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    Molecular phylogeny, character evolution and historical biogeography of Cryptanthus Otto & A. Dietr. (Bromeliaceae)

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    Cryptanthus comprises 72 species endemic to eastern Brazil with a center of diversity in the Atlantic Forest. The majority of the species are threatened due to habitat loss. We reconstructed phylogenetic relationships in Cryptanthus based on amplified fragment length polymorphisms (AFLP) including 48 species and 109 accessions. The Bayesian phylogenetic analysis revealed four major lineages in Cryptanthus and provided further evidence for the paraphyly of subgen. Hoplocryptanthus, while subgenus Cryptanthus was resolved as monophyletic. Monophyly of previously recognized morphological species groups at sectional level could not be confirmed. Based on the phylogenetic reconstruction we inferred the evolution of the sex system in Cryptanthus via maximum likelihood (ML) ancestral character reconstruction. Homoecy, the possession of hermaphrodite flowers only, was reconstructed as the ancestral state in the genus and characterizes three of the four main lineages within Cryptanthus. Andromonoecy, the possession of male and hermaphrodite flowers on the same plant, evolved only once and represents a synapomorphy of the fourth main lineage, C. subgen. Cryptanthus. The ancestral biome analysis reconstructed Cerrado (semiarid scrublands and forests) and campos rupestres (rock fields) as the most likely ancestral biomes for the genus. A shift to the Atlantic Forest biome was reconstructed to have occurred twice, in the ancestor of the first diverging lineage within the genus and in the ancestor of the C. subgen. Cryptanthus clade. A shift to the Caatinga (tropical dryland savanna) and one reversal to Cerrado (campos rupestres - rock fields) was reconstructed to have occurred once, in C. bahianus and C. arelii, respectively. The ancestral biome reconstruction indicates a high degree of niche conservatism within Cryptanthus with rare biome shifts throughout the evolution of the genus. Further, our results imply that the current infrageneric taxonomy of Cryptanthus is problematic and requires revision

    Egfr Activating Mutations And Their Association With Response To Platinum-doublet Chemotherapy In Brazilian Non-small Cell Lung Cancer Patients

