keyword
MENU ▼
Read by QxMD icon Read
search

ERBB3 AND cancer

keyword
https://www.readbyqxmd.com/read/29683256/the-immunoglobulin-like-domain-of-neuregulins-potentiates-erbb3-her3-activation-and-cellular-proliferation
#1
Ariana Centa, Ruth Rodríguez-Barrueco, Juan Carlos Montero, Atanasio Pandiella
The Neuregulins (NRGs) represent a large family of membrane-anchored growth factors, whose deregulation may contribute to the pathogenesis of several tumours. In fact, targeting of NRG-activated pathways has demonstrated clinical benefit. To improve the efficacy of anti-NRG therapies, it is essential to gain insights into the regions of NRGs that favour their pro-oncogenic properties. Here we have addressed the protumorigenic impact of different NRG domains. To do this, deletion mutants affecting different NRG domains were expressed in 293 and MCF7 cells...
April 23, 2018: Molecular Oncology
https://www.readbyqxmd.com/read/29610121/response-to-erbb3-directed-targeted-therapy-in-nrg1-rearranged-cancers
#2
Alexander Drilon, Romel Somwar, Biju P Mangatt, Henrik Edgren, Patrice Desmeules, Anja Ruusulehto, Roger S Smith, Lukas Delasos, Morana Vojnic, Andrew J Plodkowski, Joshua Sabari, Kenneth Ng, Joseph Montecalvo, Jason Chang, Huichun Tai, William W Lockwood, Victor Martinez, Gregory J Riely, Charles M Rudin, Mark G Kris, Maria E Arcila, Christopher Matheny, Ryma Benayed, Natasha Rekhtman, Marc Ladanyi, Gopinath Ganji
NRG1 rearrangements are oncogenic drivers that are enriched in invasive mucinous adenocarcinomas (IMAs) of the lung. The oncoprotein binds ERBB3-ERBB2 heterodimers and activates downstream signaling, supporting a therapeutic paradigm of ERBB3/ERBB2 inhibition. As proof of concept, a durable response was achieved with anti-ERBB3 monoclonal antibody therapy (GSK2849330) in an exceptional responder with an NRG1-rearranged IMA on a phase 1 trial (NCT01966445). In contrast, response was not achieved with anti-ERBB2 therapy (afatinib) in four NRG1-rearranged IMA patients (including the index patient post-GSK2849330)...
April 2, 2018: Cancer Discovery
https://www.readbyqxmd.com/read/29549161/dual-inhibition-of-igf-1r-and-erbb3-enhances-the-activity-of-gemcitabine-and-nab-paclitaxel-in-preclinical-models-of-pancreatic-cancer
#3
Adam J Camblin, Emily A Pace, Sharlene Adams, Michael D Curley, Victoria Rimkunas, Lin Nie, Gege Tan, Troy Bloom, Sergio Iadevaia, Jason Baum, Charlene Minx, Akos Czibere, Chrystal U Louis, Daryl C Drummond, Ulrik B Nielsen, Birgit Schoeberl, J Marc Pipas, Robert M Straubinger, Vasileios Askoxylakis, Alexey A Lugovskoy
PURPOSE: Insulin-like growth factor receptor 1 (IGF-1R) is critically involved in pancreatic cancer pathophysiology, promoting cancer cell survival and therapeutic resistance. Assessment of IGF-1R inhibitors in combination with standard-of-care chemotherapy, however, failed to demonstrate significant clinical benefit. The aim of this work is to unravel mechanisms of resistance to IGF-1R inhibition in pancreatic cancer and develop novel strategies to improve the activity of standard-of-care therapies...
March 16, 2018: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/29545332/acquired-resistance-to-a-met-antibody-in-vivo-can-be-overcome-by-the-met-antibody-mixture-sym015
#4
Sofie Ellebæk Pollmann, Valerie S Calvert, Shruti Rao, Simina M Boca, Subha Madhavan, Ivan D Horak, Andreas Kjaer, Emanuel F Petricoin, Michael Kragh, Thomas Tuxen Poulsen
Failure of clinical trials due to development of resistance to MET-targeting therapeutic agents is an emerging problem. Mechanisms of acquired resistance to MET tyrosine kinase inhibitors are well described, whereas characterization of mechanisms of resistance toward MET-targeting antibodies is limited. This study investigated mechanisms underlying in vivo resistance to two antibody therapeutics currently in clinical development: an analogue of the MET-targeting antibody emibetuzumab and Sym015, a mixture of two antibodies targeting non-overlapping epitopes of MET...
