paper marks just the first stages of the analysis, with a more detailed analysis of the genomic scan data now in progress. This additional work is being carried out at Genome Quebec. As indicated by the size of the author list on the PLoS Genetics publication, this was an enormous international collaboration headed by the Memorial Sloan Kettering  Cancer Center (MSKCC) group. We are indebted to The Lymphoma Foundation for providing the seed funds that allowed over $2M of grant funding to be secured, resulting ultimately in this high impact publication. 

The second paper to be cited underscores some of the comments above regarding findings of genome­wide association studies in cancer. That paper, published in the Journal of Clinical Oncology, provides the first analytic overview of this body of genomic research. In this paper, written by a junior faculty member of the Clinical Genetics Service, the range of risks associated with genetic variants for cancer types is presented in an analytic framework. This paper serves as a useful resource for clinicians seeking to understand the emerging literature of inherited cancer genomics. Among the points raised in the paper is the observation that one of the highest risk genomic variants associated with cancer was reported for myeloproliferative disorders (including polycythemia vera and essential thrombocytosis).

The third paper bearing support of The Lymphoma Foundation, recently published, relates to prostate cancer. In this paper, published in the journal of the American Association of Cancer Research, Clinical Cancer Research, our group defined for the first time the adverse outcome of prostate cancer occurring in the setting of an inherited mutation of the BRCA genes. This observation was conducted in Ashkenazi Jewish individuals, but should be valid across all ethnic and population subgroups. The finding that men with prostate cancer carrying BRCA mutations have a higher Gleason grade and also a much more aggressive course of disease has important clinical implications. This is because there is now a targeted therapy, consisting of PARP inhibitors, that has been shown to have activity in women with breast and ovarian cancer and BRCA mutations. We postulate in this article that a subset of men in the general population with poor prognosis prostate cancer could also benefit from this targeted therapy that has heretofore been utilized only in women with BRCA mutations. We calculate that approximately 3,000 cases of prostate cancer each year in The United States would benefit from this potential new therapeutic approach…”

September 9, 2009

TO: Mortimer Lacher, MD, FACP

President, The Lymphoma Foundation

 

This letter constitutes our annual update of research activities supported by The Lymphoma

Foundation. We will begin with the review of articles and then data that is not yet published or that

is still in progress.

 

Review of Articles

As indicated to you last year, we are increasing our emphasis on lymphoma genetics. Although

our major paper is still in the works for this year, we did have an interesting collaborative

publication in the past year. This paper, entitled, "Mutations in a gene encoding a midbody kelch

protein in familial and sporadic classical Hodgkin lymphoma lead to binucleated cells," was

published in the prestigious Proceedings of the National Academy of Sciences. It was a

collaboration with our colleague Marshall Horwitz in the Division of Medical Genetics at the

University of Washington School of Medicine in Seattle. Marshall identified a translocation in a

family with Hodgkin’s disease. We were very interested in candidate genes at this translocation

junction and explored SNPs in this and other regions in our familial lymphomas. This translocation

involved chromosomes 2 and 3. It was found to disrupt a gene KLHDC8B, which had previously

been uncharacterized. Interestingly, loss if heterozygosity was noted in the Reed-Steinberg cells

of one of the cases of Hodgkin’s disease, but not in the reactive T lymphocytes. This is a very

interesting finding and is somewhat reminiscent of the observation whereby the gene BRCA2 was

identified by loss of heterozygosity in a pancreatic cancer. As you will recall, BRCA2 was later

shown to be a major predisposing gene for breast cancer. While we played really a supportive role

in this paper by Dr. Horwitz, our contribution at the early stages was critical and we will be

continuing our collaborations with his group. He has also offered to provide DNA from his familial

cases for our family studies to be described shortly. As noted, support of The Lymphoma

Foundation was cited in this paper.

 

A second paper that identified support of The Lymphoma Foundation was published recently in
the journal Cancer Epidemiology Biomarkers and Prevention.
This paper is entitled, "The 6q22.33

Locus and Breast Cancer Susceptibility." In this paper, we expanded on our discovery of the

chromosome 6 locus for cancer susceptibility reported last year in the Proceedings of the National

Academy of Sciences and described in last year’s report to the Foundation. In the current study,

we have confirmed the significance of this locus, not only in Jewish families with breast cancer, but

also in non-Jewish families. Again, the major significance of these findings relates to their

stimulating further biologic inquiry into the mechanisms of the particular genes disrupted.

