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Molecular Oncology

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https://www.readbyqxmd.com/read/28636767/aberrant-expression-of-kallikrein-related-peptidase-7-is-correlated-to-human-melanoma-aggressiveness-by-stimulating-cell-migration-and-invasion
#1
Tiphaine Delaunay, Lydia Deschamps, Meriem Haddada, Francine Walker, Antoninus Soosaipillai, Feryel Soualmia, Chahrazade El Amri, Eleftherios P Diamandis, Maria Brattsand, Viktor Magdolen, Dalila Darmoul
Members of the tissue kallikrein-related peptidase (KLK) family not only regulate several important physiological functions, but aberrant expression has also been associated with various malignancies. Clinically, KLKs have been suggested as promising biomarkers for diagnosis and prognosis in many types of cancer. As of yet, expression of KLKs and their role in skin cancers are, however, poorly addressed. Malignant melanoma is an aggressive disease associated with poor prognosis. Hence, diagnostic biomarkers to monitor melanoma progression are needed...
June 21, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28632938/mek-inhibitors-induce-akt-activation-and-drug-resistance-by-suppressing-negative-feedback-erk-mediated-her2-phosphorylation-at-thr701
#2
Chia-Hung Chen, Te-Chun Hsia, Ming-Hsin Yeh, Tsung-Wei Chen, Yun-Ju Chen, Jung-Tsu Chen, Ya-Ling Wei, Chih-Yen Tu, Wei-Chien Huang
Targeting the MEK/ERK pathway has been viewed as a promising strategy for cancer therapy. However, MEK inhibition leads to the compensatory PI3K/AKT activation and thus contributes to the desensitization of cancer cells to MEK inhibitors. The underlying molecular mechanism of this event is not yet understood. In this study, our data showed that the induction of Akt activity by MEK inhibitors was specifically observed in HER2-positive breast cancer cells. Silence of HER2, or overexpression of HER2 kinase-dead mutant, prevents the induction of Akt activation in response to MEK inhibition, indicating HER2 as a critical regulator for this event...
June 20, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28627792/%C3%AE-catenin-in-desmoid-type-fibromatosis-deep-insights-on-the-role-of-t41a-and-s45f-mutations-on-protein-structure-and-gene-expression
#3
C Colombo, A Belfiore, N Paielli, L De Cecco, S Canevari, E Laurini, M Fermeglia, S Pricl, P Verderio, S Bottelli, M Fiore, S Stacchiotti, E Palassini, A Gronchi, S Pilotti, F Perrone
Desmoid- type fibromatosis (DF) is a rare mesenchymal lesion with high risk of local recurrence. Specific β-catenin mutations (S45F) appeared to be related to this higher risk compared to T41A mutated or wild type (WT). We explored the influence of both mutations and WT on structure stability and affinity of β-catenin for α-catenin and the pattern of gene expression that may influence DF behavior. Using 33 surgically resected primary DFs harboring T41A (n=14), S45F (n=10) or WT (n=9), we performed a comparative molecular analysis by protein/protein interaction modeling, gene expression by DASL microarrays, human inflammation gene panel and assessment of immune system-based biomarkers by immunohistochemistry...
June 19, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28618197/analysis-of-mutant-allele-fractions-in-driver-genes-in-colorectal-cancer-biological-and-clinical-insights
#4
Rodrigo Dienstmann, Elena Elez, Guillem Argiles, Ignacio Matos, Enrique Sanz-Garcia, Carolina Ortiz, Teresa Macarulla, Jaume Capdevila, Maria Alsina, Tamara Sauri, Helena Verdaguer, Marta Vilaro, Fiorella Ruiz-Pace, Cristina Viaplana, Ariadna Garcia, Stefania Landolfi, Hector G Palmer, Paolo Nuciforo, Jordi Rodon, Ana Vivancos, Josep Tabernero
Sequencing of tumors is now routine and guides personalized cancer therapy. Mutant allele fractions (MAFs, or the 'mutation dose') of a driver gene may reveal the genomic structure of tumors and influence response to targeted therapies. We performed a comprehensive analysis of MAFs of driver alterations in unpaired primary and metastatic colorectal cancer (CRC) at our institution from 2010 to 2015 and studied their potential clinical relevance. Out of 763 CRC samples, 622 had detailed annotation on overall survival in the metastatic setting (OSmet) and 89 received targeted agents matched to KRAS (MEK inhibitors), BRAF (BRAF inhibitors) or PIK3CA mutations (PI3K pathway inhibitors)...
