Benjamin Solomon

ORCID: 0000-0003-3059-5730
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Lung Cancer Treatments and Mutations
  • Lung Cancer Research Studies
  • Colorectal Cancer Treatments and Studies
  • Lung Cancer Diagnosis and Treatment
  • Cancer Genomics and Diagnostics
  • Cancer Immunotherapy and Biomarkers
  • Head and Neck Cancer Studies
  • Cancer, Hypoxia, and Metabolism
  • Gastric Cancer Management and Outcomes
  • Lymphoma Diagnosis and Treatment
  • Cancer therapeutics and mechanisms
  • RNA modifications and cancer
  • Immunotherapy and Immune Responses
  • CAR-T cell therapy research
  • Cholangiocarcinoma and Gallbladder Cancer Studies
  • Radiomics and Machine Learning in Medical Imaging
  • Brain Metastases and Treatment
  • Telomeres, Telomerase, and Senescence
  • Epigenetics and DNA Methylation
  • HER2/EGFR in Cancer Research
  • Pancreatic and Hepatic Oncology Research
  • Colorectal and Anal Carcinomas
  • Neuroendocrine Tumor Research Advances
  • Medical Imaging Techniques and Applications
  • Thyroid Cancer Diagnosis and Treatment

Peter MacCallum Cancer Centre
2016-2025

The University of Melbourne
2016-2025

Addis Ababa University
2025

Guangdong Academy of Medical Sciences
2018-2024

Cancer Services
2024

U-M Rogel Cancer Center
2020-2024

Imperial College London
2024

Southern Medical University
2024

Fudan University
2024

Zhongshan Hospital
2024

Oncogenic fusion genes consisting of EML4 and anaplastic lymphoma kinase (ALK) are present in a subgroup non-small-cell lung cancers, representing 2 to 7% such tumors. We explored the therapeutic efficacy inhibiting ALK tumors an early-phase clinical trial crizotinib (PF-02341066), orally available small-molecule inhibitor tyrosine kinase.After screening tumor samples from approximately 1500 patients with cancer for presence rearrangements, we identified 82 advanced ALK-positive disease who...

10.1056/nejmoa1006448 article EN New England Journal of Medicine 2010-10-27

In single-group studies, chromosomal rearrangements of the anaplastic lymphoma kinase gene (ALK) have been associated with marked clinical responses to crizotinib, an oral tyrosine inhibitor targeting ALK. Whether crizotinib is superior standard chemotherapy respect efficacy unknown.

10.1056/nejmoa1214886 article EN New England Journal of Medicine 2013-06-01

The efficacy of the ALK inhibitor crizotinib as compared with standard chemotherapy first-line treatment for advanced ALK-positive non-small-cell lung cancer (NSCLC) is unknown.We conducted an open-label, phase 3 trial comparing in 343 patients nonsquamous NSCLC who had received no previous systemic disease. Patients were randomly assigned to receive oral at a dose 250 mg twice daily or intravenous (pemetrexed, 500 per square meter body-surface area, plus either cisplatin, 75 meter,...

10.1056/nejmoa1408440 article EN New England Journal of Medicine 2014-12-03

10.1038/nature14664 article EN Nature 2015-07-10

The EML4-ALK fusion oncogene represents a novel molecular target in small subset of non-small-cell lung cancers (NSCLC). To aid identification and treatment these patients, we examined the clinical characteristics outcomes patients who had NSCLC with without EML4-ALK.Patients were selected for genetic screening on basis two or more following characteristics: female sex, Asian ethnicity, never/light smoking history, adenocarcinoma histology. was identified by using fluorescent situ...

10.1200/jco.2009.22.6993 article EN Journal of Clinical Oncology 2009-08-11

Chromosomal rearrangements of the gene encoding ROS1 proto-oncogene receptor tyrosine kinase (ROS1) define a distinct molecular subgroup non-small-cell lung cancers (NSCLCs) that may be susceptible to therapeutic inhibition. Crizotinib is small-molecule inhibitor anaplastic lymphoma (ALK), ROS1, and another kinase, MET.

10.1056/nejmoa1406766 article EN New England Journal of Medicine 2014-09-27

Non-small-cell lung cancer (NSCLC) harboring the anaplastic lymphoma kinase gene (ALK) rearrangement is sensitive to ALK inhibitor crizotinib, but resistance invariably develops. Ceritinib (LDK378) a new that has shown greater antitumor potency than crizotinib in preclinical studies.In this phase 1 study, we administered oral ceritinib doses of 50 750 mg once daily patients with advanced cancers genetic alterations ALK. In an expansion received maximum tolerated dose. Patients were assessed...

