p53 Loses grip on PIK3CA expression leading to enhanced cell survival during platinum resistance
Tumour suppressor p53, a master transcriptional regulator determines cell fate through preferential activation/repression of a myriad of genes during stress. Till date, activation and preferential binding of p53 on different promoters was reported to be influenced by the nature, strength and duration of stress which mediates its post translational modifications. Cisplatin, a widely used cytotoxic drug represses PIK3CA promoter activity and attenuates PI3K/AKT cell survival pathway through p53 activation in sensitive cells. (Source: Molecular Oncology)
Source: Molecular Oncology - June 28, 2016 Category: Cancer & Oncology Authors: Bhushan Thakur, Pritha Ray Source Type: research
p53 loses grip on PIK3CA expression leading to enhanced cell survival during platinum resistance
Tumor suppressor p53, a master transcriptional regulator determines cell fate through preferential activation/repression of a myriad of genes during stress. Till date, activation and preferential binding of p53 on different promoters was reported to be influenced by the nature, strength and duration of stress which mediates its post translational modifications. Cisplatin, a widely used cytotoxic drug represses PIK3CA promoter activity and attenuates PI3K/AKT cell survival pathway through p53 activation in sensitive cells. (Source: Molecular Oncology)
Source: Molecular Oncology - June 28, 2016 Category: Cancer & Oncology Authors: Bhushan Thakur, Pritha Ray Source Type: research
SNHG16 is regulated by the Wnt pathway in colorectal cancer and affects genes involved in lipid metabolism
It is well established that lncRNAs are aberrantly expressed in cancer where they have been shown to act as oncogenes or tumor suppressors. RNA profiling of 314 colorectal adenomas/adenocarcinomas and 292 adjacent normal colon mucosa samples using RNA-sequencing demonstrated that the snoRNA host gene 16 (SNHG16) is significantly up-regulated in adenomas and all stages of CRC. SNHG16 expression was positively correlated to the expression of Wnt-regulated transcription factors, including ASCL2, ETS2, and c-Myc. (Source: Molecular Oncology)
Source: Molecular Oncology - June 25, 2016 Category: Cancer & Oncology Authors: Lise Lotte Christensen, Kirsten True, Mark P. Hamilton, Morten M. Nielsen, Nkerorema D. Damas, Christian K. Damgaard, Halit Ongen, Emmanouil Dermitzakis, Jesper B. Bramsen, Jakob S. Pedersen, Anders H. Lund, S øren Vang, Katrine Stribolt, Mogens R. Madse Source Type: research
16SNHG16 is regulated by the Wnt pathway in colorectal cancer and affects genes involved in lipid metabolism
It is well established that lncRNAs are aberrantly expressed in cancer where they have been shown to act as oncogenes or tumor suppressors. RNA profiling of 314 colorectal adenomas/adenocarcinomas and 292 adjacent normal colon mucosa samples using RNA-sequencing demonstrated that the snoRNA host gene 16 (SNHG16) is significantly up-regulated in adenomas and all stages of CRC. SNHG16 expression was positively correlated to the expression of Wnt-regulated transcription factors, including ASCL2, ETS2, and c-Myc. (Source: Molecular Oncology)
Source: Molecular Oncology - June 25, 2016 Category: Cancer & Oncology Authors: Lise Lotte Christensen, Kirsten True, Mark P. Hamilton, Morten M. Nielsen, Nkerorema D. Damas, Christian K. Damgaard, Halit Ongen, Emmanouil Dermitzakis, Jesper B. Bramsen, Jakob S. Pedersen, Anders H. Lund, Søren Vang, Katrine Stribolt, Mogens R. Madsen Source Type: research
Low Merlin expression and high Survivin labeling index are indicators for poor prognosis in patients with malignant pleural mesothelioma
Alterations of the tumor suppressor Neurofibromatosis type II (NF2) have been reported in about 40% of Malignant pleural mesothelioma (MPM) patients. NF2 (Merlin) deficiency leads to alterations of the Hippo pathway; resulting in activation of the oncogenic Yes Associated Protein-1 (YAP1). Our aim was to investigate the association between these alterations and clinical outcomes. (Source: Molecular Oncology)
Source: Molecular Oncology - June 24, 2016 Category: Cancer & Oncology Authors: Mayura Meerang, Karima B érard, Martina Friess, Byron K.Y. Bitanihirwe, Alex Soltermann, Bart Vrugt, Emanuela Felley-Bosco, Raphael Bueno, William G. Richards, Burkhardt Seifert, Rolf Stahel, Walter Weder, Isabelle Opitz Source Type: research
Low Merlin Expression and High Survivin labeling Index are Indicators for Poor Prognosis in Patients with Malignant Pleural Mesothelioma
Alterations of the tumor suppressor Neurofibromatosis type II (NF2) have been reported in about 40% of Malignant pleural mesothelioma (MPM) patients. NF2 (Merlin) deficiency leads to alterations of the Hippo pathway; resulting in activation of the oncogenic Yes Associated Protein-1 (YAP1). Our aim was to investigate the association between these alterations and clinical outcomes. (Source: Molecular Oncology)
Source: Molecular Oncology - June 24, 2016 Category: Cancer & Oncology Authors: Mayura Meerang, Karima Bérard, Martina Friess, Byron K.Y. Bitanihirwe, Alex Soltermann, Bart Vrugt, Emanuela Felley-Bosco, Raphael Bueno, William G. Richards, Burkhardt Seifert, Rolf Stahel, Walter Weder, Isabelle Opitz Source Type: research
