Editorial Board
(Source: Molecular Oncology)
Source: Molecular Oncology - November 30, 2016 Category: Cancer & Oncology Source Type: research
Corrigendum to “Infiltrating T cells promote prostate cancer metastasis via modulation of FGF11→miRNA-541→androgen receptor (AR)→MMP9 signaling” [Mol Oncol 9 (1) (2015) 44–57]
It has come to the authors' attention that wrong figure panels in Figure 4 of the article, ‘Infiltrating T cells promote prostate cancer metastasis via modulation of FGF11→miRNA-541→androgen receptor (AR)→MMP9 signaling’ published In the January 2015 issue (vol. 9, Nr. 1, pages 44–57) of this JOURNAL, were provided. Upon checking the figure in question, w e found that, by oversight, during preparation of these multiple set of figure panels, some of the images that had been included were incorrect. (Source: Molecular Oncology)
Source: Molecular Oncology - November 3, 2016 Category: Cancer & Oncology Authors: Shuai Hu, Lei Li, Shuyuan Yeh, Yun Cui, Xin Li, Hong-Chiang Chang, Jie Jin, Chawnshang Chang Tags: Corrigendum Source Type: research
Prospective validation of a blood-based 9-miRNA profile for early detection of breast cancer in a cohort of women examined by clinical mammography
Mammography is the predominant screening method for early detection of breast cancer, but has limitations and could be rendered more accurate by combination with a blood-based biomarker profile. Circulating microRNAs (miRNAs) are increasingly recognized as strong biomarkers, and we previously developed a 9-miRNA profile using serum and LNA-based qPCR that effectively stratified patients with early stage breast cancer vs. healthy women. To further develop the test into routine clinical practice, we collected serum of women examined by clinical mammography (N=197) according to standard operational procedures (SOPs) of the Da...
Source: Molecular Oncology - October 31, 2016 Category: Cancer & Oncology Authors: Maria B. Lyng, Annette R. Kodahl, Harald Binder, Henrik J. Ditzel Source Type: research
Exosomal proteins as prognostic biomarkers in non-small cell lung cancer
Use of exosomes as biomarkers in non-small cell lung cancer (NSCLC) is an intriguing approach in the liquid-biopsy era. Exosomes are nano-sized vesicles with membrane-bound proteins that reflect their originating cell. Prognostic biomarkers are needed to improve patient selection for optimal treatment. We here evaluate exosomes by protein phenotyping as a prognostic biomarker in NSCLC. (Source: Molecular Oncology)
Source: Molecular Oncology - October 20, 2016 Category: Cancer & Oncology Authors: B. Sandfeld-Paulsen, N. Aggerholm-Pedersen, R. B æk, K.R. Jakobsen, P. Meldgaard, B.H. Folkersen, T.R. Rasmussen, K. Varming, M.M. Jørgensen, B.S. Sorensen Source Type: research
Editorial Board
(Source: Molecular Oncology)
Source: Molecular Oncology - October 14, 2016 Category: Cancer & Oncology Source Type: research
A Pilot Study Exploring the Molecular Architecture of the Tumor Microenvironment in Human Prostate Cancer Using a Laser Capture Microdissection and Reverse Phase Protein Microarray Workflow
The cross-talk between tumor epithelium and surrounding stromal/immune microenvironment is essential to sustain tumor growth and progression and provides new opportunities for the development of targeted treatments focused on disrupting the tumor ecology. Identification of novel approaches to study these interactions is of primary importance. Using laser capture microdissection (LCM) coupled with reverse phase protein microarray (RPPA) based protein signaling activation mapping we explored the molecular interconnection between tumor epithelium and surrounding stromal microenvironment in 18 prostate cancer (PCa) specimens. ...