Potentially, these genes could serve as targets for cancer prevention.

 

A third paper that I am including here is a technical paper entitled, "A Rapid and Reliable Test for

BRCA1 and BRCA2 Founder Mutation Analysis in Paraffin Tissue Using Pyrosequencing."

This paper recognizes the support of the Dannheiser Foundation [contributed via the Lymphoma Foundation] and the Edward Spiegel Memorial Fund [of the Lymphoma Foundation].

 

This is a technical genetics paper that describes a new method of finding genetic mutations in material embedded in paraffin tissue. As you know, most biopsy specimens from patients taken by pathology departments, is embedded in beeswax (paraffin). In this paper, we have shown that we are able to recover DNA from this material and use it for diagnostic testing. While this paper addresses the use of this technique for determining mutations in the BRCA genes, the method could, in theory, be used for detection of other genetic abnormalities, as well.

 

Research Findings Not Yet Published

As an update to last year’s report, at that time we were very excited about an extremely high association with a particular gene in the TGF signaling pathway. When we repeated the genotyping on an expanded dataset, the findings were considerably weaker, but still significant. This was somewhat disappointing, but such are the realities of scientific research.

 

On a more promising front, this past summer we have completed our whole genome association

study of non-Hodgkin’s lymphoma. This study now involves over two hundred and fifty families,

including approximately one-third from our colleague at the Dana-Farber Cancer Institute.

These families all have two individuals with a lymphoid cancer in them, either non-Hodgkin’s

lymphoma, Hodgkin’s disease, CLL or a plasma cell neoplasm. The genotyping has been

completed here in New York and at the Coriell Institute and we are in the process of analyzing that

data at the present time. The preliminary findings in these families will be confirmed in a series of

fifteen-hundred lymphoma cases and fifteen-hundred normal controls. The pathology specimens

for these have been independently reviewed by the Research Assistant working with Dr. Andrew

Zelenetz, Chief of the Lymphoma Service, at Memorial SIoan-Kettering Cancer Center.

Dr. ZeIenetz will be a collaborator in this study. Once this data is analyzed, it will be submitted this

fall to a high impact journal and will constitute one of the first whole genome association studies of

non-Hodgkin’s lymphoma. We are very excited about this project, which has been the recipient of

considerable funding support from The Lymphoma Foundation, as well as other sources. An effort

will also be made over the course of the fall to submit several grants in addition, to generate the

approximately $150,000 cost of the second phase replication study of the fifteen-hundred cases

and controls mentioned above:

 

Conclusion

The above constitutes a review of activities, papers and projects underway with the support of

The Lymphoma Foundation. We continue to be grateful for this ongoing support, which is vital to

move research forward in the area of the genetics of lymphoma, as well as the genetics of other

malignancies. A key aspect of our work is that any individual cancer, whether lymphoma or breast

cancer, offers the genetic clues that will allow the targeted prevention and treatment of all cancers.

 

Submitted by
Kenneth Offit, MD, MPH

Chief, Clinical Genetics Service

Vice Chairman, Academic Affairs, Department of Medicine,

Vice Chairman, Program in Cancer Prevention and Population Research,

Memorial SIoan-Kettering Cancer Center;

Member, Cancer Biology and Genetics Program (joint),

SIoan-Kettering Institute;

Professor of Medicine and Public Health,

Weill College of Medicine, Cornell University


THE FOLLOWING PUBLICATIONS BY DR. KENNETH OFFIT and his research colleagues (2002-2006) ARE A RECORD OF ADDITIONAL INNOVATIVE CLINICAL AND LABORATORY GENETIC RESEARCH SUPPORTED IN PART BY LYMPHOMA FOUNDATION GRANTS

CANCER AND LYMPHOMA GENETICS
2006
Localization of Breast Cancer Susceptibility Loci by Genome-Wide SNP Linkage Disequilibrium Mapping
Ellis NA, KirchhoffT, MitraN, Ye T, Chuai S, Huang H, Nafa K, Norton L, Neuhausen S, Gordon D, Streuwing JP, Naiod S   Offit K.. Genetic Epidemiology 2006,30(1):48-61

