ArticleOncotarget2020
Resistance to allosteric SHP2 inhibition in FGFR-driven cancers through rapid feedback activation of FGFR.
Article in Oncotarget, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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
21 citing papers in PubMed, 40 citations in OpenAlex.
- Recent Advances in Research on SHP Family Phosphatases: Signal Regulation Mechanisms and Disease Associations.Cell biochemistry and function · 2026Review
- MBNL1 Promotes Intestinal Fibrosis via RAS-MAPK Pathway-Mediated Fibroblast Activation and Proliferation.Biomedicines · 2026Article
- Multiplexed single-cell transcriptomics reveals diverse phenotypic outcomes for pathogenic SHP2 variants.Science advances · 2026Article
- Dual inhibition of BRAF for cancer treatment: advances and therapeutic potential.Future medicinal chemistry · 2025Review
- TNO155 is a selective SHP2 inhibitor to targetHeliyon · 2024Article
- Review
- Tyrosine phosphataseFrontiers in immunology · 2024Review
- CRISPR Screening Identifies Mechanisms of Resistance to KRASG12C and SHP2 Inhibitor Combinations in Non-Small Cell Lung Cancer.Cancer research · 2023Article
- SHP2 clinical phenotype, cancer, or RASopathies, can be predicted by mutant conformational propensities.Cellular and molecular life sciences : CMLS · 2023Article
- Review
- Discovery of a SHP2 Degrader with In Vivo Anti-Tumor Activity.Molecules (Basel, Switzerland) · 2023Article
- SHP2 participates in decidualization by activating ERK to maintain normal nuclear localization of progesterone receptor.Reproduction (Cambridge, England) · 2023Article
- PI3K inhibition circumvents resistance to SHP2 blockade in metastatic triple-negative breast cancer.Journal of mammary gland biology and neoplasia · 2023Article
- Strategies to inhibit FGFR4 V550L-driven rhabdomyosarcoma.British journal of cancer · 2022Article
- Phosphorylation of SHP2 at Tyr62 Enables Acquired Resistance to SHP2 Allosteric Inhibitors in FLT3-ITD-Driven AML.Cancer research · 2022Article
- Targeted Degradation of the Oncogenic Phosphatase SHP2.Biochemistry · 2021Article
- Exceptional response to the ALK and ROS1 inhibitor lorlatinib and subsequent mechanism of resistance in relapsedCold Spring Harbor molecular case studies · 2021Article
- Diacylglycerol Kinase alpha in X Linked Lymphoproliferative Disease Type 1.International journal of molecular sciences · 2021Review
- Polyphyllin D Shows Anticancer Effect through a Selective Inhibition of Src Homology Region 2-Containing Protein Tyrosine Phosphatase-2 (SHP2).Molecules (Basel, Switzerland) · 2021Article
- Combined Inhibition of SHP2 and MEK Is Effective in Models of NF1-Deficient Malignant Peripheral Nerve Sheath Tumors.Cancer research · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SHP2 mediates RAS activation downstream of multiple receptor tyrosine kinases (RTKs) and cancer cell lines dependent on RTKs are in general dependent on SHP2. Profiling of the allosteric SHP2 inhibitor SHP099 across cancer cell lines harboring various RTK dependencies reveals that FGFR-dependent cells are often insensitive to SHP099 when compared to EGFR-dependent cells. We find that FGFR-driven cells depend on SHP2 but exhibit resistance to SHP2 inhibitors
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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.