Activating KRAS mutations are characteristic of oncocytic sinonasal papilloma and associated sinonasal squamous cell carcinoma
dc.contributor.author | Udager, Aaron M | |
dc.contributor.author | McHugh, Jonathan B | |
dc.contributor.author | Betz, Bryan L | |
dc.contributor.author | Montone, Kathleen T | |
dc.contributor.author | Livolsi, Virginia A | |
dc.contributor.author | Seethala, Raja R | |
dc.contributor.author | Yakirevich, Evgeny | |
dc.contributor.author | Iwenofu, O Hans | |
dc.contributor.author | Perez‐ordonez, Bayardo | |
dc.contributor.author | DuRoss, Kathleen E | |
dc.contributor.author | Weigelin, Helmut C | |
dc.contributor.author | Lim, Megan S | |
dc.contributor.author | Elenitoba‐johnson, Kojo Sj | |
dc.contributor.author | Brown, Noah A | |
dc.date.accessioned | 2016-09-17T23:54:28Z | |
dc.date.available | 2017-11-01T15:31:29Z | en |
dc.date.issued | 2016-08 | |
dc.identifier.citation | Udager, Aaron M; McHugh, Jonathan B; Betz, Bryan L; Montone, Kathleen T; Livolsi, Virginia A; Seethala, Raja R; Yakirevich, Evgeny; Iwenofu, O Hans; Perez‐ordonez, Bayardo ; DuRoss, Kathleen E; Weigelin, Helmut C; Lim, Megan S; Elenitoba‐johnson, Kojo Sj ; Brown, Noah A (2016). "Activating KRAS mutations are characteristic of oncocytic sinonasal papilloma and associated sinonasal squamous cell carcinoma." The Journal of Pathology 239(4): 394-398. | |
dc.identifier.issn | 0022-3417 | |
dc.identifier.issn | 1096-9896 | |
dc.identifier.uri | https://hdl.handle.net/2027.42/133586 | |
dc.description.abstract | Oncocytic sinonasal papillomas (OSPs) are benign tumours of the sinonasal tract, a subset of which are associated with synchronous or metachronous sinonasal squamous cell carcinoma (SNSCC). Activating EGFR mutations were recently identified in nearly 90% of inverted sinonasal papillomas (ISPs) â a related tumour with distinct morphology. EGFR mutations were, however, not found in OSP, suggesting that different molecular alterations drive the oncogenesis of these tumours. In this study, tissue from 51 cases of OSP and five cases of OSPâ associated SNSCC was obtained retrospectively from six institutions. Tissue was also obtained from 50 cases of ISP, 22 cases of ISPâ associated SNSCC, ten cases of exophytic sinonasal papilloma (ESP), and 19 cases of SNSCC with no known papilloma association. Using targeted nextâ generation and conventional Sanger sequencing, we identified KRAS mutations in 51/51 (100%) OSPs and 5/5 (100%) OSPâ associated SNSCCs. The somatic nature of KRAS mutations was confirmed in a subset of cases with matched germline DNA, and four matched pairs of OSP and concurrent associated SNSCC had concordant KRAS genotypes. In contrast, KRAS mutations were present in only one (5%) SNSCC with no known papilloma association and none of the ISPs, ISPâ associated SNSCCs, or ESPs. This is the first report of somatic KRAS mutations in OSP and OSPâ associated SNSCC. The presence of identical mutations in OSP and concurrent associated SNSCC supports the putative role of OSP as a precursor to SNSCC, and the high frequency and specificity of KRAS mutations suggest that OSP and OSPâ associated SNSCC are biologically distinct from other similar sinonasal tumours. The identification of KRAS mutations in all studied OSP cases represents an important development in our understanding of the pathogenesis of this disease and may have implications for diagnosis and therapy. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. | |