MDM2 SNP309 accelerates tumor formation in a gender-specific and hormone-dependent manner Bond GL, Hirshfield KM, KirchhoffT, Alexe G, Bond EE, Robins H, Basrtel F, Taubert H, Wuerl P, Hait W, Toppmeyer D, Offit K, Levine AJ.. Cancer Research 2006,66(10):5104-10

Accuracy of BRCAI and BRCA2 founder mutation analysis in formalin-fixed and paraffin-embedded (FFPE) tissue Adank MA, Brogi E, Bogomolniy F, Wadsworth EA, Lafaro KJ, Yee CJ, KirchhoffT, Meijers-Heijboer EJ, KauffNK, Boyd J, Offit K.. Familial Cancer 2006 (in press)

Cancer Genetic Testing and Assisted Reproduction. Offit K, Kohut K, Clagett B, Wadsworth E, Cummings S, White M, Sagi M, Bernstein D, Davis JG. Journal of Clinical Oncology 2006.  Electronically published online by the Journal of Clinical Oncology in July, 2006 and was formally published in October 2006

2004-2005
The Genetics of Familial Lymphomas
, R. Siddiqui, K. Onel, F. Facio, K. Offit, Current Oncology Reports 2004, 6:380-387

 The TP53 Mutational spectrum and frequency of CHEK2* 1100delC in Li Fraumeni-like kindreds Siddiqui, R, Onel K, Facio F, Nafa D, Robles-Diaz R, Kauff N, Huang H, Robson M, Ellis N, Offit K  Familial Cancer 2005; 4(2):177-81

Combined genetic assessment of transforming growth factor-beta signaling pathway variants may predict breast cancer risk. Kaklamani VG, Baddi L, Liu J, Rosman D, Phukan S, Bradley C, Hegarty C, McDaniel B, Rademaker A, Oddoux C, Ostrer H, Michel LS, Huang H, Chen Y, Ahsan H, Offit K, Pasche B. Cancer Research 2005; 65(8):3454-61.

Estrogen receptor genotypes and haplotypes associated with breast cancer risk. Gold B, Kalush F, Bergeron J, Scott K, Mitra N, Wilson K, Ellis N, Huang H, Chen M, Lippert R, Halldorsson BV, Woodworth B, White T, Clark AG, Parl FF, Broder S, Dean M, Offit K.   Cancer Research 2004; 64:8891-900.

Localization of cancer susceptibility genes by genome-wide single-nucleotide polymorphism linkage-disequilibrium mapping. Mitra N, Ye TZ, Smith A, Chuai S, Kirchhoff T, Peterlongo P, Nafa K, Phillips MS, Offit K, Ellis NA.  Cancer Research 2004; 64: 8116-25.
 

Hereditary ovarian cancer in Ashkenazi Jews. Robles-Diaz L, Goldfrank D, Kauff N, Robson M, Offit K  Familial  Cancer 2004; 3:259-64

 A636P testing in Ashkenazi Jews. Guillem JG, Moore HG, Palmer, C, Glogowski E, Finch R, Nafa K, Markowitz AJ,
Offit K, Ellis NA.  Familial Cancer 2004; 3:223-227

 Pleomorphic expression of a germline kit mutation in a large kindred with gastrointestinal stromal tumors, hyperpigmentation, and dysphagia. Robson ME, Glogowski E, Sommer G, Antonescu CR, Khedoudja N, Maki RG, Ellis N, Besmer P, Brennan M, Offit K.   Clinical Cancer Research 2004;10:1250-4.

Functional and genomic approaches reveal an ancient CHEK2 allele associated with breast cancer in the Ashkenazi Jewish population. Shaag A, Walsh T, Renbaum P, Kirchhoff T, Nafa K, Shiovitz S, Mandell JB, Welcsh P, Lee MK, Ellis N, Offit K, Levy-Lahad E, King MC.   Human Molecular Genetics 2005; 14:555-63
 

2002-2003
TGFBR1*6A and Cancer Risk:  A Meta-Analysis of Seven Case-Control Studies, 
V.G. Kaklamani, N. Hou, Y. Bian, J. Reich, K. Offit, L.S. Michel, W.S. Rubinstein, A. Rademaker, B. Pasche,  Journal of Clinical Oncology, Vol 21, No 17 (September 1), 2003: pp3236-3243

Rare Variants of ATM and Risk for Hodgkin’s Disease and Radiation-associated Breast Cancers, 
K. Offit,, S. Gilad, S. Paglin, P. Kolachana, L.C. Roisman, K. Nafa, V. Yeugelewitz, M. Gonzales, M. Robson, D. McDermott, H.H. Pierce, N.D. Kauff, P. Einat, S. Jhanwar, J.M. Satagopan, C. Oddoux, N. Ellis, R. Skaliter, J. Yahalom,  Clinical Cancer Research, Vol. 8, 3813-3819, December 2002.