March 15, 2018: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/29506988/phase-ii-study-of-the-dual-egfr-her3-inhibitor-duligotuzumab-mehd7945a-vs-cetuximab-in-combination-with-folfiri-in-ras-wild-type-metastatic-colorectal-cancer
#5
Andrew Graham Hill, Michael Findlay, Matthew Burge, Christopher Jackson, Pilar García Alfonso, Leslie Samuel, Vinod Ganju, Meinolf Karthaus, Alessio Amatu, Mark Jeffery, Maria Di Bartolomeo, John Bridgewater, Andrew L Coveler, Manuel Hidalgo, Amy V Kapp, Roxana Sufan, Bruce McCall, William Hanley, Elicia Penuel, Andrea Pirzkall, Josep Tabernero
PURPOSE: Duligotuzumab is a dual-action antibody directed against EGFR and HER3. EXPERIMENTAL DESIGN: mCRC patients with KRAS ex2 wild-type received duligotuzumab or cetuximab and FOLFIRI until progression or intolerable toxicity. Mandatory tumor samples underwent mutation and biomarker analysis. Efficacy analysis was conducted in patients with RAS exon 2/3 wild-type tumors. RESULTS: Of 134 randomized patients, 98 were RAS ex2/3 wild-type...
March 5, 2018: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/29453410/molecular-characterization-of-colorectal-adenomas-with-and-without-malignancy-reveals-distinguishing-genome-transcriptome-and-methylome-alterations
#6
Brooke R Druliner, Panwen Wang, Taejeong Bae, Saurabh Baheti, Seth Slettedahl, Douglas Mahoney, Nikolaos Vasmatzis, Hang Xu, Minsoo Kim, Matthew Bockol, Daniel O'Brien, Diane Grill, Nathaniel Warner, Miguel Munoz-Gomez, Kimberlee Kossick, Ruth Johnson, Mohamad Mouchli, Donna Felmlee-Devine, Jill Washechek-Aletto, Thomas Smyrk, Ann Oberg, Junwen Wang, Nicholas Chia, Alexej Abyzov, David Ahlquist, Lisa A Boardman
The majority of colorectal cancer (CRC) arises from precursor lesions known as polyps. The molecular determinants that distinguish benign from malignant polyps remain unclear. To molecularly characterize polyps, we utilized Cancer Adjacent Polyp (CAP) and Cancer Free Polyp (CFP) patients. CAPs had tissues from the residual polyp of origin and contiguous cancer; CFPs had polyp tissues matched to CAPs based on polyp size, histology and dysplasia. To determine whether molecular features distinguish CAPs and CFPs, we conducted Whole Genome Sequencing, RNA-seq, and RRBS on over 90 tissues from 31 patients...
February 16, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29434871/mechanisms-for-dna-damaging-agent-induced-inactivation-of-erbb2-and-erbb3-via-the-erk-and-p38-signaling-pathways
#7
Chul Min Park, Yuki Kawasaki, Alaa Refaat, Hiroaki Sakurai
Cisplatin (CDDP) and doxorubicin (DOX) are chemotherapeutic drugs that trigger apoptosis by inducing DNA-damage. A previous study using breast cancer cells demonstrated the negative feedback modulation of the epidermal growth factor receptor (EGFR) and receptor tyrosine-protein kinase erbB-2 (ErbB2) via extracellular signal-regulated kinase (ERK)-mediated phosphorylation of conserved Thr-669 and Thr-677 residues, respectively, in the juxtamembrane domain. In addition, CDDP has been identified to cause negative feedback inhibition of activated EGFR in lung cancer cells...
