Noah Kauff

Positions:

Instructor, Temporary in the Obstetrics and Gynecology

Obstetrics and Gynecology, Gynecologic Oncology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

M.D. 1993

University of Pennsylvania

Grants:

Kastan Gray Foundation Project

Administered By
Duke Cancer Institute
Role
Researcher
Start Date
End Date

Publications:

Adenoma Prevalence in Blacks and Whites Having Equal Adherence To Screening Colonoscopy: The National Colonoscopy Study.

Authors
Mendelsohn, RB; Winawer, SJ; Jammula, A; Mills, G; Jordan, P; O'Brien, MJ; Close, GM; Dorfman, M; Church, TR; Mandelson, MT; Allen, J; Feld, A; Kauff, ND; Morgan, GA; Kumar, JMR; Serrano, V; Bayuga-Miller, S; Fischer, SE; Kuk, D; Zauber, AG
MLA Citation
Mendelsohn, Robin B., et al. “Adenoma Prevalence in Blacks and Whites Having Equal Adherence To Screening Colonoscopy: The National Colonoscopy Study..” Clin Gastroenterol Hepatol, vol. 15, no. 9, Sept. 2017, pp. 1469–70. Pubmed, doi:10.1016/j.cgh.2017.04.014.
URI
https://scholars.duke.edu/individual/pub1258511
PMID
28419856
Source
pubmed
Published In
Clinical Gastroenterology and Hepatology : the Official Clinical Practice Journal of the American Gastroenterological Association
Volume
15
Published Date
Start Page
1469
End Page
1470
DOI
10.1016/j.cgh.2017.04.014

Assessing associations between the AURKA-HMMR-TPX2-TUBG1 functional module and breast cancer risk in BRCA1/2 mutation carriers.