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    Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)The aim of the study was to analyze the frequency of epidermal growth factor receptor (EGFR) mutations in Brazilian non-small cell lung cancer patients and to correlate these mutations with response to benefit of platinum-based chemotherapy in non-small cell lung cancer (NSCLC). Our cohort consisted of prospective patients with NSCLCs who received chemotherapy (platinum derivates plus paclitaxel) at the [UNICAMP], Brazil. EGFR exons 18–21 were analyzed in tumor-derived DNA. Fifty patients were included in the study (25 with adenocarcinoma). EGFR mutations were identified in 6/50 (12 %) NSCLCs and in 6/25 (24 %) adenocarcinomas; representing the frequency of EGFR mutations in a mostly self-reported White (82.0 %) southeastern Brazilian population of NSCLCs. Patients with NSCLCs harboring EGFR exon 19 deletions or the exon 21 L858R mutation were found to have a higher chance of response to platinum-paclitaxel (OR 9.67 [95 % CI 1.03–90.41], p = 0.047). We report the frequency of EGFR activating mutations in a typical southeastern Brazilian population with NSCLC, which are similar to that of other countries with Western European ethnicity. EGFR mutations seem to be predictive of a response to platinum-paclitaxel, and additional studies are needed to confirm or refute this relationship.9438939409/52574-5; FAPESP; São Paulo Research FoundationFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Ramalingam, S.S., Owonikoko, T.K., Khuri, F.R., Lung cancer: new biological insights and recent therapeutic advances (2011) CA Cancer J Clin, 61 (2), pp. 91-112. , PID: 21303969Siegel, R., Naishadham, D., Jemal, A., Cancer statistics (2013) CA Cancer J Clin, 63 (1), pp. 11-30. , PID: 23335087Ettinger, D.S., Akerley, W., Borghaei, H., Non-small cell lung cancer (2012) J Natl Compr Canc Netw, 10 (10), pp. 1236-1271. , COI: 1:CAS:528:DC%2BC38XhslynsrrL, PID: 23054877Schiller, J.H., Harrington, D., Belani, C.P., Comparison of four chemotherapy regimens for advanced non-small-cell lung cancer (2002) N Engl J Med, 346, pp. 92-98. , COI: 1:CAS:528:DC%2BD38Xkt1OlsQ%3D%3D, PID: 11784875Shepherd, F.A., Rosell, R., Weighing tumor biology in treatment decisions for patients with non-small cell lung cancer (2007) J Thorac Oncol, 2, pp. S68-S76. , PID: 17589302Danzinger, S., Filipitz, M., Biomarkers—the way towards individualized chemotherapy in non-small cell lung cancer (NSCLC) (2007) Wien Med Wochenschr, 157 (21-22), pp. 554-561. , PID: 18157593Ferraldeschi, R., Baka, S., Jyoti, B., Modern management of small-cell lung cancer (2007) Drugs, 67 (15), pp. 2135-2152. , COI: 1:CAS:528:DC%2BD2sXhsVWkt7bK, PID: 17927281Lee, W., Lockhart, A.C., Kim, R.B., Cancer pharmacogenomics: powerful tools in cancer chemotherapy and drug development (2005) Oncologist, 10, pp. 104-111. , COI: 1:CAS:528:DC%2BD2MXis1KnsbY%3D, PID: 15709212Rosell, R., Cobo, M., Isla, D., Application of genomics in NSCLC (2005) Lung Cancer, pp. S33-S40Sandler, A., Gray, R., Perry, M.C., Paclitaxel-carboplatin alone or with bevacizumab for non-small-cell lung cancer (2006) N Engl J Med, 355, pp. 2542-2550. , COI: 1:CAS:528:DC%2BD28XhtlWqsbzI, PID: 17167137Zhou, C., Wu, Y.L., Chen, G., Erlotinib versus chemotherapy as first-line treatment for patients with advanced EGFR mutation-positive non-small cell lung cancer (OPTIMAL, CTONG-0802): a multicentre, open-label, randomized, phase 3 study (2011) Lancet Oncol, 12, pp. 735-742. , COI: 1:CAS:528:DC%2BC3MXpslKhsbY%3D, PID: 21783417De Luca, A., Carotenuto, A., Rachiglio, A., The role of the EGFR signaling in tumor microenvironment (2008) J Cell Physiol, 214, pp. 559-567. , PID: 17894407Jackman, D.M., Yeap, B.Y., Sequist, L.V., Exon 19 deletion mutations of epidermal growth factor receptor are associated with prolonged survival in non-small cell lung cancer patients treated with gefitinib or erlotinib (2006) Clin Cancer Res, 12 (13), pp. 3908-3914. , COI: 1:CAS:528:DC%2BD28XmsValt7k%3D, PID: 16818686Herbst, R.S., Heymach, J.V., Lippman, S.M., Lung cancer (2008) N Engl J Med, 359 (13), pp. 1367-1380. , COI: 1:CAS:528:DC%2BD1cXhtFKjt7bM, PID: 18815398Pao, W., Miller, V.A., Politi, K.A., Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain (2005) PLoS Med, 2 (3), p. e73. , PID: 15737014Bacchi, C.E., Ciol, H., Queiroga, E.M., Epidermal growth factor receptor and KRAS mutations in Brazilian lung cancer patients (2012) Clinics (São Paulo, Brazil), 67 (5), pp. 419-424Paez, J.G., Janne, P.A., Lee, J.C., EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy (2004) Science, 304 (5676), pp. 1497-1500. , COI: 1:CAS:528:DC%2BD2cXksVGmsbs%3D, PID: 15118125Johnson, B.E., Janne, P.A., Epidermal growth factor receptor mutations in patients with non–small cell lung cancer (2005) Cancer Res, 65, pp. 7525-7529. , COI: 1:CAS:528:DC%2BD2MXpslait7s%3D, PID: 16140912Lin, C.C., Hsu, H.H., Sun, C.T., Chemotherapy response in East Asian non-small cell lung cancer patients harboring wild-type or activating mutation of epidermal growth factor receptors (2010) Thorac Oncol, 9, pp. 1424-1429Kim, H.T., Lee, J.E., Shin, E.S., Effect of BRCA1 haplotype on survival of non-small-cell lung cancer patients treated with platinum-based chemotherapy (2008) J Clin Oncol, 26 (36), pp. 5972-5979. , COI: 1:CAS:528:DC%2BD1MXhs1Ggu74%3D, PID: 19018088Zambon, L., Carcinoma Brônquico: Análise de uma série de casos atendidos no ambulatório de oncopneumologia das disciplinas de Pneumologia e Cirúrgia Torácica da Faculdade de Ciências Médicas da UNICAMP. Dissertation (1994) State University of Campinas, , UNICAMP, Brasil:Dogan, S., Shen, R., Ang, D.C., Molecular epidemiology of EGFR and KRAS mutations in 3,026 lung adenocarcinomas: higher susceptibility of women to smoking-related KRAS-mutant cancers (2012) Clin Cancer Res, 18 (22), pp. 6169-6177. , COI: 1:CAS:528:DC%2BC38Xhs12jur%2FK, PID: 23014527Mok, T.S., Wu, Y.L., Thongprasert, S., Gefitinib or carboplatin–paclitaxel in pulmonary adenocarcinoma (2009) N Engl J Med, 36 (10), pp. 947-957Rosell, R., Carcereny, E., Gervais, R., Erlotinib versus standard chemotherapy as first-line treatment for European patients with advanced EGFR mutation-positive non-small-cell lung cancer (EURTAC): a multicentre, open-label, randomised phase 3 trial (2012) Lancet Oncol, 13 (3), pp. 239-246. , COI: 1:CAS:528:DC%2BC38XjsVCgsbk%3D, PID: 2228516
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