February 2018: Oncology Letters
https://www.readbyqxmd.com/read/29420467/her-kinase-inhibition-in-patients-with-her2-and-her3-mutant-cancers
#8
David M Hyman, Sarina A Piha-Paul, Helen Won, Jordi Rodon, Cristina Saura, Geoffrey I Shapiro, Dejan Juric, David I Quinn, Victor Moreno, Bernard Doger, Ingrid A Mayer, Valentina Boni, Emiliano Calvo, Sherene Loi, Albert C Lockhart, Joseph P Erinjeri, Maurizio Scaltriti, Gary A Ulaner, Juber Patel, Jiabin Tang, Hannah Beer, S Duygu Selcuklu, Aphrothiti J Hanrahan, Nancy Bouvier, Myra Melcer, Rajmohan Murali, Alison M Schram, Lillian M Smyth, Komal Jhaveri, Bob T Li, Alexander Drilon, James J Harding, Gopa Iyer, Barry S Taylor, Michael F Berger, Richard E Cutler, Feng Xu, Anna Butturini, Lisa D Eli, Grace Mann, Cynthia Farrell, Alshad S Lalani, Richard P Bryce, Carlos L Arteaga, Funda Meric-Bernstam, José Baselga, David B Solit
Somatic mutations of ERBB2 and ERBB3 (which encode HER2 and HER3, respectively) are found in a wide range of cancers. Preclinical modelling suggests that a subset of these mutations lead to constitutive HER2 activation, but most remain biologically uncharacterized. Here we define the biological and therapeutic importance of known oncogenic HER2 and HER3 mutations and variants of unknown biological importance by conducting a multi-histology, genomically selected, 'basket' trial using the pan-HER kinase inhibitor neratinib (SUMMIT; clinicaltrials...
February 8, 2018: Nature
https://www.readbyqxmd.com/read/29413684/human-epidermal-receptor-family-inhibitors-in-patients-with-erbb3-mutated-cancers-entering-the-back-door
#9
Loic Verlingue, Antoine Hollebecque, Ludovic Lacroix, Sophie Postel-Vinay, Andrea Varga, Yolla El Dakdouki, Capucine Baldini, Rastilav Balheda, Anas Gazzah, Jean-Marie Michot, Aurélien Marabelle, Olivier Mir, Monica Arnedos, Etienne Rouleau, Eric Solary, Thierry De Baere, Eric Angevin, Jean-Pierre Armand, Stefan Michiels, Fabrice André, Eric Deutsch, Jean-Yves Scoazec, Jean-Charles Soria, Christophe Massard
INTRODUCTION: Therapeutic inhibition of the human epidermal receptor 3 (ERBB3, HER3) has been challenged by the low frequency of ERBB3 somatic alterations across cancer types. We have evaluated the clinical utility to use available inhibitors of the HER family in the context of ERBB3 mutations. PATIENTS AND METHODS: In this study, we have selected patients with somatic ERBB3 alterations detected in their tumours from the molecular screening programs running at our institution...
March 2018: European Journal of Cancer
https://www.readbyqxmd.com/read/29413056/egfr-mediated-interleukin-enhancer-binding-factor-3-contributes-to-formation-and-survival-of-cancer-stem-like-tumorspheres-as-a-therapeutic-target-against-egfr-positive-non-small-cell-lung-cancer
#10
Chun-Chia Cheng, Kuei-Fang Chou, Cheng-Wen Wu, Nai-Wen Su, Cheng-Liang Peng, Ying-Wen Su, Jungshan Chang, Ai-Sheng Ho, Huan-Chau Lin, Caleb Gon-Shen Chen, Bi-Ling Yang, Yu-Cheng Chang, Ya-Wen Chiang, Ken-Hong Lim, Yi-Fang Chang
OBJECTIVES: YM155, an inhibitor of interleukin enhancer-binding factor 3 (ILF3), significantly suppresses cancer stemness property, implying that ILF3 contributes to cell survival of cancer stem cells. However, the molecular function of ILF3 inhibiting cancer stemness remains unclear. This study aimed to uncover the potential function of ILF3 involving in cell survival of epidermal growth factor receptor (EGFR)-positive lung stem-like cancer, and to investigate the potential role to improve the efficacy of anti-EGFR therapeutics...
February 2018: Lung Cancer: Journal of the International Association for the Study of Lung Cancer
https://www.readbyqxmd.com/read/29388752/iron-oxide-nanoparticles-synergize-with-erlotinib-to-suppress-refractory-non-small-cell-lung-cancer-cell-proliferation-through-the-inhibition-of-erbb-pi3k-akt-and-pten-activation
#11
Meili Zhang, Buqing Sai, Pengfei Cao, Zheng Li, Liyang Zhang, Cijun Shuai, Xinye Wang, Jia Wang, Guiyuan Li, Juanjuan Xiang, Jingqun Tang
Non-small cell lung cancer (NSCLC) accounts for 85% of lung cancer cases. EGFR tyrosine kinase inhibitors (EGFR-TKIs) such as erlotinib and gefitinib, are currently approved for the management of NSCLC. However, primary and acquired resistances to EGFR-TKIs are the major obstacles in the treatment of NSCLC. These resistances have been associated with the development of secondary mutations in EGFR or continued oncogenic signaling despite TKI treatment. In this study, NSCLC cells with wild-type EGFR, A549, H460, H358, H157 which do not respond to EGFR-TKIs, were used...