While interplay between BRCA1 and AURKA-RHAMM-TPX2-TUBG1 regulates mammary epithelial polarization, common genetic variation in HMMR (gene product RHAMM) may be associated with risk of breast cancer in BRCA1 mutation carriers. Following on these observations, we further assessed the link between the AURKA-HMMR-TPX2-TUBG1 functional module and risk of breast cancer in BRCA1 or BRCA2 mutation carriers. Forty-one single nucleotide polymorphisms (SNPs) were genotyped in 15,252 BRCA1 and 8,211 BRCA2 mutation carriers and subsequently analyzed using a retrospective likelihood approach. The association of HMMR rs299290 with breast cancer risk in BRCA1 mutation carriers was confirmed: per-allele hazard ratio (HR) = 1.10, 95% confidence interval (CI) 1.04-1.15, p = 1.9 x 10(-4) (false discovery rate (FDR)-adjusted p = 0.043). Variation in CSTF1, located next to AURKA, was also found to be associated with breast cancer risk in BRCA2 mutation carriers: rs2426618 per-allele HR = 1.10, 95% CI 1.03-1.16, p = 0.005 (FDR-adjusted p = 0.045). Assessment of pairwise interactions provided suggestions (FDR-adjusted pinteraction values > 0.05) for deviations from the multiplicative model for rs299290 and CSTF1 rs6064391, and rs299290 and TUBG1 rs11649877 in both BRCA1 and BRCA2 mutation carriers. Following these suggestions, the expression of HMMR and AURKA or TUBG1 in sporadic breast tumors was found to potentially interact, influencing patients' survival. Together, the results of this study support the hypothesis of a causative link between altered function of AURKA-HMMR-TPX2-TUBG1 and breast carcinogenesis in BRCA1/2 mutation carriers.
Authors
Blanco, I; Kuchenbaecker, K; Cuadras, D; Wang, X; Barrowdale, D; de Garibay, GR; Librado, P; Sánchez-Gracia, A; Rozas, J; Bonifaci, N; McGuffog, L; Pankratz, VS; Islam, A; Mateo, F; Berenguer, A; Petit, A; Català, I; Brunet, J; Feliubadaló, L; Tornero, E; Benítez, J; Osorio, A; Ramón y Cajal, T; Nevanlinna, H; Aittomäki, K; Arun, BK; Toland, AE; Karlan, BY; Walsh, C; Lester, J; Greene, MH; Mai, PL; Nussbaum, RL; Andrulis, IL; Domchek, SM; Nathanson, KL; Rebbeck, TR; Barkardottir, RB; Jakubowska, A; Lubinski, J; Durda, K; Jaworska-Bieniek, K; Claes, K; Van Maerken, T; Díez, O; Hansen, TV; Jønson, L; Gerdes, A-M; Ejlertsen, B; de la Hoya, M; Caldés, T; Dunning, AM; Oliver, C; Fineberg, E; Cook, M; Peock, S; McCann, E; Murray, A; Jacobs, C; Pichert, G; Lalloo, F; Chu, C; Dorkins, H; Paterson, J; Ong, K-R; Teixeira, MR; Teixeira,; Hogervorst, FBL; van der Hout, AH; Seynaeve, C; van der Luijt, RB; Ligtenberg, MJL; Devilee, P; Wijnen, JT; Rookus, MA; Meijers-Heijboer, HEJ; Blok, MJ; van den Ouweland, AMW; Aalfs, CM; Rodriguez, GC; Phillips, K-AA; Piedmonte, M; Nerenstone, SR; Bae-Jump, VL; O'Malley, DM; Ratner, ES; Schmutzler, RK; Wappenschmidt, B; Rhiem, K; Engel, C; Meindl, A; Ditsch, N; Arnold, N; Plendl, HJ; Niederacher, D; Sutter, C; Wang-Gohrke, S; Steinemann, D; Preisler-Adams, S; Kast, K; Varon-Mateeva, R; Gehrig, A; Bojesen, A; Pedersen, IS; Sunde, L; Jensen, UB; Thomassen, M; Kruse, TA; Foretova, L; Peterlongo, P; Bernard, L; Peissel, B; Scuvera, G; Manoukian, S; Radice, P; Ottini, L; Montagna, M; Agata, S; Maugard, C; Simard, J; Soucy, P; Berger, A; Fink-Retter, A; Singer, CF; Rappaport, C; Geschwantler-Kaulich, D; Tea, M-K; Pfeiler, G; BCFR,; John, EM; Miron, A; Neuhausen, SL; Terry, MB; Chung, WK; Daly, MB; Goldgar, DE; Janavicius, R; Dorfling, CM; van Rensburg, EJ; Fostira, F; Konstantopoulou, I; Garber, J; Godwin, AK; Olah, E; Narod, SA; Rennert, G; Paluch, SS; Laitman, Y; Friedman, E; SWE-BRCA,; Liljegren, A; Rantala, J; Stenmark-Askmalm, M; Loman, N; Imyanitov, EN; Hamann, U; kConFab Investigators,; Spurdle, AB; Healey, S; Weitzel, JN; Herzog, J; Margileth, D; Gorrini, C; Esteller, M; Gómez, A; Sayols, S; Vidal, E; Heyn, H; GEMO,; Stoppa-Lyonnet, D; Léoné, M; Barjhoux, L; Fassy-Colcombet, M; de Pauw, A; Lasset, C; Ferrer, SF; Castera, L; Berthet, P; Cornelis, F; Bignon, Y-J; Damiola, F; Mazoyer, S; Sinilnikova, OM; Maxwell, CA; Vijai, J; Robson, M; Kauff, N; Corines, MJ; Villano, D; Cunningham, J; Lee, A; Lindor, N; Lázaro, C; Easton, DF; Offit, K; Chenevix-Trench, G; Couch, FJ; Antoniou, AC; Pujana, MA
MLA Citation
Blanco, Ignacio, et al. “Assessing associations between the AURKA-HMMR-TPX2-TUBG1 functional module and breast cancer risk in BRCA1/2 mutation carriers..” Plos One, vol. 10, no. 4, 2015. Pubmed, doi:10.1371/journal.pone.0120020.
URI
https://scholars.duke.edu/individual/pub1327351
PMID
25830658
Source
pubmed
Published In
Plos One
Volume
10
Published Date
Start Page
e0120020
DOI
10.1371/journal.pone.0120020

Outcomes of primary surgical cytoreduction in patients with BRCA-associated high-grade serous ovarian carcinoma.

OBJECTIVE: BRCA-associated and sporadic ovarian cancers have different pathologic and clinical features. Our goal was to determine if BRCA mutation status is an independent predictor of residual tumor volume following primary surgical cytoreduction. METHODS: We conducted a retrospective analysis of patients with FIGO stage IIIC-IV high-grade serous ovarian cancer classified for the presence or absence of germline BRCA mutations. The primary outcome was tumor-debulking status categorized as complete gross resection (0mm), optimal but visible disease (1-10 mm), or suboptimal debulking (>10 mm) following primary surgical cytoreduction. Overall survival by residual tumor size and BRCA status was also assessed as a secondary endpoint. RESULTS: Data from 367 patients (69 BRCA mutated, 298 BRCA wild-type) were analyzed. Rate of optimal tumor debulking (0-10 mm) in BRCA wild-type and BRCA-mutated patients were 70.1% and 84.1%, respectively (P=0.02). On univariate analysis, increasing age (10-year OR, 1.33; 95% CI, 1.07-1.65; P=0.01) and wild-type BRCA status (OR, 0.47; 95% CI, 0.23-0.94, P=0.03) were both significantly associated with suboptimal surgical outcome. On multivariate analysis, BRCA mutation status was no longer associated with residual tumor volume (OR, 0.63; 95% CI, 0.31-1.29; P=0.21) while age remained a borderline significant predictor (10-year OR, 1.25; 95% CI, 1.01-1.56; P=0.05). Both smaller residual tumor volume and mutant BRCA status were significantly associated with improved overall survival. CONCLUSION: BRCA mutation status is not associated with the rate of optimal tumor debulking at primary surgery after accounting for differences in patient age. Improved survival of BRCA carriers is unlikely the result of better surgical outcomes but instead intrinsic tumor biology.
Authors
Hyman, DM; Long, KC; Tanner, EJ; Grisham, RN; Arnold, AG; Bhatia, J; Phillips, MF; Spriggs, DR; Soslow, RA; Kauff, ND; Levine, DA
MLA Citation
Hyman, David M., et al. “Outcomes of primary surgical cytoreduction in patients with BRCA-associated high-grade serous ovarian carcinoma..” Gynecol Oncol, vol. 126, no. 2, Aug. 2012, pp. 224–28. Pubmed, doi:10.1016/j.ygyno.2012.05.001.
URI
https://scholars.duke.edu/individual/pub1327364
PMID
22579790
Source
pubmed
Published In
Gynecol Oncol
Volume
126
Published Date
Start Page
224
End Page
228
DOI
10.1016/j.ygyno.2012.05.001

