Results 81 to 90 of about 1,302,502 (304)

Plecstatin inhibits hepatocellular carcinoma tumorigenesis and invasion through cytolinker plectin

Molecular Oncology, EarlyView.
The ruthenium‐based metallodrug plecstatin exerts its anticancer effect in hepatocellular carcinoma (HCC) primarily through selective targeting of plectin. By disrupting plectin‐mediated cytoskeletal organization, plecstatin inhibits anchorage‐dependent growth, cell polarization, and tumor cell dissemination.
Zuzana Outla, Jan Kosla, Magdalena Prechova, Lukas Frick, Patricia Bortel, Yasmin Borutzki, Andrea Bileck, Christopher Gerner, Samuel M. Meier‐Menches, Selma Osmanagic‐Myers, Martin Gregor   +10 more
wiley   +1 more source

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

Molecular Oncology, EarlyView.
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala, Sini Ahonen, Sara Peltola, Aura Tuohisto‐Kokko, Olaya Esparta, Peppi Suominen, Anne Jokilammi, Iman Farahani, Deepankar Chakroborty, Nikol Dibus, Steffen Boettcher, Tomi T. Airenne, Mark S. Johnson, Lisa D. Eli, Klaus Elenius, Kari J. Kurppa   +15 more
wiley   +1 more source

Gene amplification in Rhynchosciara (1955-1987)

Memorias do Instituto Oswaldo Cruz, 1987
A review is made of the evidence indicating the existence of gene amplification in Rhynchosciara, from the early cytological work to the more recent studies using cloned sequences from the DNA puffs.
Francisco J. S. Lara
doaj   +1 more source

Epigenetic regulation affects gene amplification in Drosophila development

Frontiers in Bioscience-Landmark, 2020
In Drosophila melanogaster, in response to developmental transcription factors, and by repeated initiation of DNA replication of four chorion genes, ovarian follicle cells, form an onion skin-type structure at the replication origins. The DNA replication
Hidetsugu Kohzaki, Maki Asano, Yota Murakami, Alexander Mazo   +3 more
doaj   +1 more source

Integrative analyses identify modulators of response to neoadjuvant aromatase inhibitors in patients with early breast cancer [PDF]

, 2015
Introduction Aromatase inhibitors (AIs) are a vital component of estrogen receptor positive (ER+) breast cancer treatment. De novo and acquired resistance, however, is common.
A Mackay, AK Dunbier, AK Dunbier, Alan Mackay, Alexey Larionov, Anita K Dunbier, Aradhana Rani, Ash Nerurkar, B Weigelt, BP Coe, C Curtis, C Kent, D Generali, DG Albertson, DS Tan, Elena López-Knowles, F Kreisel, Helen Anderson, HW Cheung, IE Smith, IE Smith, J Hicks, J Michael Dixon, Jorge S Reis-Filho, JS Foster, K Lundgren, L Osterberg, LA Martin, LA Martin, LA Martin, Lesley-Ann Martin, LG Leon, Lorna Renshaw, M Dowsett, M Mello-Grand, M Scaltriti, Mitch Dowsett, MJ Ellis, MT Weigel, N Turner, P Darbre, P Lal, Paul M Wilkerson, Peter Osin, PM Wilkerson, PM Wilkerson, PT Simpson, R Beroukhim, R Duprez, R Katz-Brull, R Natrajan, R Natrajan, R Natrajan, Ricardo Ribas, T Miyake, T Troiani, TK Lam, William R Miller, WR Miller, WR Miller, WR Miller, WR Miller, X Huo, Y Zhao, Z Ghazoui, Zara Ghazoui   +65 more
core   +3 more sources

Peroxidasin enables melanoma immune escape by inhibiting natural killer cell cytotoxicity

Molecular Oncology, EarlyView.
Peroxidasin (PXDN) is secreted by melanoma cells and binds the NK cell receptor NKG2D, thereby suppressing NK cell activation and cytotoxicity. PXDN depletion restores NKG2D signaling and enables effective NK cell–mediated melanoma killing. These findings identify PXDN as a previously unrecognized immune evasion factor and a potential target to improve
Hsu‐Min Sung, David Bickel, Lena C. M. Krause, Daria Ezeriņa, Christian Ickes, Julian Wojtachnia, Christine S. Gibhardt, Magdalena Shumanska, Khadija Wahni, Andrea Paluschkiwitz, Julia Malo Pueyo, Ekaterina Baranova, Wim Vranken, Hedwig Stanisz, Ioana Stejerean‐Todoran, Michael P. Schön, Joris Messens, Ivan Bogeski   +17 more
wiley   +1 more source

Assessment of ERBB2 and EGFR gene amplification and protein expression in gastric carcinoma by immunohistochemistry and fluorescence in situ hybridization

Molecular Cytogenetics, 2011
Background The goal of this study was to investigate ERBB2(HER2) and EGFR gene amplification and protein expression in gastric cancer. Fluorescence in situ hybridization (FISH) and immunohistochemistry were used to analyze ERBB2 and EGFR gene ...
XX Lv, XW Zhang, Z Chen, T Yun, CF Gao, YK Wang, NL Meng, WZ Zhao   +7 more
doaj   +1 more source

Crucial parameters for precise copy number variation detection in formalin‐fixed paraffin‐embedded solid cancer samples

Molecular Oncology, EarlyView.
This study shows that copy number variations (CNVs) can be reliably detected in formalin‐fixed paraffin‐embedded (FFPE) solid cancer samples using ultra‐low‐pass whole‐genome sequencing, provided that key (pre)‐analytical parameters are optimized.
Hanne Goris, Vasiliki Siozopoulou, Léon C van Kempen, Anne Sieben, Ella Roelant, Stig Hellemans, Elyne Backx, Laure Sorber, Koen De Winne, Senada Koljenović, Karen Zwaenepoel   +10 more
wiley   +1 more source

Fluorescence in situ hybridization analysis of the hTERC region in acute myeloid leukemia patients

Turkish Journal of Hematology, 2011
OBJECTIVE: The telomerase RNA component (hTERC) gene is located at 3q26. Increased hTERC gene expression has been frequently observed and amplification was shown using fluorescence in situ hybridization (FISH) in different cancers.
Özge Özer, Tuğçe Bulakbaşı Balcı, Zerrin Yılmaz, Feride İffet Şahin   +3 more
doaj   +1 more source

Gene amplifications associated with the development of hormone- resistant prostate cancer [PDF]

, 2003
Purpose: Hormone resistance remains a significant clinical problem in prostate cancer with few therapeutic options. Research into mechanisms of hormone resistance is essential.
Bartlett, J.M.S., Edwards, J., Krishnan, S., Witton, C.J.   +3 more
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