Source: Molecular Oncology - October 13, 2016 Category: Cancer & Oncology Authors: Elisa Pin, Steven Stratton, Claudio Belluco, Lance Liotta, Ray Nagle, K. Alex Hodge, Jianghong Deng, Ting Dong, Elisa Baldelli, Emanuel Petricoin, Mariaelena Pierobon Source Type: research
Somatic mutation detection using various targeted detection assays in paired samples of circulating tumor DNA, primary tumor and metastases from patients undergoing resection of colorectal liver metastases
Assessing circulating tumor DNA (ctDNA) is a promising method to evaluate somatic mutations from solid tumors in a minimally-invasive way. In a group of twelve metastatic colorectal cancer (mCRC) patients undergoing liver metastasectomy, from each patient DNA from cell-free DNA (cfDNA), the primary tumor, metastatic liver tissue, normal tumor-adjacent colon or liver tissue, and whole blood were obtained. Investigated was the feasibility of a targeted NGS approach to identify somatic mutations in ctDNA. (Source: Molecular Oncology)
Source: Molecular Oncology - October 7, 2016 Category: Cancer & Oncology Authors: Nick Beije, Jean C. Helmijr, Marjolein J.A. Weerts, Corine M. Beaufort, Matthew Wiggin, Andre Marziali, Cornelis Verhoef, Stefan Sleijfer, Maurice P.H.M. Jansen, John W.M. Martens Source Type: research
Epigenetic determinants of metastasis
Genetic analyses of cancer progression in patient samples and model systems have thus far failed to identify specific mutational drivers of metastasis. Yet, at least in experimental systems, metastatic cancer clones display stable traits that can facilitate progression through the many steps of metastasis. How cancer cells establish and maintain the transcriptional programmes required for metastasis remains mostly unknown. Emerging evidence suggests that metastatic traits may arise from epigenetically altered transcriptional output of the oncogenic signals that drive tumour initiation and early progression. (Source: Molecular Oncology)
Source: Molecular Oncology - October 6, 2016 Category: Cancer & Oncology Authors: Saroor A. Patel, Sakari Vanharanta Tags: Review Source Type: research
Tumor cell dormancy
Metastasis is the primary cause of death in cancer patients and current treatments fail to provide durable responses. Efforts to treat metastatic disease are hindered by the fact that metastatic cells often remain dormant for prolonged intervals of years, or even decades. Tumor dormancy reflects the capability of disseminated tumor cells (DTCs), or micrometastases, to evade treatment and remain at low numbers after primary tumor resection. Unfortunately, dormant cells will eventually produce overt metastasis. (Source: Molecular Oncology)
Source: Molecular Oncology - October 6, 2016 Category: Cancer & Oncology Authors: Roger R. Gomis, Sylwia Gawrzak Tags: Review Source Type: research
Corrigendum to “Molecular imaging for personalized cancer care” [Mol. Oncol. 6(2) (2012) 182–195]
In the review article, “Molecular Imaging for Personalized Cancer Care” (Mol. Oncol. 2012 Apr; 6(2):182–195. PMID: 2246961), we represented certain concepts that were previously presented by us in chapter 2 of the IOM report, “A National Cancer Clinical Trials System for the 21st Century: Reinvigorating the NCI Co operative Group.” We regret that we omitted to include a reference to the IOM report, but we wish to note that we have received permission from the IOM for use of the material in question. (Source: Molecular Oncology)
Source: Molecular Oncology - October 1, 2016 Category: Cancer & Oncology Authors: Moritz F. Kircher, Hedvig Hricak, Steven M. Larson Tags: Corrigendum Source Type: research
VCP inhibitors induce endoplasmic reticulum stress, cause cell cycle arrest, trigger caspase-mediated cell death and synergistically kill ovarian cancer cells in combination with Salubrinal
Valosin-containing protein (VCP) or p97, a member of AAA-ATPase protein family, has been associated with various cellular functions including endoplasmic reticulum-associated degradation (ERAD), Golgi membrane reassembly, autophagy, DNA repair, and cell division. Recent studies identified VCP and ubiquitin proteasome system (UPS) as synthetic lethal targets in ovarian cancer. Here, we describe the preclinical activity of VCP inhibitors in ovarian cancer. Results from our studies suggest that quinazoline-based VCP inhibitors initiate G1 cell cycle arrest, attenuate cap-dependent translation and induce programmed cell death ...
