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Your search keyword '"Iafrate, A.J."' showing total 28 results
Start Over Author "Iafrate, A.J."
28 results on '"Iafrate, A.J."'

7. Implementing multiplexed genotyping of non-small-cell lung cancers into routine clinical practice

Author

Sequist, L.V., Heist, R.S., Shaw, A.T., Fidias, P., Rosovsky, R., Temel, J.S., Lennes, I.T., Digumarthy, S., Waltman, B.A., Bast, E., Tammireddy, S., Morrissey, L., Muzikansky, A., Goldberg, S.B., Gainor, J., Channick, C.L., Wain, J.C., Gaissert, H., Donahue, D.M., Muniappan, A., Wright, C., Willers, H., Mathisen, D.J., Choi, N.C., Baselga, J., Lynch, T.J., Ellisen, L.W., Mino-Kenudson, M., Lanuti, M., Borger, D.R., Iafrate, A.J., Engelman, J.A., and Dias-Santagata, D.

Published
2011
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10. Association between PIK3CA mutation status and development of brain metastases in HR+/HER2- metastatic breast cancer

Author

Fitzgerald, D.M., primary, Muzikansky, A., additional, Pinto, C., additional, Henderson, L., additional, Walmsley, C., additional, Allen, R., additional, Ferraro, G.B., additional, Isakoff, S., additional, Moy, B., additional, Oh, K., additional, Shih, H.A., additional, Dias-Santagata, D., additional, Iafrate, A.J., additional, Bardia, A., additional, Brastianos, P.K., additional, and Juric, D., additional

Published
2019
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11. MA26.03 Activity of Osimertinib and the Selective RET Inhibitor BLU-667 in an EGFR-Mutant Patient with Acquired RET Rearrangement

Author

Piotrowska, Z., primary, Isozaki, H., additional, Lennerz, J., additional, Digumarthy, S., additional, Gainor, J., additional, Marcoux, N., additional, Banwait, M., additional, Dias-Santagata, D., additional, Iafrate, A.J., additional, Mino-Kenudson, M., additional, Nagy, R., additional, Lanman, R., additional, Evans, E., additional, Clifford, C., additional, Wolf, B., additional, Hata, A., additional, and Sequist, L., additional

Published
2018
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13. Correlation of extent of ALK FISH positivity and crizotinib efficacy in three prospective studies of ALK-positive patients with non-small-cell lung cancer

Author

Soria, J.-C., primary, Ho, S.N., additional, Varella-Garcia, M., additional, Iafrate, A.J., additional, Solomon, B.J., additional, Shaw, A.T., additional, Blackhall, F., additional, Mok, T.S., additional, Wu, Y.-L., additional, Pestova, K., additional, Wilner, K.D., additional, Polli, A., additional, Paolini, J., additional, Lanzalone, S., additional, Green, S., additional, and Camidge, D.R., additional

Published
2018
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14. A systematic liquid biopsy program identifies novel and heterogeneous mechanisms of acquired resistance in gastrointestinal (GI) cancer patients

Author

Parikh, A., primary, Kwak, E., additional, Goyal, L., additional, Blaszkowsky, L., additional, Hazar-Rethinam, M., additional, Siravegna, G., additional, Russo, M., additional, Van Seventer, E., additional, Nadres, B., additional, Shahzade, H., additional, Clark, J., additional, Allen, J., additional, Iafrate, A.J., additional, Bardellli, A., additional, Ryan, D., additional, Murphy, J., additional, Zhu, A., additional, Hong, T., additional, and Corcoran, R., additional

Published
2016
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28. SOD1A4V-mediated ALS: Absence of a closely linked modifier gene and origination in Asia

Author

Broom, W.J., Johnson, D.V., Auwarter, K.E., Iafrate, A.J., Russ, C., Al-Chalabi, A., Sapp, P.C., McKenna-Yasek, D., Andersen, P.M., and Brown, R.H.

Subjects
*AMYOTROPHIC lateral sclerosis, *GENETIC polymorphisms, *POPULATION genetics, *GENETICS
Abstract

Abstract: Familial amyotrophic lateral sclerosis (ALS) accounts for 10% of all ALS. Approximately 20% of cases are due to mutations in the Cu/Zn superoxide dismutase gene (SOD1). In North America, SOD1A4V is the most common SOD1 mutation. Carriers of the SOD1A4V mutation share a common phenotype with rapid disease progression and death on average occurring at 1.4 years (versus 3–5 years with other dominant SOD1 mutations). Previous studies of SOD1A4V carriers identified a common haplotype around the SOD1 locus, suggesting a common founder for most SOD1A4V patients. In the current study we sequenced the entire common haplotypic region around SOD1 to test the hypothesis that polymorphisms in either previously undescribed coding regions or non-coding regions around SOD1 are responsible for the more aggressive phenotype in SOD1A4V–mediated ALS. We narrowed the conserved region around the SOD1 gene in SOD1A4V ALS to 2.8Kb and identified five novel SNPs therein. None of these variants was specifically found in all SOD1A4V patients. It therefore appears likely that the aggressive nature of the SOD1A4V mutation is not a result of a modifying factor within the region around the SOD1 gene. Founder analysis estimates that the A4V mutation occurred 540 generations (∼12,000 years) ago (95% CI 480–700). The conserved minimal haplotype is statistically more similar to Asian than European population DNA sets, suggesting that the A4V mutation arose in native Asian–Americans who reached the Americas through the Bering Strait. [Copyright &y& Elsevier]

Published
2008
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