Analysis of Mismatch Repair Defects in the Familial Occurrence of Lymphoma and Colorectal Cancer, Teruya-Feldstein, J., Greene, J., Cohen, L., Popplewell, L., Ellis, N.A., Offit, K., Leukemia and Lymphoma, 2002 Vol. 43 (8), pp. 1619-1626.


Similar Patterns of Genomic Alterations Characterize Primary Mediastinal Large-B-Cell Lymphoma and Diffuse Large-B-Cell Lymphoma
,
Palanisamy, N., Abou-Elella, A., Chaganti, S.R., Houldsworth, J. Offit, K., Louie, D.C., Terayu-Feldstein, J., Cigudosa, J.C., Rao, P.H., Sanger, W.G., Weisenburger, D.D., Chaganti, R.S.K., Genes, Chromosomes & Cancer, 33:114-122 (2002).


Differential recruitment of caspase 8 to cFlip confers sensitivity or resistance to Fas-mediated apoptosis in a subset of familial lymphoma patients
,
 C. Bäumler, F. Duan, K. Onel, B. Rapaport, S. Jhanwas, K. Offit, K.B. Elkon,  Leukemia Research 27 (2003) 841-851

 

 
BREAST AND OVARIAN CANCER GENETICS

2002-2005

Combined genetic assessment of transforming growth factor-beta signaling pathway variants may predict breast cancer risk. Kaklamani VG, Baddi L, Liu J, Rosman D, Phukan S, Bradley C, Hegarty C, McDaniel B, Rademaker A, Oddoux C, Ostrer H, Michel LS, Huang H, Chen Y, Ahsan H, Offit K, Pasche B. Cancer Research 2005; 65(8):3454-61.

Estrogen receptor genotypes and haplotypes associated with breast cancer risk. Gold B, Kalush F, Bergeron J, Scott K, Mitra N, Wilson K, Ellis N, Huang H, Chen M, Lippert R, Halldorsson BV, Woodworth B, White T, Clark AG, Parl FF, Broder S, Dean M, Offit K.   Cancer Research 2004; 64:8891-900.

Hereditary ovarian cancer in Ashkenazi Jews. Robles-Diaz L, Goldfrank D, Kauff N, Robson M, Offit K  Familial  Cancer 2004; 3:259-64

 Functional and genomic approaches reveal an ancient CHEK2 allele associated with breast cancer in the Ashkenazi Jewish population. Shaag A, Walsh T, Renbaum P, Kirchhoff T, Nafa K, Shiovitz S, Mandell JB, Welcsh P, Lee MK, Ellis N, Offit K, Levy-Lahad E, King MC.   Human Molecular Genetics 2005; 14:555-63


Shared Genetic Susceptibility to Breast Cancer, Brain Tumors, and Fanconi Anemia, K. Offit, O. Levran, B. Mullaney, K. Mah, K. Nafa, S.D. Batish, R. Diotti, H. Schneider, A. Deffenbaugh, T. Scholl, V.K. Proud, M. Robson, L. Norton, N. Ellis, H. Hanenberg, A.D. Auerbach, Journal of the National Cancer Institute, Vol. 95, No. 20, October 15, 2003

Localization of Breast Cancer Susceptibility Loci by Genome-Wide SNP Linkage Disequilibrium Mapping, N.A. Ellis, T. Kirchhoff, N. Mitra, T.-Z. Ye, S. Chuai, H. Huang, K. Nafa, L. Norton, S. Neuhausen, J.P. Struewing, S. Narod, K. Offit, (in preparation).

Outcome of Preventive Surgery and Screening for Breast and Ovarian Cancer in BRCA Mutation Carriers,
Scheuer, L., Kauff, N., Robson, M., Kelly, B., Barakat, R., Satagopan, J., Ellis, N., Hensley, M., Boyd, J., Borgen, P., Norton, L., Offit, K.,
J Clin Oncol
, Vol 20, No 5 (March 1), 2002: pp 1260-1268.