Source: Molecular Oncology - September 26, 2016 Category: Cancer & Oncology Authors: Prabhakar Bastola, Lisa Neums, Frank J. Schoenen, Jeremy Chien Source Type: research
VCP inhibitors induce endoplasmic reticulum stress, cause cell cycle arrest, trigger caspase-mediated cell death and synergistically kill ovarian cancer cells in combination with salubrinal
Valosin-containing protein (VCP) or p97, a member of AAA-ATPase protein family, has been associated with various cellular functions including endoplasmic reticulum-associated degradation (ERAD), Golgi membrane reassembly, autophagy, DNA repair, and cell division. Recent studies identified VCP and ubiquitin proteasome system (UPS) as synthetic lethal targets in ovarian cancer. Here, we describe the preclinical activity of VCP inhibitors in ovarian cancer. Results from our studies suggest that quinazoline-based VCP inhibitors initiate G1 cell cycle arrest, attenuate cap-dependent translation and induce programmed cell death ...
Source: Molecular Oncology - September 26, 2016 Category: Cancer & Oncology Authors: Prabhakar Bastola, Lisa Neums, Frank J. Schoenen, Dr. Jeremy Chien Source Type: research
Concordance of Immune Checkpoints within Tumor Immune Contexture and Their Prognostic Significance in Gastric Cancer
This study aims to investigate the expression and prognostic significance of immune checkpoints within gastric cancer. In the study, a cohort of 398 cancer tissues from stage I to IV gastric cancer patients were assessed for programmed cell death 1 ligand 1 (PD-L1) expression and tumor-infiltrating lymphocyte (TIL) infiltration using immunohistochemistry to ascertain their survival correlation. (Source: Molecular Oncology)
Source: Molecular Oncology - September 23, 2016 Category: Cancer & Oncology Authors: Congqi Dai, Ruixuan Geng, Chenchen Wang, Angela Wong, Ming Qing, Jianjun Hu, Yu Sun, A.W.I. Lo, Jin Li Source Type: research
Dysregulation of histone methyltransferases in breast cancer – Opportunities for new targeted therapies?
Histone methyltransferases (HMTs) catalyze the methylation of lysine and arginine residues on histone tails and non-histone targets. These important post-translational modifications are exquisitely regulated and affect chromatin compaction and transcriptional programs leading to diverse biological outcomes. There is accumulating evidence that genetic alterations of several HMTs impinge on oncogenic or tumor-suppressor functions and influence both cancer initiation and progression. HMTs therefore represent an opportunity for therapeutic targeting in those patients with tumors in which HMTs are dysregulated, to reverse the h...
Source: Molecular Oncology - September 22, 2016 Category: Cancer & Oncology Authors: Ewa M. Michalak, Jane E. Visvader Tags: Review Source Type: research
Dysregulation of Histone Methyltransferases in Breast Cancer- Opportunities for New Targeted Therapies?
Histone methyltransferases (HMTs) catalyze the methylation of lysine and arginine residues on histone tails and non-histone targets. These important post-translational modifications are exquisitely regulated and affect chromatin compaction and transcriptional programs leading to diverse biological outcomes. There is accumulating evidence that genetic alterations of several HMTs impinge on oncogenic or tumor-suppressor functions and influence both cancer initiation and progression. HMTs therefore represent an opportunity for therapeutic targeting in those patients with tumors in which HMTs are dysregulated, to reverse the h...
Source: Molecular Oncology - September 22, 2016 Category: Cancer & Oncology Authors: Ewa M. Michalak, Jane E. Visvader Tags: Review Source Type: research
