Browsing by Author "Cruz, M"

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Clinicopathological predictors of long-term benefit in breast cancer treated with neoadjuvant chemotherapy
(Baishideng Publishing Group, 2018) Galvez, M; Castaneda, CA; Sanchez, J; Castillo, M; Rebaza, LP; Calderon, G; Cruz, M; Cotrina, JM; Abugattas, J; Dunstan, J; Guerra, H; Mejia, O; Gomez, HL
Aim: To investigate the survival impact of clinicopathological factors, including pathological complete response (pCR) and tumor-infiltrating lymphocytes (sTIL) levels according to subtypes, in breast cancer (BC) patients who received neo-adjuvant chemotherapy (NAC). Methods: We evaluated 435 BC patients who presented and received NAC at the Instituto Nacional de Enfermedades Neoplasicas from 2003 to 2014. sTIL was analyzed as the proportion of tumor stroma occupied by lymphocytes, and was prospectively evaluated on hematoxylin and eosin-stained sections of the preNAC core biopsy. pCR was considered in the absence of infiltrating cancer cells in primary tumor and axillary lymph nodes. Analysis of statistical association between clinical pathological features, sTIL, pCR and survival were carried out using SPSSvs19. Results: Median age was 49 years (range 24-84 years) and the most frequent clinical stage was IIIB (58.3%). Luminal A, Luminal B, HER2-enriched and (triple-negative) TN phenotype was found in 24.6%, 37.9%, 17.7% and 19.8%, respectively. pCR was observed in 11% and median percentage of sTIL was 40% (2%-95%) in the whole population. pCR was associated to Ct1-2 (P = 0.045) and to high sTIL (P = 0.029) in the whole population. There was a slight trend towards significance for sTIL (P = 0.054) in Luminal A. sTIL was associated with grade III (P < 0.001), no-Luminal A subtype (P < 0.001), RE-negative (P < 0.001), PgR-negative (P < 0.001), HER2-positive (P = 0.002) and pCR (P = 0.029) in the whole population. Longer disease-free survival was associated with grade I-II (P = 0.006), cN0 (P < 0.001), clinical stage II (P = 0.004), ER-positive (P < 0.001), PgR-positive (P < 0.001), luminal A (P < 0.001) and pCR (P = 0.002). Longer disease-free survival was associated with grade I-II in Luminal A (P < 0.001), N0-1 in Luminal A (P = 0.045) and TNBC (P = 0.01), clinical stage II in Luminal A (P = 0.003) and TNBC (P = 0.038), and pCR in TNBC (P < 0.001). Longer overall survival was associated with grade I-II (P < 0.001), ER-positive (P < 0.001), PgR-positive (P < 0.001), Luminal A (P < 0.001), cN0 (P = 0.002) and pCR (P = 0.002) in the whole population. Overall survival was associated with clinical stage II (P = 0.017) in Luminal A, older age (P = 0.042) in Luminal B, and pCR in TNBC (P = 0.005). Conclusion: Predictive and prognostic values of clinicopathological features, like pCR and sTIL, differ depending on the evaluated molecular subtype.
Gene content, phage cycle regulation model and prophage inactivation disclosed by prophage genomics in the Helicobacter pylori Genome Project
(Taylor and Francis Ltd., 2024) Vale, FF; Roberts, RJ; Kobayashi, I; Camargo, MC; Rabkin, CS; Wang, D; Hicks, B; Zhu, B; Yeager, M; Hutchinson, A; Teshome, K; Jones, K; Luo, W; Goldstein, AM; Hu, N; Taylor, PR; Song, M; Gutiérrez-Escobar, AJ; Yu, K; Abnet, CC; Chanock, SJ; Romero-Gallo, J; Krishna, U; Peek, RM; Piazuelo, MB; Wilson, KT; Loh, JT; Cover, TL; Raaf, N; Aftab, H; Akada, J; Matsumoto, T; Yamaoka, Y; Haesebrouck, F; Bartelli, TF; Nunes, DN; Pelosof, A; Sztokfisz, CZ; Dias-Neto, E; Assumpção, PP; Tishkov, I; Goodman, KJ; Geary, J; Cromarty, TJ; Price, NL; Quilty, D; Corvalan, AH; Serrano, CA; Gonzalez, R; Riquelme, A; García-Cancino, A; Parra-Sepúlveda, C; Castillo, F; Bravo, MM; Pazos, A; Bravo, LE; Fox, JG; Ramírez-Mayorga, V; Molina-Castro, S; Durán-Bermúdez, S; Campos-Núñez, C; Chaves-Cervantes, M; Tshibangu-Kabamba, E; Tumba, GD; Tshimpi-Wola, A; de Jesus