Risk-Reducing Salpingo-Oophorectomy in Women with a BRCA1 or BRCA2 Mutation,  Kauff, N.D., Satagopan, J.M., Robson, M.E., Scheuer, L., Hensley, M., Hudis, C.A., Ellis, N.A., Boyd, J., Borgen, P.I., Barakat, R.R., Norton, L., Offit, K., N Engl J Med, Vol. 346 , No. 21 May 23, 2002: pp 1609-1615.
 

Frequency of CHEK2*1100delC in New York breast cancer cases and controls, K. Offit, H. Pierce, T. Kirchhoff, P. Kolachana, B. Rapaport, P. Gregersen, S. Johnson, O. Yossepowitch, H. Huang, J. Satagopan, M. Robson, L. Scheuer,  BMC Medical Genetics, 2003, 4, http://www.biomedcentral.com/1471-2350/4/1.

 

BRCA1 AND BRCA2 Germline Mutations in Lymphoma Patients, O. Yossepowitch, N. Olvera, J. M. Satagopan, H. Huang, S. Jhanwar, B. Rapaport, J. J. Boyd, K. Offit, Leukemia and Lymphoma, 2003 Vol. 44 (1), pp. 127-131

COLON CANCER and OTHER GASTROINTESTINAL GENETICS

2004
Pleomorphic Characteristics of a Germ-Line KIT Mutatioin in a Large Kindred with Gastrointestinal Stromal Tumors, Hyperpigmentation, and Dysphagia M.E. Robson, E. Glogowski, G. Sommer, C.R. Antonescu, K. Nafa, R.G. Maki, N. Ellis, P. Besmer, M. Brennan, K. Offit, Clinical Cancer Research, Vol. 10, 1250-1254, February 15, 2004

2002-2003
BLM  Heterozygosity and the Risk of Colorectal Cancer,  Gruber, S.B., Ellis, N.A., Rennert, G., Offit, K., et al.  Science, Vol 297, 20 September 2002

The Founder Mutation MSH2*1906G®C Is an Important Cause of Herditary Nonpolyposis Colorectal Cancer in the Ashkenazi Jewish Population,  W.D. Foulkes, I. Thiffault, S.B. Gruber, M. Horwitz, N. Hamel, C. Lee, J. Shia, A. Markowitz, A. Figer, E. Friedman, D. Farber, C.M.T. Greenwood, J.D. Bonner, K. Nafa, T. Walsh, V. Marcus, L. Tomsho, J. Gebert, F.A. Macrae, C.L. Gaff, B. Bressac-de Paillerets, P.K. Gregersen, J.N. Weitzel, P.H. Gordon, E. MacNamara, M.-C. King, H. Hampel, A. de la Chapelle, J Boyd, K. Offit, G. Rennert, G. Chong, and N.A. Ellis.  Am. J. Hum. Genet. 71:1395-1412, 2002.


A636P Is Associated with Early-Onset Colon Cancer in Ashkenazi Jews,
  J.G. Guillem, B.S. Rapaport, T. Kirchhoff, P. Kolachana, K. Nafa, E. Glogowski, R. Finch, H. Huang, W.D. Foulkes, A. Markowitz, N.A. Ellis, K. Offit,   J Am Coll Surg., Vol. 196, No. 2, 222-225, February 2003.


PEDIATRIC CANCER GENETICS
 

2004-2005

The TP53 Mutational spectrum and frequency of CHEK2* 1100delC in Li Fraumeni-like kindreds Siddiqui, R, Onel K, Facio F, Nafa D, Robles-Diaz R, Kauff N, Huang H, Robson M, Ellis N, Offit K  Familial Cancer 2005; 4(2):177-81

The FANCD1/BRCA2*6174DELT Mutation is Rare in Sporadic Pediatric Medulloblastoma, K. Onel, T. Kirchhoff, J.C. Allen, E. Jiminez, K. Offit, (in preparation)

 

 

**Dr. Kenneth Offit  is the Director of the Clinical Genetics Service at the Memorial Sloan Kettering Cancer Center and author of Clinical Cancer Genetics 
 

 

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