dc.publisher | John Wiley & Sons, Ltd | |
dc.subject.other | squamous cell carcinoma | |
dc.subject.other | Schneiderian | |
dc.subject.other | sinonasal | |
dc.subject.other | papilloma | |
dc.subject.other | oncocytic | |
dc.subject.other | KRAS | |
dc.title | Activating KRAS mutations are characteristic of oncocytic sinonasal papilloma and associated sinonasal squamous cell carcinoma | |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | |
dc.subject.hlbsecondlevel | Pathology | |
dc.subject.hlbtoplevel | Health Sciences | |
dc.description.peerreviewed | Peer Reviewed | |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/133586/1/path4750.pdf | |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/133586/2/path4750_am.pdf | |
dc.identifier.doi | 10.1002/path.4750 | |
dc.identifier.source | The Journal of Pathology | |
dc.identifier.citedreference | Szablewski V, Solassol J, Poizat F, et al. EGFR expression and KRAS and BRAF mutational status in intestinalâ type sinonasal adenocarcinoma. Int J Mol Sci 2013; 14: 5170 â 5181. | |
dc.identifier.citedreference | Projetti F, Durand K, Chaunavel A, et al. Epidermal growth factor receptor expression and KRAS and BRAF mutations: study of 39 sinonasal intestinalâ type adenocarcinomas. Hum Pathol 2013; 44: 2116 â 2125. | |
dc.identifier.citedreference | Hu Y, Lu W, Chen G, et al. Kâ ras G12V transformation leads to mitochondrial dysfunction and a metabolic switch from oxidative phosphorylation to glycolysis. Cell Res 2012; 22: 399 â 412. | |
dc.identifier.citedreference | Radkay LA, Chiosea SI, Seethala RR, et al. Thyroid nodules with KRAS mutations are different from nodules with NRAS and HRAS mutations with regard to cytopathologic and histopathologic outcome characteristics. Cancer Cytopathol 2014; 122: 873 â 882. | |
dc.identifier.citedreference | Strojan P, Ferlito A, Lund VJ, et al. Sinonasal inverted papilloma associated with malignancy: the role of human papillomavirus infection and its implications for radiotherapy. Oral Oncol 2012; 48: 216 â 218. | |
dc.identifier.citedreference | Stolze B, Reinhart S, Bulllinger L, et al. Comparative analysis of KRAS codon 12, 13, 18, 61, and 117 mutations using human MCF10A isogenic cell lines. Sci Rep 2015; 5: 8535. | |
dc.identifier.citedreference | Park JT, Johnson N, Liu S, et al. Differential in vivo tumorigenicity of diverse KRAS mutations in vertebrate pancreas: a comprehensive survey. Oncogene 2015; 34: 2801 â 2806. | |
dc.identifier.citedreference | Modest DP, Camaj P, Heinemann V, et al. KRAS alleleâ specific activity of sunitinib in an isogenic disease model of colorectal cancer. J Cancer Res Clin Oncol 2013; 139: 953 â 961. | |
dc.identifier.citedreference | Fatrai S, van Gosliga D, Han L, et al. KRAS(G12V) enhances proliferation and initiates myelomonocytic differentiation in human stem/progenitor cells via intrinsic and extrinsic pathways. J Biol Chem 2011; 286: 6061 â 6070. | |
dc.identifier.citedreference | Haigis KM, Kendall KR, Wang Y, et al. Differential effects of oncogenic Kâ Ras and Nâ Ras on proliferation, differentiation and tumor progression in the colon. Nature Genet 2008; 40: 600 â 608. | |
dc.identifier.citedreference | Davies BR, Logie A, McKay JS, et al. AZD6244 (ARRYâ 142886), a potent inhibitor of mitogenâ activated protein kinase/extracellular signalâ regulated kinase kinase 1/2 kinases: mechanism of action in vivo, pharmacokinetic/pharmacodynamic relationship, and potential for combination in preclinical models. Mol Cancer Ther 2007; 6: 2209 â 2219. | |