June 15, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28618162/zeb1-regulated-inflammatory-phenotype-in-breast-cancer-cells
#5
Akihiro Katsura, Yusuke Tamura, Satoshi Hokari, Mayumi Harada, Masato Morikawa, Tsubasa Sakurai, Kei Takahashi, Anna Mizutani, Jun Nishida, Yuichiro Yokoyama, Yasuyuki Morishita, Takashi Murakami, Shogo Ehata, Kohei Miyazono, Daizo Koinuma
Zinc finger E-box binding protein 1 (ZEB1) and ZEB2 induce epithelial-mesenchymal transition (EMT) and enhance cancer progression. However, the global view of transcriptional regulation by ZEB1 and ZEB2 is yet to be elucidated. Here, we identified a ZEB1-regulated inflammatory phenotype in breast cancer cells using chromatin immunoprecipitation-sequencing and RNA sequencing, followed by gene set enrichment analysis (GSEA) of ZEB1-bound genes. Knockdown of ZEB1 and/or ZEB2 resulted in the down-regulation of genes encoding inflammatory cytokines related to poor prognosis in cancer patients, including IL6 and IL8, therefore suggesting that ZEB1 and ZEB2 have similar functions in terms of the regulation of production of inflammatory cytokines...
June 15, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28614631/trpm4-regulates-akt-gsk3-%C3%AE-activity-and-enhances-%C3%AE-catenin-signaling-and-cell-proliferation-in-prostate-cancer-cells
#6
Alfredo I Sagredo, Eduardo A Sagredo, Claudio Cappelli, Pablo Báez, Andaur M Rodrigo, Constanza Blanco, Julio C Tapia, César Echeverría, Oscar Cerda, Andrés Stutzin, Felipe Simon, Katherine Marcelain, Ricardo Armisén
Increased expression of the TRPM4 channel has been reported to be associated with the progression of prostate cancer. However, the molecular mechanism underlying its effect remains unknown. This work found that decreasing TRPM4 levels leads to the reduced proliferation of PC3 cells. This effect was associated with a decrease in total β-catenin protein levels and its nuclear localization, and a significant reduction in Tcf/Lef transcriptional activity. Moreover, TRPM4 silencing increases the Ser33/Ser37/Thr41 β-catenin phosphorylated population and reduces the phosphorylation of GSK-3β at Ser9, suggesting an increase in β-catenin degradation as the underlying mechanism...
June 14, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28614624/new-insights-into-the-role-of-emt-in-tumor-immune-escape
#7
REVIEW
Stéphane Terry, Pierre Savagner, Sandra Ortiz-Cuaran, Linda Mahjoubi, Pierre Saintigny, Jean-Paul Thiery, Salem Chouaib
Novel immunotherapy approaches have provided durable remission in a significant number of cancer patients with cancers previously considered rapidly lethal. Nonetheless, the high degree of non-responders, and in some cases the emergence of resistance in patients who do initially respond, represents a significant challenge in the field of cancer immunotherapy. These issues prompt much more extensive studies to better understand how cancer cells escape immune surveillance and resist immune attacks. Here, we review the current knowledge of how cellular heterogeneity and plasticity could be involved in shaping the tumor microenvironment and in controlling anti-tumor immunity...
June 14, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28599100/emt-and-inflammation-inseparable-actors-of-cancer-progression
#8
REVIEW
Meggy Suarez-Carmona, Julien Lesage, Didier Cataldo, Christine Gilles
Tumors can be depicted as wounds that never heal, and are infiltrated by a large array of inflammatory and immune cells. Tumor-associated chronic inflammation is a hallmark of cancer that fosters progression to a metastatic stage, as has been extensively reviewed lately. Indeed, inflammatory cells persisting in the tumor establish a cross-talk with tumor cells that may result in a phenotype switch into tumor-supporting cells. This has been particularly well described for macrophages and is referred to as tumor-associated "M2" polarization...
June 9, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28590039/emt-present-and-future-in-clinical-oncology
#9
REVIEW
Patricia G Santamaria, Gema Moreno-Bueno, Francisco Portillo, Amparo Cano
Epithelial-mesenchymal transition (EMT) has emerged as a key regulator of metastasis by facilitating tumor cell invasion and dissemination to distant organs. Recent evidences support that the reverse mesenchymal-epithelial transition (MET) is required for metastatic outgrowth; moreover, the existence of hybrid epithelial/mesenchymal (E/M) phenotypes is increasingly being reported in different tumor contexts. The accumulated data strongly support that plasticity between epithelial and mesenchymal states underlies the dissemination and metastatic potential of carcinoma cells...
