The Experts below are selected from a list of 42540 Experts worldwide ranked by ideXlab platform
Yoshitaka Fujii - One of the best experts on this subject based on the ideXlab platform.
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kif5b ret Fusion Gene in surgically treated adenocarcinoma of the lung
Oncology Reports, 2012Co-Authors: Keisuke Yokota, Shigeki Shimizu, Masayuki Shitara, Yuu Hikosaka, Hidefumi Sasaki, Motoki Yano, Satoru Moriyama, Katsuhiro Okuda, Yoshitaka FujiiAbstract:: Recently, a novel Fusion Gene resulting from a linkage between the kinesin family member 5B Gene (KIF5B; 10p11.22) and the rearranged during transfection Gene (RET; 10q11.21) was identified in non-small cell lung cancer (NSCLC). However, the correlation between the KIF5B/RET Fusion Gene status and the clinicopathological features of surgically-treated lung cancer has not been well characterized. In this study, we have independently investigated the KIF5B/RET Fusion Gene status in 371 surgically-treated NSCLCs (270 were adenocarcinomas and 101 were squamous cell carcinomas), 60 breast cancers, 11 metastatic lung cancers from colon cancers and thyroid papillary adenocarcinoma cases at the Nagoya City University Hospital. The Fusion Gene status was analyzed by an RT-PCR-based assay and by using direct sequencing. We detected 3 of 270 cases of KIF5B/RET Fusion Genes in adenocarcinomas (1.1%) consisting of female and never smokers with mixed subtype adenocarcinomas. The Fusion Genes were detected exclusively with other mutations, such as EGFR, Kras, Braf, erbB2 mutations, and EML4/ALK Fusion. KIF5B/RET Fusion was not detected in the cases with squamous cell carcinoma or other types of cancers. From the 3 cases, 2 were KIF5B (exon 15); RET (exon 12) Fusions with papillary dominant and 1 case was KIF5B (exon 22); RET (exon 12) Fusion with solid dominant adenocarcinoma. The matched normal lung tissues did not display translocation. We reported KIF5B/RET Fusion Genes as a driver somatic mutation of lung adenocarcinomas. The cinicopathological backgrounds of the KIF5B/RET Fusion-positive patients were similar with those of the EML4/ALK Fusion-positive patients. The chimeric oncoGene may be a promising molecular target for the personalized diagnosis and treatment of NSCLC.
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KIF5B/RET Fusion Gene in surgically-treated adenocarcinoma of the lung.
Oncology Reports, 2012Co-Authors: Keisuke Yokota, Shigeki Shimizu, Masayuki Shitara, Yuu Hikosaka, Hidefumi Sasaki, Motoki Yano, Satoru Moriyama, Katsuhiro Okuda, Yoshitaka FujiiAbstract:: Recently, a novel Fusion Gene resulting from a linkage between the kinesin family member 5B Gene (KIF5B; 10p11.22) and the rearranged during transfection Gene (RET; 10q11.21) was identified in non-small cell lung cancer (NSCLC). However, the correlation between the KIF5B/RET Fusion Gene status and the clinicopathological features of surgically-treated lung cancer has not been well characterized. In this study, we have independently investigated the KIF5B/RET Fusion Gene status in 371 surgically-treated NSCLCs (270 were adenocarcinomas and 101 were squamous cell carcinomas), 60 breast cancers, 11 metastatic lung cancers from colon cancers and thyroid papillary adenocarcinoma cases at the Nagoya City University Hospital. The Fusion Gene status was analyzed by an RT-PCR-based assay and by using direct sequencing. We detected 3 of 270 cases of KIF5B/RET Fusion Genes in adenocarcinomas (1.1%) consisting of female and never smokers with mixed subtype adenocarcinomas. The Fusion Genes were detected exclusively with other mutations, such as EGFR, Kras, Braf, erbB2 mutations, and EML4/ALK Fusion. KIF5B/RET Fusion was not detected in the cases with squamous cell carcinoma or other types of cancers. From the 3 cases, 2 were KIF5B (exon 15); RET (exon 12) Fusions with papillary dominant and 1 case was KIF5B (exon 22); RET (exon 12) Fusion with solid dominant adenocarcinoma. The matched normal lung tissues did not display translocation. We reported KIF5B/RET Fusion Genes as a driver somatic mutation of lung adenocarcinomas. The cinicopathological backgrounds of the KIF5B/RET Fusion-positive patients were similar with those of the EML4/ALK Fusion-positive patients. The chimeric oncoGene may be a promising molecular target for the personalized diagnosis and treatment of NSCLC.
