In cancer drug resistance, germline matters too.

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

11 citing papers in PubMed.

1. Understanding of Immune Escape Mechanisms and Advances in Cancer Immunotherapy.Journal of oncology · 2022
   Review
2. The pharmacogenomics of drug resistance to protein kinase inhibitors.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2016
   Review
3. NF-κB-driven suppression of FOXO3a contributes to EGFR mutation-independent gefitinib resistance.Proceedings of the National Academy of Sciences of the United States of America · 2016
   Article
4. Epidermal growth factor receptor mutations in lung adenocarcinoma.Laboratory investigation; a journal of technical methods and pathology · 2014
   Review
5. Pharmacogenomics in oncology care.Frontiers in genetics · 2014
   Review
6. Network-based drug discovery by integrating systems biology and computational technologies.Briefings in bioinformatics · 2013
   Article
7. PUMA and BIM are required for oncogene inactivation-induced apoptosis.Science signaling · 2013
   Article
8. A mechanism of resistance to gefitinib mediated by cellular reprogramming and the acquisition of an FGF2-FGFR1 autocrine growth loop.Oncogenesis · 2013
   Article
9. Bim, a proapoptotic protein, up-regulated via transcription factor E2F1-dependent mechanism, functions as a prosurvival molecule in cancer.The Journal of biological chemistry · 2013
   Article
10. The EphB4 receptor tyrosine kinase promotes lung cancer growth: a potential novel therapeutic target.PloS one · 2013
    Article
11. Single nucleotide polymorphisms (SNPs) in non-small cell lung cancer (NSCLC) patients.The oncologist · 2012
    Article

Corrections and comments

• Comment on
  A common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer.2012

Authors and funding

2 authors.

Funding

No grant is acknowledged in the PubMed record.

Abstract

PubMed holds no abstract for this paper.

Indexed as