June 7, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28590032/epithelial-mesenchymal-transition-in-cancer-metastasis-through-the-lymphatic-system
#10
REVIEW
Mikael C Karlsson, Santiago F Gonzalez, Josefin Welin, Jonas Fuxe
It was already in the 18th century when the French surgeon Le Dran first noted that breast cancer patients with spread of tumor cells to their axillary lymph nodes had a drastically worse prognosis than patients without spread (leDran et al., 1752). Since then, metastatic spread of cancer cells to regional lymph nodes has been established as the most important prognostic factor in many types of cancer (Carter et al., 1989; Elston and Ellis, 1991). However, despite its clinical importance, lymph metastasis remains an underexplored area of tumor biology...
June 7, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28580773/hbx-mediated-decrease-of-aim2-contributes-to-hepatocellular-carcinoma-metastasis
#11
Shi-Lu Chen, Li-Li Liu, Shi-Xun Lu, Rong-Zhen Luo, Chun-Hua Wang, Hong Wang, Shao-Hang Cai, Xia Yang, Dan Xie, Chris Zhiyi Zhang, Jing-Ping Yun
Tumor metastasis is responsible for the high mortality rates in patients with hepatocellular carcinoma (HCC). Absent in Melanoma 2 (AIM2) has been implicated in inflammation and carcinogenesis, but its role in HCC metastasis remains unknown. Here, we show that AIM2 protein expression was noticeably reduced in HCC cell lines and clinical samples. A reduction in AIM2 was closely associated with higher serum AFP levels, vascular invasion, poor tumor differentiation, an incomplete tumor capsule and unfavorable postsurgical survival odds...
June 5, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28580735/ddah1-mediates-gastric-cancer-cell-invasion-and-metastasis-via-wnt-%C3%AE-catenin-signaling-pathway
#12
Jianxin Ye, Jie Xu, Yun Li, Qiang Huang, Jinsheng Huang, Jinzhou Wang, Wenjing Zhong, Xinjian Lin, Wannan Chen, Xu Lin
Gastric cancer (GC) represents the fourth most common malignant neoplasm and the second leading cause of cancer death. Despite therapeutic advances in recent decades, the clinical outcome remains dismal owing to the fact that most GC patients show advanced disease at diagnosis and current chemotherapy only confers a modest survival advantage. Identification of key molecular signaling pathways involved in gastric carcinogenesis and progression would aid in early diagnosis and provide a rational design for targeted therapies in selected patients with advanced GC, to improve their outcome...
June 5, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28557340/trka-is-a-binding-partner-of-npm-alk-that-promotes-the-survival-of-alk-t-cell-lymphoma
#13
Wenyu Shi, Suraj Konnath George, Bhawana George, Choladda V Curry, Albina Murzabdillaeva, Serhan Alkan, Hesham M Amin
Nucleophosmin-anaplastic lymphoma kinase-expressing (NPM-ALK(+) ) T-cell lymphoma is an aggressive neoplasm that is more commonly seen in children and young adults. The pathogenesis of NPM-ALK(+) T-cell lymphoma is not completely understood. It is characterized by the expression of the chimeric tyrosine kinase NPM-ALK. Wild-type ALK is a receptor tyrosine kinase that is physiologically expressed in neural tissues during early stages of human development, which suggests that ALK may interact with neurotrophic factors...
May 30, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28557306/sk4-channels-modulate-ca-2-signalling-and-cell-cycle-progression-in-murine-breast-cancer
#14
Friederike A Steudel, Corinna J Mohr, Benjamin Stegen, Hoang Y Nguyen, Andrea Barnert, Marc Steinle, Sandra Beer-Hammer, Pierre Koch, Wing-Yee Lo, Werner Schroth, Reiner Hoppe, Hiltrud Brauch, Peter Ruth, Stephan M Huber, Robert Lukowski
Oncogenic signalling via Ca(2+) -activated K(+) channels of intermediate conductance (SK4, also known as KCa 3.1 or IK) has been implicated in different cancer entities including breast cancer. Yet, the role of endogenous SK4 channels for tumourigenesis is unclear. Herein, we generated SK4-negative tumours by crossing SK4-deficient (SK4 KO) mice to the polyoma middle T-antigen (PyMT) and epidermal growth factor receptor 2 (cNeu) breast cancer models in which oncogene expression is driven by the retroviral promotor MMTV...
May 30, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28556483/drug-sensitivity-and-resistance-testing-identifies-plk1-inhibitors-and-gemcitabine-as-potent-drugs-for-malignant-peripheral-nerve-sheath-tumors-mpnst
#15
Matthias Kolberg, Jarle Bruun, Astrid Murumägi, John P Mpindi, Christian H Bergsland, Maren Høland, Ina A Eilertsen, Stine A Danielsen, Olli Kallioniemi, Ragnhild A Lothe
Patients with malignant peripheral nerve sheath tumor (MPNST), a rare soft tissue cancer associated with loss of the tumor suppressor neurofibromin (NF1), have poor prognosis and typically respond poorly to adjuvant therapy. We evaluated the effect of 299 clinical and investigational compounds on seven MPNST cell lines, two primary cultures of human Schwann cells, and five normal bone marrow aspirates, to identify potent drugs for MPNST treatment with few side effects. Top hits included Polo-like kinase 1 (PLK1) inhibitors (volasertib and BI2536) and the fluoronucleoside gemcitabine, which were validated in orthogonal assays measuring viability, cytotoxicity and apoptosis...