Genome-wide association studies of cancer.

Knowledge of the inherited risk for cancer is an important component of preventive oncology. In addition to well-established syndromes of cancer predisposition, much remains to be discovered about the genetic variation underlying susceptibility to common malignancies. Increased knowledge about the human genome and advances in genotyping technology have made possible genome-wide association studies (GWAS) of human diseases. These studies have identified many important regions of genetic variation associated with an increased risk for human traits and diseases including cancer. Understanding the principles, major findings, and limitations of GWAS is becoming increasingly important for oncologists as dissemination of genomic risk tests directly to consumers is already occurring through commercial companies. GWAS have contributed to our understanding of the genetic basis of cancer and will shed light on biologic pathways and possible new strategies for targeted prevention. To date, however, the clinical utility of GWAS-derived risk markers remains limited.
Authors
Stadler, ZK; Thom, P; Robson, ME; Weitzel, JN; Kauff, ND; Hurley, KE; Devlin, V; Gold, B; Klein, RJ; Offit, K
MLA Citation
Stadler, Zsofia K., et al. “Genome-wide association studies of cancer..” J Clin Oncol, vol. 28, no. 27, Sept. 2010, pp. 4255–67. Pubmed, doi:10.1200/JCO.2009.25.7816.
URI
https://scholars.duke.edu/individual/pub1327402
PMID
20585100
Source
pubmed
Published In
Journal of Clinical Oncology
Volume
28
Published Date
Start Page
4255
End Page
4267
DOI
10.1200/JCO.2009.25.7816

BRCA mutations in women with ductal carcinoma in situ.

PURPOSE: The strength of the association between ductal carcinoma in situ (DCIS) and BRCA mutations has not been defined. EXPERIMENTAL DESIGN: Mutation frequency was compared in three groups: (1) a prevalent series of women with DCIS, (2) an incident series of women with DCIS, and (3) a clinic-based series of women with DCIS referred for hereditary cancer risk assessment. In groups 1 and 2, limited to Ashkenazi Jewish (AJ) cases, mutation frequency was compared with that in age-matched AJ controls with invasive breast cancer (IBC). RESULTS: In group 1, 3 of 62 (4.8%) women with DCIS and 15 of 130 (11.5%) controls with IBC had BRCA mutations. In group 2, 0 of 58 (0%) women with DCIS and 6 of 116 (5.2%) controls with IBC had BRCA mutations [combined odds ratios (OR) in groups 1 and 2: 3.64, 95% confidence interval (95% CI), 1.06-12.46; P=0.04]. In group 3, deleterious mutations were identified in 10 of 79 (12.7%) probands with DCIS, similar to the frequency in IBC probands. In group 3, mutations were associated with family history of ovarian cancer (OR, 13.35; 95% CI, 2.48-71.94; P=0.003) or early onset breast cancer (OR, 16.23; 95% CI, 1.68-157.01; P=0.02) but not with AJ ethnicity or age at diagnosis. CONCLUSIONS: BRCA mutations were less frequent in women with DCIS not selected for family history or age at diagnosis than in women with IBC. Nonetheless, mutations were found in a significant proportion of women with DCIS who presented for hereditary risk assessment.
Authors
Smith, KL; Adank, M; Kauff, N; Lafaro, K; Boyd, J; Lee, JB; Hudis, C; Offit, K; Robson, M
MLA Citation
Smith, Karen Lisa, et al. “BRCA mutations in women with ductal carcinoma in situ..” Clin Cancer Res, vol. 13, no. 14, July 2007, pp. 4306–10. Pubmed, doi:10.1158/1078-0432.CCR-07-0146.
URI
https://scholars.duke.edu/individual/pub1327390
PMID
17634561
Source
pubmed
Published In
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
Volume
13
Published Date
Start Page
4306
End Page
4310
DOI
10.1158/1078-0432.CCR-07-0146