April 2017: Journal of Biomedical Nanotechnology
https://www.readbyqxmd.com/read/29383036/development-of-a-personalized-therapeutic-strategy-for-erbb-gene-mutated-cancers
#12
Malgorzata Milewska, Mattia Cremona, Clare Morgan, John O'Shea, Aoife Carr, Sri H Velanki, Ann M Hopkins, Sinead Toomey, Stephen F Madden, Bryan T Hennessy, Alex J Eustace
Background: The application of genomic technologies to patient tumor samples identified groups of signaling pathways which acquire activating mutations. Some cancers are dependent on these mutations and the aberrant proteins resulting from these mutations can be targeted by novel drugs which can eradicate the cancer. Methods: We used www.cbioportal.org to determine the frequency of ERBB mutations in solid tumors. We then determined the sensitivity of a panel of cell lines to clinically available PI3K inhibitors...
2018: Therapeutic Advances in Medical Oncology
https://www.readbyqxmd.com/read/29338072/targeting-her2-in-colorectal-cancer-the-landscape-of-amplification-and-short-variant-mutations-in-erbb2-and-erbb3
#13
Jeffrey S Ross, Marwan Fakih, Siraj M Ali, Julia A Elvin, Alexa B Schrock, James Suh, Jo-Anne Vergilio, Shakti Ramkissoon, Eric Severson, Sugganth Daniel, David Fabrizio, Garrett Frampton, James Sun, Vincent A Miller, Philip J Stephens, Laurie M Gay
BACKGROUND: In contrast to lung cancer, few precision treatments are available for colorectal cancer (CRC). One rapidly emerging treatment target in CRC is ERBB2 (human epidermal growth factor receptor 2 [HER2]). Oncogenic alterations in HER2, or its dimerization partner HER3, can underlie sensitivity to HER2-targeted therapies. METHODS: In this study, 8887 CRC cases were evaluated by comprehensive genomic profiling for genomic alterations in 315 cancer-related genes, tumor mutational burden, and microsatellite instability...
April 1, 2018: Cancer
https://www.readbyqxmd.com/read/29326437/insertional-mutagenesis-in-a-her2-positive-breast-cancer-model-reveals-eras-as-a-driver-of-cancer-and-therapy-resistance
#14
Gerjon J Ikink, Mandy Boer, Elvira R M Bakker, Annabel Vendel-Zwaagstra, Chris Klijn, Jelle Ten Hoeve, Jos Jonkers, Lodewyk F Wessels, John Hilkens
Personalized medicine for cancer patients requires a deep understanding of the underlying genetics that drive cancer and the subsequent identification of predictive biomarkers. To discover new genes and pathways contributing to oncogenesis and therapy resistance in HER2+ breast cancer, we performed Mouse Mammary Tumor Virus (MMTV)-induced insertional mutagenesis screens in ErbB2/cNeu-transgenic mouse models. The screens revealed 34 common integration sites (CIS) in mammary tumors of MMTV-infected mice, highlighting loci with multiple independent MMTV integrations in which potential oncogenes are activated, most of which had never been reported as MMTV CIS...
March 2018: Oncogene
https://www.readbyqxmd.com/read/29321661/differential-recruitment-of-cd44-isoforms-by-erbb-ligands-reveals-an-involvement-of-cd44-in-breast-cancer
#15
Iris Morath, Christian Jung, Romain Lévêque, Chen Linfeng, Robert-Alain Toillon, Arne Warth, Véronique Orian-Rousseau
Members of the CD44 family of transmembrane glycoproteins control cell signaling pathways from numerous cell surface receptors, including receptor tyrosine kinases (RTKs). The decisive factor (ligand, RTKs or both) that controls the recruitment of specific CD44 isoforms is still unknown. We investigated this question by using the EGFR signaling pathway, in which one receptor can be activated by a broad range of ligands. By means of siRNA-mediated downregulation of CD44 expression and blocking experiments, we identified CD44v6 as a co-receptor for EGF- and ER-induced ErbB1 activation and for NRG1-induced ErbB3 and ErbB4 activation...