Jiang Liyua - One of the best experts on this subject based on the ideXlab platform.
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kif5b ret Fusion Gene and non small cell lung cancer
Chinese clinical oncology, 2013Co-Authors: Jiang LiyuaAbstract:Lung cancer is the leading cause of mortality in cancer worldwide.Molecular targeted therapy is the hotpot of lung cancer study in recent years.In 2012,a novel Fusion Gene KIF5B-RET was identified in non-small cell lung cancer.This Fusion Gene is more frequently detected in the lung adenocarcinoma,with no or little history of cigarette smoking.The mutually exclusive nature of the RET Fusions and other oncogenic alterations such as EGFR,K-Ras,ALK,etc.,suggests that the KIF5B-RET Fusion is a new driver mutation.It could be a promising molecular target for the personalized diagnosis and treatment of non-small cell lung cancer.
Keisuke Yokota - One of the best experts on this subject based on the ideXlab platform.
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kif5b ret Fusion Gene in surgically treated adenocarcinoma of the lung
Oncology Reports, 2012Co-Authors: Keisuke Yokota, Shigeki Shimizu, Masayuki Shitara, Yuu Hikosaka, Hidefumi Sasaki, Motoki Yano, Satoru Moriyama, Katsuhiro Okuda, Yoshitaka FujiiAbstract:: Recently, a novel Fusion Gene resulting from a linkage between the kinesin family member 5B Gene (KIF5B; 10p11.22) and the rearranged during transfection Gene (RET; 10q11.21) was identified in non-small cell lung cancer (NSCLC). However, the correlation between the KIF5B/RET Fusion Gene status and the clinicopathological features of surgically-treated lung cancer has not been well characterized. In this study, we have independently investigated the KIF5B/RET Fusion Gene status in 371 surgically-treated NSCLCs (270 were adenocarcinomas and 101 were squamous cell carcinomas), 60 breast cancers, 11 metastatic lung cancers from colon cancers and thyroid papillary adenocarcinoma cases at the Nagoya City University Hospital. The Fusion Gene status was analyzed by an RT-PCR-based assay and by using direct sequencing. We detected 3 of 270 cases of KIF5B/RET Fusion Genes in adenocarcinomas (1.1%) consisting of female and never smokers with mixed subtype adenocarcinomas. The Fusion Genes were detected exclusively with other mutations, such as EGFR, Kras, Braf, erbB2 mutations, and EML4/ALK Fusion. KIF5B/RET Fusion was not detected in the cases with squamous cell carcinoma or other types of cancers. From the 3 cases, 2 were KIF5B (exon 15); RET (exon 12) Fusions with papillary dominant and 1 case was KIF5B (exon 22); RET (exon 12) Fusion with solid dominant adenocarcinoma. The matched normal lung tissues did not display translocation. We reported KIF5B/RET Fusion Genes as a driver somatic mutation of lung adenocarcinomas. The cinicopathological backgrounds of the KIF5B/RET Fusion-positive patients were similar with those of the EML4/ALK Fusion-positive patients. The chimeric oncoGene may be a promising molecular target for the personalized diagnosis and treatment of NSCLC.
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KIF5B/RET Fusion Gene in surgically-treated adenocarcinoma of the lung.