May 29, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28556516/emt-and-met-related-processes-in-non-epithelial-tumors-importance-for-disease-progression-prognosis-and-therapeutic-opportunities
#16
REVIEW
Ulf D Kahlert, Justin V Joseph, Frank A E Kruyt
The epithelial-to mesenchymal (EMT) process is increasingly recognized for playing a key role in the progression, dissemination and therapy resistance of epithelial tumors. Accumulating evidence suggests that EMT inducers also lead to a gain in mesenchymal properties and promote malignancy of non-epithelial tumors. In this review we present and discuss current findings, illustrating the importance of EMT inducers in tumors originating from non-epithelial/ mesenchymal tissues, including: brain tumors, hematopoietic malignancies and sarcomas...
May 28, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28548388/epithelial-mesenchymal-plasticity-how-have-quantitative-mathematical-models-helped-improve-our-understanding
#17
REVIEW
Mohit Kumar Jolly, Satyendra C Tripathi, Jason A Somarelli, Samir M Hanash, Herbert Levine
Phenotypic plasticity, the ability of cells to reversibly alter their phenotypes in response to signals, presents a significant clinical challenge to treating solid tumors. Tumor cells utilize phenotypic plasticity to evade therapies, metastasize, and colonize distant organs. As a result, phenotypic plasticity can accelerate tumor progression. A well-studied example of phenotypic plasticity is the bidirectional conversions among epithelial, mesenchymal, and hybrid epithelial/mesenchymal phenotype(s). These conversions can alter a repertoire of cellular traits associated with multiple hallmarks of cancer, such as metabolism, immune-evasion, invasion and metastasis...
May 26, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28548345/emt-and-met-necessary-or-permissive-for-metastasis
#18
REVIEW
Mohit Kumar Jolly, Kathryn E Ware, Shivee Gilja, Jason A Somarelli, Herbert Levine
Epithelial-to-mesenchymal transition (EMT) and its reverse mesenchymal-to-epithelial transition (MET) have been suggested to play crucial roles in metastatic dissemination of carcinomas. These phenotypic transitions between states are not binary. Instead, carcinoma cells often exhibit a spectrum of epithelial/mesenchymal phenotype(s). While epithelial-mesenchymal plasticity has been observed pre-clinically and clinically, whether any of these phenotypic transitions are indispensable for metastatic outgrowth remains an unanswered question...
May 26, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28544747/k-ras-mutation-and-amplification-status-is-predictive-of-resistance-and-high-basal-pakt-is-predictive-of-sensitivity-to-everolimus-in-biliary-tract-cancer-cell-lines
#19
Yvonne Yeung, David K Lau, Fiona Chionh, Hoanh Tran, Janson W T Tse, Andrew J Weickhardt, Mehrdad Nikfarjam, Andrew M Scott, Niall C Tebbutt, John M Mariadason
Advanced biliary tract cancer (BTC) has a poor prognosis and limited treatment options. The PI3K/Akt/mTOR signaling pathway is hyperactivated in a subset of BTCs and clinical activity to the mTOR inhibitor everolimus has been observed in some BTC patients. The goal of this study was to identify biomarkers predictive of everolimus response. Twenty BTC cell lines were assessed for everolimus sensitivity with a spectrum of growth inhibitory responses observed. Molecular biomarkers of sensitivity and resistance were identified by interrogation of the activation status of the Ras/MAPK and PI3K/Akt/mTOR pathways...
May 24, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28544627/epithelial-to-mesenchymal-transition-transcription-factors-in-cancer-associated-fibroblasts
#20
REVIEW
Josep Baulida
Beyond inducing epithelial-to-mesenchymal transcription (EMT), transcriptional factors of the Snail, ZEB and Twist families (EMT-TFs) control global plasticity programs affecting cell stemness and fate. Literature addressing the reactivation of these factors in adult tumour cells is very extensive, as they enable cancer cell plasticity and fuel both tumour initiation and metastatic spread. Incipient data reveal that EMT-TFs are also expressed in fibroblasts, providing these with additional properties. Here, I will review recent reports on the expression of EMT-TFs in cancer-associated fibroblasts (CAFs)...
May 24, 2017: Molecular Oncology
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