Ngoma-Kisoko, P; Ngoyi, DM; Cruz, M; Hosking, C; Abreu, JJ; Varon, C; Benejat, L; Jehanne, Q; Lehours, P; Megraud, F; Secka, O; Link, A; Malfertheiner, P; Adinortey, MB; Bockarie, AS; Adinortey, CA; Ofori, EG; Sgouras, DN; Martinez-Gonzalez, B; Michopoulos, S; Georgopoulos, S; Hernandez, E; Dominguez, RL; Morgan, DR; Harðardóttir, H; Gunnarsdóttir, AI; Guðjónsson, H; Jónasson, JG; Björnsson, ES; Ballal, M; Shetty, V; Miftahussurur, M; Sugihartono, T; Alfaray, RI; Waskito, LA; Fauzia, KA; Syam, AF; Maulahela, H; Malekzadeh, R; Sotoudeh, M; Peretz, A; Azrad, M; On, A; De, Re, V; Zanussi, S; Cannizzaro, R; Canzonieri, V; Shimura, T; Tokunaga, K; Osaki, T; Kamiya, S; Jadallah, K; Matalka, I; Sagynbekuly, IN; Moldobaeva, MS; Rakhat, A; Choi, IJ; Kim, JG; Kim, N; Leja, M; Vangravs, R; Šķenders, Ģ; Rūdule, A; Kikuste, I; Vanags, A; Rudzīte, D; Kupcinskas, J; Skieceviciene, J; Jonaitis, L; Kiudelis, G; Jonaitis, P; Kiudelis, V; Varkalaite, G; Vadivelu, J; Loke, MF; Vellasamy, KM; Herrera-Goepfert, R; Alonso-Larraga, JO; Yee, TT; Htet, K; Matsuhisa, T; Shrestha, PK; Ansari, S; Abiodun, O; Jemilohun, C; Akande, KO; Olu-Abiodun, O; Magaji, FA; Omotoso, A; Okonkwo, U; Osuagwu, CC; Owoseni, OO; Castaneda, C; Castillo, M; Velapatino, B; Gilman, RH; Krzyżek, P; Gościniak, G; Pawełka, D; Korona-Glowniak, I; Cichoz-Lach, H; Oleastro, M; Figueiredo, C; Machado, JC; Ferreira, RM; Bordin, DS; Livzan, MA; Tsukanov, VV; Tan, P; Yeoh, KG; Zhu, F; Ally, R; Haas, R; Fischer, W; Montes, M; Fernández-Reyes, M; Tamayo, E; Lizasoain, J; Bujanda, L; Lario, S; Ramírez-Lázaro, MJ; Calvet, X; Brunet-Mas, E; Domper-Arnal, MJ; García-Mateo, S; Abad-Baroja, D; Delgado-Guillena, P; Moreira, L; Botargues, J; Pérez-Martínez, I; Barreiro-Alonso, E; Flores, V; Gisbert, JP; Muro, EA; Linares, P; Alcoba, L; Martin, V; Fleitas-Kanonnikoff, T; Altayeb, HN; Engstrand, L; Enroth, H; Keller, PM; Wagner, K; Pohl, D; Lee, Y-C; Liou, J-M; Wu, M-S; Kocazeybek, B; Sarıbas, S; Tasçı, İ; Demiryas, S; Kepil, N; Quiel, L; Villagra, M; Norton, M; Johnson, D; Huang, RJ; Hwang, JH; Szymczak, W; Rajagopalan, S; Asare, E; Jacobs, WR; In, H; Bollag, R; Lopez, A; Kruse, EJ; White, J; Graham, DY; Lane, C; Gao, Y; Gold, BD; Cruz-Correa, M; González-Pons, M; Rodriguez, LM; Tuan, VP; Dung, HDQ; Binh, TT; Trang, TTH; Van, Khien, V; Chen, X; Zhao, Y; Raley, C; Kessing, B; Tran, B; Katsura, Y; Gonzalez-Hormazabal, P; Didelot, X; Sheppard, S; Tarazona-Santos, E; Zamudio, R; Mariño-Ramírez, L; Backert, S; Naumann, M; Smet, A; Berg, DE; Chiner-Oms, Á; Comas, I; Martínez-Martínez, FJ; Yahara, K; Blaser, MJ; Vincze, T; Morgan, RD; Dekker, JP; Torres, J; Noureen, M; Cherry, JL; Osada, N; Fukuyo, M; Arita, M; Sandoval-Motta, S; Agostini, RB; Ghirotto, S; Muñoz-Ramírez, ZY; Torres, RC; Falush, D; Thorell, K; Uchiyama, I
Prophages can have major clinical implications through their ability to change pathogenic bacterial traits. There is limited understanding of the prophage role in ecological, evolutionary, adaptive processes and pathogenicity of Helicobacter pylori, a widespread bacterium causally associated with gastric cancer. Inferring the exact prophage genomic location and completeness requires complete genomes. The international Helicobacter pylori Genome Project (HpGP) dataset comprises 1011 H. pylori complete clinical genomes enriched with epigenetic data. We thoroughly evaluated the H. pylori prophage genomic content in the HpGP dataset. We investigated population evolutionary dynamics through phylogenetic and pangenome analyses. Additionally, we identified genome rearrangements and assessed the impact of prophage presence on bacterial gene disruption and methylome. We found that 29.5% (298) of the HpGP genomes contain prophages, of which only 32.2% (96) were complete, minimizing the burden of prophage carriage. The prevalence of H. pylori prophage sequences was variable by geography and ancestry, but not by disease status of the human host. Prophage insertion occasionally results in gene disruption that can change the global bacterial epigenome. Gene function prediction allowed the development of the first model for lysogenic-lytic cycle regulation in H. pylori. We have disclosed new prophage inactivation mechanisms that appear to occur by genome rearrangement, merger with other mobile elements, and pseudogene accumulation. Our analysis provides a comprehensive framework for H. pylori prophage biological and genomics, offering insights into lysogeny regulation and bacterial adaptation to prophages. © 2024 The Author(s). Published with license by Taylor & Francis Group, LLC.