Oncology Reports, 2012Co-Authors: Keisuke Yokota, Shigeki Shimizu, Masayuki Shitara, Yuu Hikosaka, Hidefumi Sasaki, Motoki Yano, Satoru Moriyama, Katsuhiro Okuda, Yoshitaka FujiiAbstract:: Recently, a novel Fusion Gene resulting from a linkage between the kinesin family member 5B Gene (KIF5B; 10p11.22) and the rearranged during transfection Gene (RET; 10q11.21) was identified in non-small cell lung cancer (NSCLC). However, the correlation between the KIF5B/RET Fusion Gene status and the clinicopathological features of surgically-treated lung cancer has not been well characterized. In this study, we have independently investigated the KIF5B/RET Fusion Gene status in 371 surgically-treated NSCLCs (270 were adenocarcinomas and 101 were squamous cell carcinomas), 60 breast cancers, 11 metastatic lung cancers from colon cancers and thyroid papillary adenocarcinoma cases at the Nagoya City University Hospital. The Fusion Gene status was analyzed by an RT-PCR-based assay and by using direct sequencing. We detected 3 of 270 cases of KIF5B/RET Fusion Genes in adenocarcinomas (1.1%) consisting of female and never smokers with mixed subtype adenocarcinomas. The Fusion Genes were detected exclusively with other mutations, such as EGFR, Kras, Braf, erbB2 mutations, and EML4/ALK Fusion. KIF5B/RET Fusion was not detected in the cases with squamous cell carcinoma or other types of cancers. From the 3 cases, 2 were KIF5B (exon 15); RET (exon 12) Fusions with papillary dominant and 1 case was KIF5B (exon 22); RET (exon 12) Fusion with solid dominant adenocarcinoma. The matched normal lung tissues did not display translocation. We reported KIF5B/RET Fusion Genes as a driver somatic mutation of lung adenocarcinomas. The cinicopathological backgrounds of the KIF5B/RET Fusion-positive patients were similar with those of the EML4/ALK Fusion-positive patients. The chimeric oncoGene may be a promising molecular target for the personalized diagnosis and treatment of NSCLC.
J Trachtenberg - One of the best experts on this subject based on the ideXlab platform.
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expression of the tmprss2 erg Fusion Gene predicts cancer recurrence after surgery for localised prostate cancer
British Journal of Cancer, 2007Co-Authors: Linda Sugar, Wenyi Yang, S Srivastava, Laurence Klotz, L Y Yang, Aleksandra Stanimirovic, E Encioiu, M Neill, D A Loblaw, J TrachtenbergAbstract:The prostate-specific Gene, TMPRSS2 is fused with the Gene for the transcription factor ERG in a large proportion of human prostate cancers. The prognostic significance of the presence of the TMPRSS2:ERG Gene Fusion product remains controversial. We examined prostate cancer specimens from 165 patients who underwent surgery for clinically localised prostate cancer between 1998 and 2006. We tested for the presence of TMPRSS2:ERG Gene Fusion product, using RT–PCR and direct sequencing. We conducted a survival analysis to determine the prognostic significance of the presence of the TMPRSS2:ERG Fusion Gene on the risk of prostate cancer recurrence, adjusting for the established prognostic factors. We discovered that the Fusion Gene was expressed within the prostate cancer cells in 81 of 165 (49.1%) patients. Of the 165 patients, 43 (26.1%) developed prostate-specific antigen (PSA) relapse after a mean follow-up of 28 months. The subgroup of patients with the Fusion protein had a significantly higher risk of recurrence (58.4% at 5 years) than did patients who lacked the Fusion protein (8.1%, P<0.0001). In a multivariable analysis, the presence of Gene Fusion was the single most important prognostic factor; the adjusted hazard ratio for disease recurrence for patients with the Fusion protein was 8.6 (95% CI=3.6–20.6, P<0.0001) compared to patients without the Fusion protein. Among prostate cancer patients treated with surgery, the expression of TMPRSS2:ERG Fusion Gene is a strong prognostic factor and is independent of grade, stage and PSA level.
Anthony M. Vergis - One of the best experts on this subject based on the ideXlab platform.
