ReviewNature reviews. Clinical oncology2013
Safety and feasibility of targeted agent combinations in solid tumours.
Review in Nature reviews. Clinical oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Does the addition of drugs targeting the vascular endothelial growth factor pathway to first-line chemotherapy increase complete response? A meta-analysis of randomized clinical trials.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Pooled it
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- Inhibition of the RAF/MEK/ERK Signaling Cascade in Pancreatic Cancer: Recent Advances and Future Perspectives.International journal of molecular sciences · 2024Review
- Disrupting cellular memory to overcome drug resistance.Nature communications · 2023Article
- The role of macrophages in non-small cell lung cancer and advancements in 3D co-cultures.eLife · 2023Article
- The Next Generation of KRAS Targeting: Reasons for Excitement and Concern.Molecular cancer therapeutics · 2022Review
- Prognostic comparative genes predict targets for sorafenib combination therapies in hepatocellular carcinoma.Computational and structural biotechnology journal · 2022Article
- Inhibition of cytoplasmic EZH2 induces antitumor activity through stabilization of the DLC1 tumor suppressor protein.Nature communications · 2021Article
- Lack of predictive tools for conventional and targeted cancer therapy: Barriers to biomarker development and clinical translation.Advanced drug delivery reviews · 2021Review
- driveR: a novel method for prioritizing cancer driver genes using somatic genomics data.BMC bioinformatics · 2021Article
- Targeted drug delivery strategies for precision medicines.Nature reviews. Materials · 2021Article
- PRODIGY: personalized prioritization of driver genes.Bioinformatics (Oxford, England) · 2020Article
- CLytA-DAAO, Free and Immobilized in Magnetic Nanoparticles, induces Cell Death in Human Cancer Cells.Biomolecules · 2020Article
- A Phase I/II first-line study of R-CHOP plus B-cell receptor/NF-κB-double-targeting to molecularly assess therapy response.International journal of hematologic oncology · 2019Article
- Overcoming the challenges of cancer drug resistance through bacterial-mediated therapy.Chronic diseases and translational medicine · 2019Article
- let‑7 and miR‑17 promote self‑renewal and drive gefitinib resistance in non‑small cell lung cancer.Oncology reports · 2019Article
- Polytherapy and Targeted Cancer Drug Resistance.Trends in cancer · 2019Review
- A Phase I Study of Ganetespib and Ziv-Aflibercept in Patients with Advanced Carcinomas and Sarcomas.The oncologist · 2018Article
- Exploiting vulnerabilities in cancer signalling networks to combat targeted therapy resistance.Essays in biochemistry · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The plethora of novel molecular-targeted agents (MTAs) has provided an opportunity to selectively target pathways involved in carcinogenesis and tumour progression. Combination strategies of MTAs are being used to inhibit multiple aberrant pathways in the hope of optimizing antitumour efficacy and to prevent development of resistance. While the selection of specific agents in a given combination has been based on biological considerations (including the role of the putative targets in cancer) and the interactions of the agents used in combination, there has been little exploration of the possible enhanced toxicity of combinations resulting from alterations in multiple signalling pathways in normal cell biology. Owing to the complex networks and crosstalk that govern normal and tumour cell proliferation, inhibiting multiple pathways with MTA combinations can result in unpredictable disturbances in normal physiology. This Review focuses on the main toxicities and the lack of tolerability of some common MTA combinations, particularly where evidence of enhanced toxicity compared to either agent alone is documented or there is development of unexpected toxicity. Toxicities caused by MTA combinations highlight the need to introduce new preclinical testing paradigms early in the drug development process for the assessment of chronic toxicities resulting from such combinations.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.