dc.identifier.citedreference | Biankin AV, Waddell N, Kassahn KS, et al. Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes. Nature 2012; 491: 399 â 405. | |
dc.identifier.citedreference | Cancer Genome Atlas Research Network. Comprehensive molecular profiling of lung adenocarcinoma. Nature 2014; 511: 543 â 550. | |
dc.identifier.citedreference | Gasparre G, Romeo G, Rugolo M, et al. Learning from oncocytic tumors: why choose inefficient mitochondria? Biochim Biophys Acta 2011; 1807: 633 â 642. | |
dc.identifier.citedreference | Chang A, Harawi SJ. Oncocytes, oncocytosis, and oncocytic tumors. Pathol Annu 1992; 27 ( Pt 1 ): 263 â 304. | |
dc.identifier.citedreference | Udager AM, McHugh JB, Elenitobaâ Johnson KS, et al. EGFR mutations in sinonasal squamous tumors: oncogenic and therapeutic implications. Oncoscience 2015; 2: 908 â 909. | |
dc.identifier.citedreference | Neuzillet C, Tijerasâ Raballand A, de Mestier L, et al. MEK in cancer and cancer therapy. Pharmacol Ther 2014; 141: 160 â 171. | |
dc.identifier.citedreference | Lopez F, Garcia Inclan C, Perezâ Escuredo J, et al. KRAS and BRAF mutations in sinonasal cancer. Oral Oncol 2012; 48: 692 â 697. | |
dc.identifier.citedreference | Cancer Genome Atlas Network. Comprehensive molecular characterization of human colon and rectal cancer. Nature 2012; 487: 330 â 337. | |
dc.identifier.citedreference | Udager AM, Rolland DC, McHugh JB, et al. Highâ frequency targetable EGFR mutations in sinonasal squamous cell carcinomas arising from inverted sinonasal papilloma. Cancer Res 2015; 75: 2600 â 2606. | |
dc.identifier.citedreference | Barnes L, Bedetti C. Oncocytic Schneiderian papilloma: a reappraisal of cylindrical cell papilloma of the sinonasal tract. Hum Pathol 1984; 15: 344 â 351. | |
dc.identifier.citedreference | Barnes L. Schneiderian papillomas and nonsalivary glandular neoplasms of the head and neck. Mod Pathol 2002; 15: 279 â 297. | |
dc.identifier.citedreference | Garciaâ Inclan C, Lopez F, Perezâ Escuredo J, et al. EGFR status and KRAS/BRAF mutations in intestinalâ type sinonasal adenocarcinomas. Cell Oncol 2012; 35: 443 â 450. | |
dc.identifier.citedreference | Timar J. The clinical relevance of KRAS gene mutation in nonâ smallâ cell lung cancer. Curr Opin Oncol 2014; 26: 138 â 144. | |
dc.identifier.citedreference | Arrington AK, Heinrich EL, Lee W, et al. Prognostic and predictive roles of KRAS mutation in colorectal cancer. Int J Mol Sci 2012; 13: 12153 â 12168. | |
dc.identifier.citedreference | Bornholdt J, Hansen J, Steiniche T, et al. Kâ ras mutations in sinonasal cancers in relation to wood dust exposure. BMC Cancer 2008; 8: 53. | |
dc.identifier.citedreference | Cancer Genome Atlas Network. Comprehensive genomic characterization of head and neck squamous cell carcinomas. Nature 2015; 517: 576 â 582. | |
dc.identifier.citedreference | Stransky N, Egloff AM, Tward AD, et al. The mutational landscape of head and neck squamous cell carcinoma. Science 2011; 333: 1157 â 1160. | |
dc.identifier.citedreference | Agrawal N, Frederick MJ, Pickering CR, et al. Exome sequencing of head and neck squamous cell carcinoma reveals inactivating mutations in NOTCH1. Science 2011; 333: 1154 â 1157. | |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
Files in this item
Remediation of Harmful Language
The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.
Accessibility
If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.