March 2018: Oncogene
https://www.readbyqxmd.com/read/29286064/mir-152-is-involved-in-the-proliferation-and-metastasis-of-ovarian-cancer-through-repression-of-erbb3
#16
Lian-Wei Li, Hong-Qi Xiao, Rong Ma, Meng Yang, Wan Li, Ge Lou
MicroRNAs (miRNAs) participate in post-transcriptional regulation by targeting the 3' untranslated region of target genes that are involved in diverse biological processes. To the best of our knowledge, the association between miR‑152 and ERBB3 in ovarian cancer remains unclear. In the present study, a negative correlation between miR‑152 and ERBB3 in ovarian cancer was observed. The luciferase reporter gene assay results demonstrated that miR‑152 negatively regulated ERBB3 in SKOV3 and OVCAR3 ovarian cancer cells...
March 2018: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/29199595/epidermal-growth-factor-receptor-tyrosine-kinase-a-potential-target-in-treatment-of-non-small-cell-lung-carcinoma
#17
REVIEW
Venugopal Vinod Prabhu, Niranjali Devaraj
Lung cancer is responsible for 1.6 million deaths. Approximately 80%-85% of lung cancers are of the non-small-cell variety, which includes squamous cell carcinoma, adenocarcinoma, and large-cell carcinoma. Knowing the stage of cancer progression is a requisite for determining which management approach-surgery, chemotherapy, radiotherapy, and/or immunotherapy-is optimal. Targeted therapeutic approaches with antiangiogenic monoclonal antibodies or tyrosine kinase inhibitors are one option if tumors harbor oncogene mutations...
2017: Journal of Environmental Pathology, Toxicology and Oncology
https://www.readbyqxmd.com/read/29182685/mir205-inhibits-stem-cell-renewal-in-sum159pt-breast-cancer-cells
#18
Víctor Mayoral-Varo, Annarica Calcabrini, María Pilar Sánchez-Bailón, Jorge Martín-Pérez
miR205 has a dual activity, as tumor suppressor and as oncogene. Here we analyzed the impact of miR205 ectopic expression in the initial tumorigenic processes of SUM159PT, a triple negative breast cancer cell line with low endogenous levels of miR205. In SUM159PT, miR205 inhibited expression of its targets VEGFA, ErbB3, Zeb1, Fyn and Lyn A/B; it reduced cell proliferation, and Myc/cyclin D1 levels, while increased p27kip1 expression. miR205 abolished anchorage-independent growth, inhibited migration and invasion, Src-kinases/Stat3 axis activation, and levels of secreted MMP9...
2017: PloS One
https://www.readbyqxmd.com/read/29113229/fatty-acid-synthase-affects-expression-of-erbb-receptors-in-epithelial-to-mesenchymal-transition-of-breast-cancer-cells-and-invasive-ductal-carcinoma
#19
Tingting Chen, Lan Zhou, Hua Li, Yuan Tian, Junqin Li, Lihua Dong, Yuhua Zhao, Dapeng Wei
The aim of the present study was to investigate changes in the expression of ErbBs during epithelial-mesenchymal transition (EMT) of breast cancer cells and its association with the expression of fatty acid synthase (FASN). MCF-7-MEK5 cells were used as the experimental model, while MCF-7 cells were used as a control. Tumor cells were implanted into nude mice for in vivo analysis. Cerulenin was used as a FASN inhibitor. Reverse transcription-polymerase chain reaction and western blot analysis were used to detect expression levels of FASN and ErbB1-4...
November 2017: Oncology Letters
https://www.readbyqxmd.com/read/29080385/evaluation-of-patritumab-with-or-without-erlotinib-in-combination-with-standard-cytotoxic-agents-against-pediatric-sarcoma-xenograft-models
#20
Abhik Bandyopadhyay, Edward Favours, Doris A Phelps, Vanessa Del Pozo, Samson Ghilu, Dias Kurmashev, Joel Michalek, Aron Trevino, Denis Guttridge, Cheryl London, Kenji Hirotani, Ling Zhang, Raushan T Kurmasheva, Peter J Houghton
BACKGROUND: Integrating molecularly targeted agents with cytotoxic drugs used in curative treatment of pediatric cancers is complex. An evaluation was undertaken with the ERBB3/Her3-specific antibody patritumab (P) either alone or with the ERBB1/epidermal growth factor receptor inhibitor erlotinib (E) in combination with standard cytotoxic agents, cisplatin, vincristine, and cyclophosphamide, in pediatric sarcoma xenograft models that express receptors and ligands targeted by these agents...
February 2018: Pediatric Blood & Cancer
keyword
keyword
119202
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"