Insulin-like growth factor-1 receptor regulates repair of ultraviolet B-induced DNA damage in human keratinocytes in vivo
The activation status of the insulin-like growth factor-1 receptor (IGF-1R) regulates the cellular response of keratinocytes to ultraviolet B (UVB) exposure, both in vitro and in vivo. Geriatric skin is deficient in IGF-1 expression resulting in an aberrant IGF-1R-dependent UVB response which contributes to the development of aging-associated squamous cell carcinoma. Furthermore, our lab and others have reported that geriatric keratinocytes repair UVB-induced DNA damage less efficiently than young adult keratinocytes. (Source: Molecular Oncology)
Source: Molecular Oncology - June 14, 2016 Category: Cancer & Oncology Authors: Mathew M. Loesch, Ann E. Collier, David H. Southern, Rachel E. Ward, Sunil S. Tholpady, Davina A. Lewis, Jeffrey B. Travers, Dan F. Spandau Source Type: research
Insulin-like growth factor-1 receptor regulates repair of ultraviolet B-induced DNA damage in human keratinocytes in vivo
The activation status of the insulin-like growth factor-1 receptor (IGF-1R) regulates the cellular response of keratinocytes to ultraviolet B (UVB) exposure, both in vitro and in vivo. Geriatric skin is deficient in IGF-1 expression resulting in an aberrant IGF-1R-dependent UVB response which contributes to the development of aging-associated squamous cell carcinoma. Furthermore, our lab and others have reported that geriatric keratinocytes repair UVB-induced DNA damage less efficiently than young adult keratinocytes. (Source: Molecular Oncology)
Source: Molecular Oncology - June 14, 2016 Category: Cancer & Oncology Authors: Mathew M. Loesch, Ann E. Collier, David H. Southern, Rachel E. Ward, Sunil S. Tholpady, Davina A. Lewis, Jeffrey B. Travers, Dan F. Spandau Source Type: research
A novel approach to detect resistance mechanisms reveals FGR as a factor mediating HDAC inhibitor SAHA resistance in B-cell lymphoma
Histone deacetylase (HDAC) inhibitors such as suberoylanilide hydroxamic acid (SAHA) are not commonly used in clinical practice for treatment of B-cell lymphomas, although a subset of patients with refractory or relapsed B-cell lymphoma achieved partial or complete remissions.Therefore, the purpose of this study was to identify molecular features that predict the response of B-cell lymphomas to SAHA treatment. We designed an integrative approach combining drug efficacy testing with exome and captured target analysis (DETECT). (Source: Molecular Oncology)
Source: Molecular Oncology - June 8, 2016 Category: Cancer & Oncology Authors: Maria Joosten, Sebastian Ginzel, Christian Blex, Dmitri Schmidt, Michael Gombert, Cai Chen, Ren é Martin Linka, Olivia Gräbner, Anika Hain, Burkhard Hirsch, Anke Sommerfeld, Anke Seegebarth, Uschi Gruber, Corinna Maneck, Langhui Zhang, Katharina Stenin, Source Type: research
A rare DNA contact mutation in cancer confers p53 gain-of-function and tumor cell survival via TNFAIP8 induction
The p53 tumor suppressor gene encodes a sequence-specific transcription factor. Mutations in the coding sequence of p53 occur frequently in human cancer and often result in single amino acid substitutions (missense mutations) in the DNA binding domain (DBD), blocking normal tumor suppressive functions. In addition to the loss of canonical functions, some missense mutations in p53 confer gain-of-function (GOF) activities to tumor cells. While many missense mutations in p53 cluster at six “hotspot” amino acids, the majority of mutations in human cancer occur elsewhere in the DBD and at a much lower frequency. (Source: Molecular Oncology)
Source: Molecular Oncology - June 6, 2016 Category: Cancer & Oncology Authors: Jessica A. Monteith, Hestia Mellert, Morgan A. Sammons, Laudita A. Kuswanto, Stephen M. Sykes, Lois Resnick-Silverman, James J. Manfredi, Shelley L. Berger, Steven B. McMahon Source Type: research
Droplet digital PCR of circulating tumor cells from colorectal cancer patients can predict KRAS mutations before surgery
In this study we explored the capacity of a size-based device for capturing CTCs coupled with a multiplex KRAS screening assay using droplet digital PCR (ddPCR). (Source: Molecular Oncology)
Source: Molecular Oncology - June 5, 2016 Category: Cancer & Oncology Authors: J érôme Alexandre Denis, Alexia Patroni, Erell Guillerm, Dominique Pépin, Naoual Benali-Furet, Janine Wechsler, Gilles Manceau, Maguy Bernard, Florence Coulet, Annette K. Larsen, Mehdi Karoui, Jean-Marc Lacorte Source Type: research
Droplet Digital PCR of circulating tumor cells from colorectal cancer patients can predict KRAS mutations before surgery
In this study we explored the capacity of a size-based device for capturing CTCs coupled with a multiplex KRAS screening assay using droplet digital PCR (ddPCR). (Source: Molecular Oncology)
Source: Molecular Oncology - June 5, 2016 Category: Cancer & Oncology Authors: Jérôme Alexandre Denis, Alexia Patroni, Erell Guillerm, Dominique Pépin, Naoual Benali-Furet, Janine Weschler, Gilles Manceau, Maguy Bernard, Florence Coulet, Annette K. Larsen, Mehdi Karoui, Jean-Marc Lacorte Source Type: research