10.1056/nejmoa1311107 article EN New England Journal of Medicine 2014-03-26
Martin Peifer Lynnette Fernández-Cuesta Martin L. Sos Julie George Danila Seidel and 88 more Lawryn H. Kasper Dennis Plenker Frauke Leenders Ruping Sun Thomas Zander Roopika Menon Mirjam Koker Ilona Dahmen Christian Müller Vincenzo Di Cerbo Hans‐Ulrich Schildhaus Janine Altmüller Ingelore Baessmann Christian Becker Bram De Wilde Jo Vandesompele Diana Böhm Sascha Ansén Franziska Gabler Ines Wilkening Stefanie Heynck Johannes M. Heuckmann Xin Lü Scott L. Carter Kristian Cibulskis Shantanu Banerji Gad Getz Kwon-Sik Park Daniel Rauh Christian Grütter Matthias Fischer Laura Pasqualucci Gavin Wright Zoe Wainer Prudence A. Russell Iver Petersen Yuan Chen Erich Stoelben Corinna Ludwig Philipp A. Schnabel Hans Hoffmann Thomas Muley Michael Brockmann Walburga Engel-Riedel Lucia Anna Muscarella Vito Michele Fazio Harry J.M. Groen Wim Timens Hannie Sietsma Erik Thunnissen Egbert F. Smit Daniëlle A.M. Heideman Peter J.F. Snijders Federico Cappuzzo Claudia Ligorio Stefania Damiani John K. Field Steinar Solberg Odd Terje Brustugun Marius Lund‐Iversen Jörg Sänger Joachim H. Clement Alex Soltermann Holger Moch Walter Weder Benjamin Solomon Jean‐Charles Soria Pierre Validire Benjamin Besse Élisabeth Brambilla Christian Brambilla Sylvie Lantuéjoul Philippe Lorimier Peter M. Schneider Michael Hallek William Pao Matthew Meyerson Julien Sage Jay Shendure Robert C. Schneider Reinhard Büttner Jürgen Wolf Peter Nürnberg Sven Perner Lukas C. Heukamp Paul K. Brindle Stefan A. Haas Roman K. Thomas

10.1038/ng.2396 article EN Nature Genetics 2012-09-02

Multiple mechanisms of crizotinib resistance were identified in lung cancer patients including new secondary ALK mutations and activation receptor tyrosine kinases.

10.1126/scitranslmed.3003316 article EN Science Translational Medicine 2012-01-26

Lorlatinib, a third-generation inhibitor of anaplastic lymphoma kinase (ALK), has antitumor activity in previously treated patients with ALK-positive non–small-cell lung cancer (NSCLC). The efficacy lorlatinib, as compared that crizotinib, first-line treatment for advanced NSCLC is unclear.

10.1056/nejmoa2027187 article EN New England Journal of Medicine 2020-11-18

Context.— In 2013, an evidence-based guideline was published by the College of American Pathologists, International Association for Study Lung Cancer, and Molecular Pathology to set standards molecular analysis lung cancers guide treatment decisions with targeted inhibitors. New evidence has prompted evaluation additional laboratory technologies, targetable genes, patient populations, tumor types testing. Objective.— To systematically review update 2013 affirm its validity; assess new...

10.5858/arpa.2017-0388-cp article EN Archives of Pathology & Laboratory Medicine 2018-01-22

To determine the prognostic importance of p16 and human papillomavirus (HPV) in patients with oropharyngeal cancer treated on a phase III concurrent chemoradiotherapy trial.Patients stage or IV head neck squamous cell were randomly assigned to radiotherapy cisplatin without tirapazamine. In this substudy, analyses restricted cancer. was detected by immunohistochemistry, HPV situ hybridization polymerase chain reaction.Slides available for assay 206 465 patients, which 185 eligible, evaluable...

10.1200/jco.2010.29.2904 article EN Journal of Clinical Oncology 2010-08-10

RET fusions are oncogenic drivers in 1 to 2% of non-small-cell lung cancers (NSCLCs). In patients with fusion-positive NSCLC, the efficacy and safety selective inhibition unknown.We enrolled advanced NSCLC who had previously received platinum-based chemotherapy those were untreated separately a phase 1-2 trial selpercatinib. The primary end point was an objective response (a complete or partial response) as determined by independent review committee. Secondary points included duration...

10.1056/nejmoa2005653 article EN New England Journal of Medicine 2020-08-26

Non-small-cell lung cancer (NSCLC) with a mutation in the gene encoding epidermal growth factor receptor (EGFR) is sensitive to approved EGFR inhibitors, but resistance develops, mediated by T790M most cases. Rociletinib (CO-1686) an inhibitor active preclinical models of EGFR-mutated NSCLC or without T790M.In this phase 1-2 study, we administered rociletinib patients who had disease progression during previous treatment existing inhibitor. In expansion (phase 2) part T790M-positive received...

10.1056/nejmoa1413654 article EN New England Journal of Medicine 2015-04-29

Crizotinib is an oral kinase inhibitor approved for the treatment of ALK-rearranged non-small-cell lung cancer (NSCLC). The clinical benefits crizotinib in patients with brain metastases have not been previously studied.Patients advanced NSCLC enrolled onto trial PROFILE 1005 or 1007 (randomly assigned to crizotinib) were included this retrospective analysis. Patients asymptomatic (nontarget target lesions) allowed enroll. Tumor assessments evaluated every 6 weeks using RECIST (version...

10.1200/jco.2014.59.0539 article EN Journal of Clinical Oncology 2015-01-27
Coming Soon ...