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fancd2 is a potential therapeutic target and biomarker in alveolar rhabdomyosarcoma harboring the pax3 foxo1 Fusion Gene
Clinical Cancer Research, 2014Co-Authors: Mamata Singh, Justin M. Leasure, Christopher Chronowski, Kathryn Bondra, Lauren A. Hensley, Miguel A Villalonacalero, Wenrui Duan, Ning Li, Brian A Geier, Anthony M. VergisAbstract:Purpose: Alveolar rhabdomyosarcoma that harbors the PAX3–FOXO1 Fusion Gene (t-ARMS) is a common and lethal subtype of this childhood malignancy. Improvement in clinical outcomes in this disease is predicated upon the identification of novel therapeutic targets. Experimental Design: Robust mouse models were used for in vivo analysis, and molecular studies were performed on xenografts treated in parallel. Two independent patient sets ( n = 101 and 124) of clinically annotated tumor specimens were used for analysis of FANCD2 levels and its association with clinical and molecular characteristics and outcomes. Results: Our xenograft studies reveal a selective suppression of FANCD2 by m-TOR kinase inhibition and radiosensitization of the t-ARMS line only. In the initial patient set, we show that FANCD2 transcript levels are prognostic in univariate analysis, and are significantly associated with metastatic disease and that the copresence of the translocation and high expression of FANCD2 is independently prognostic. We also demonstrate a significant and nonrandom enrichment of mTOR-associated Genes that correlate with FANCD2 Gene expression within the t-ARMS samples, but not within other cases. In the second patient set, we show that on a protein level, FANCD2 expression correlates with PAX3–FOXO1 Fusion Gene and is strongly associated with phospho-P70S6K expression in cases with the Fusion Gene. Conclusions: Our data demonstrate that FANCD2 may have a significant role in the radiation resistance and virulence of t-ARMS. Indirectly targeting this DNA repair protein, through mTOR inhibition, may represent a novel and selective treatment strategy. Clin Cancer Res; 20(14); 3884–95. ©2014 AACR .
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FANCD2 is a potential therapeutic target and biomarker in alveolar rhabdomyosarcoma harboring the PAX3-FOXO1 Fusion Gene
Clinical Cancer Research, 2014Co-Authors: Mamata Singh, Justin M. Leasure, Christopher Chronowski, Kathryn Bondra, Lauren A. Hensley, Miguel Villalona-calero, B Geier, Wenrui Duan, Ning Li, Anthony M. VergisAbstract:PURPOSE: Alveolar rhabdomyosarcoma that harbors the PAX3-FOXO1 Fusion Gene (t-ARMS) is a common and lethal subtype of this childhood malignancy. Improvement in clinical outcomes in this disease is predicated upon the identification of novel therapeutic targets.\n\nEXPERIMENTAL DESIGN: Robust mouse models were used for in vivo analysis, and molecular studies were performed on xenografts treated in parallel. Two independent patient sets (n = 101 and 124) of clinically annotated tumor specimens were used for analysis of FANCD2 levels and its association with clinical and molecular characteristics and outcomes.\n\nRESULTS: Our xenograft studies reveal a selective suppression of FANCD2 by m-TOR kinase inhibition and radiosensitization of the t-ARMS line only. In the initial patient set, we show that FANCD2 transcript levels are prognostic in univariate analysis, and are significantly associated with metastatic disease and that the copresence of the translocation and high expression of FANCD2 is independently prognostic. We also demonstrate a significant and nonrandom enrichment of mTOR-associated Genes that correlate with FANCD2 Gene expression within the t-ARMS samples, but not within other cases. In the second patient set, we show that on a protein level, FANCD2 expression correlates with PAX3-FOXO1 Fusion Gene and is strongly associated with phospho-P70S6K expression in cases with the Fusion Gene.\n\nCONCLUSIONS: Our data demonstrate that FANCD2 may have a significant role in the radiation resistance and virulence of t-ARMS. Indirectly targeting this DNA repair protein, through mTOR inhibition, may represent a novel and selective treatment strategy.
