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Paper · 15313890

SPRY2 is an inhibitor of the ras/extracellular signal-regulated kinase pathway in melanocytes and melanoma cells with wild-type BRAF but not with the V599E mutant.

Tsavachidou D and 6 others. Cancer Res, 2004. Cited by 98 papers, by iCite.

11 sourcespapers-2026-11-12-0.1.0

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ConductScience Library. SPRY2 is an inhibitor of the ras/extracellular signal-regulated kinase pathway in melanocytes and melanoma cells with wild-type BRAF but not with the V599E mutant. Papers, record 15313890. Release papers-2026-11-12-0.1.0, 12 Nov 2026. https://conductscience.org/library/papers/15313890

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Paper

PubMed's record of the paper, with iCite's citation figures. No abstract is shown.

Title
SPRY2 is an inhibitor of the ras/extracellular signal-regulated kinase pathway in melanocytes and melanoma cells with wild-type BRAF but not with the V599E mutant.
PubMed
Journal
Cancer Res
PubMed
Year
2004
PubMed
Publication types
Journal Article, Research Support, U.S. Gov't, P.H.S.
PubMed
Citations, by iCite
98
iCite
Relative citation ratio, by iCite
1.64
iCite
Revised in PubMed
2014-11-20
PubMed

Authors7

The authors in the order PubMed's record lists them, with the ORCID iDs it states.

OrderAuthorForenameKindORCID iD
1Tsavachidou DDimitra
2Coleman MLMathew L
3Athanasiadis GGalene
4Li SShuixing
5Licht JDJonathan D
6Olson MFMichael F
7Weber BLBarbara L

Source PubMed

Topics18

NLM's MeSH indexing of the paper, its major topics first.

MeSH termMajor
MelanocytesMajor topic
MelanomaMajor topic
Mitogen-Activated Protein KinasesMajor topic
ProteinsMajor topic
Proto-Oncogene Proteins c-rafMajor topic
ras ProteinsMajor topic
Cell Line, Tumor
Gene Expression Profiling
Humans
Intracellular Signaling Peptides and Proteins
MAP Kinase Signaling System
Membrane Proteins
Mutation
Oligonucleotide Array Sequence Analysis
Protein Biosynthesis
Proto-Oncogene Proteins B-raf
RNA, Small Interfering
Transfection

Source PubMed

Grants3

Each grant PubMed's record writes, matched to the NIH project NIH's grant and paper links name for this paper, and each of those links the record does not write.

Grant, as the record writes itAgencyCountryNIH projectStated bySource
CA030721-01A1NCI NIH HHSUnited StatesPubMedPubMed
CA59998NCI NIH HHSUnited StatesR01CA059998PubMed and NIHNIH RePORTER
R01CA030721NIHNIH RePORTER

Trials0

The trials whose ClinicalTrials.gov record lists the paper, and the trial numbers the paper's PubMed record names.

None in this release.

Comments and corrections0

PubMed's comments and corrections, NLM's own indexing: retractions first, then expressions of concern, errata and updates, and comments last.

None in this release.

References0

The papers the reference list in PubMed's record names, those in our copy of PubMed, in the list's order.

None in this release.

Cited by62

The papers in our copy of PubMed whose reference list names this one, newest first. iCite, which reads more sources, counts 98 citations.

PMIDTitleJournalYearIn PapersSource
42,979,327Concurrent loss of RB1 facilitates EGFR-TKI resistance in EGFR-mutant lung cancer by modulating histone crotonylation.Acta Pharm Sin B2026https://conductscience.org/library/papers/42979327PubMed
39,494,610Model ensembling as a tool to form interpretable multi-omic predictors of cancer pharmacosensitivity.Brief Bioinform2024https://conductscience.org/library/papers/39494610PubMed
38,012,755Therapeutic effect and transcriptome-methylome characteristics of METTL3 inhibition in liver hepatocellular carcinoma.Cancer Cell Int2023https://conductscience.org/library/papers/38012755PubMed
37,845,209TRAF7-targeted HOXA5 acts as a tumor suppressor in prostate cancer progression and stemness via transcriptionally activating SPRY2 and regulating MEK/ERK signaling.Cell Death Discov2023https://conductscience.org/library/papers/37845209PubMed
37,444,145Examining the Effects of Gestational Physical Activity and Hofbauer Cell Polarization on Angiogenic Factors.Int J Environ Res Public Health2023https://conductscience.org/library/papers/37444145PubMed
36,765,910ABL1/2 and DDR1 Drive MEKi Resistance in NRAS-Mutant Melanomas by Stabilizing RAF/MYC/ETS1 and Promoting RAF Homodimerization.Cancers (Basel)2023https://conductscience.org/library/papers/36765910PubMed
36,139,698RNA-seq and ChIP-seq Identification of Unique and Overlapping Targets of GLI Transcription Factors in Melanoma Cell Lines.Cancers (Basel)2022https://conductscience.org/library/papers/36139698PubMed
35,707,123The DNA methylation landscape of five pediatric-tumor types.PeerJ2022https://conductscience.org/library/papers/35707123PubMed
35,116,291The role of TRIM51 as a multipurpose biomarker in melanoma.Transl Cancer Res2021https://conductscience.org/library/papers/35116291PubMed
34,048,471Sprouty4 negatively regulates ERK/MAPK signaling and the transition from in situ to invasive breast ductal carcinoma.PLoS One2021https://conductscience.org/library/papers/34048471PubMed

1 to 10 of 62

See all 62 cited by

Genes5

The genes the Gene search release ties to the paper: Swiss-Prot's references first, then PubTator's text mining.

GeneNCBI Gene IDLinked byIn GenesSource
BRAF673PubTator's text mininghttps://conductscience.org/library/genes/673NCBI Gene
MAPK15,594PubTator's text mininghttps://conductscience.org/library/genes/5594NCBI Gene
RAF15,894PubTator's text mininghttps://conductscience.org/library/genes/5894NCBI Gene
SPRY210,253PubTator's text mininghttps://conductscience.org/library/genes/10253NCBI Gene
SPRY481,848PubTator's text mininghttps://conductscience.org/library/genes/81848NCBI Gene

Drugs0

The drugs whose trials, in the Pipelines release, list the paper.

None in this release.

Data0

The data bank entries PubMed's record names. Trial numbers are under Trials.

None in this release.

Data dates

The date of each source this release read.

PubMed
2026-11-06
PubMed
iCite
2026-11-05
iCite
PMC's ID file
2026-11-05
PMC's ID file
NIH RePORTER's grant and paper links
2026-11-01
NIH RePORTER's grant and paper links
Trials
2026-11-12
Gene search
2026-11-11
Pipelines
2026-09-18

Sources 11

  • ChEMBL, through Open TargetsCC BY-SA 3.0
  • ClinicalTrials.govNo license stated
  • HGNCCC0
  • iCiteCC BY 4.0
  • NCBI GenePublic domain (US government)
  • NIH RePORTER's grant and paper linksPublic domain
  • Open TargetsCC0 1.0
  • PMC's ID filePublic domain (US government)
  • PubMedNLM's terms
  • PubTator 3Public domain
  • UniProtCC BY 4.0
Each source's terms
  • ChEMBL, through Open TargetsCC BY-SA 3.0, for the parts from ChEMBL. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
  • ClinicalTrials.govnone stated
  • HGNCCC0: https://www.genenames.org/about/license/
  • iCiteCC BY 4.0
  • NCBI GeneNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
  • NIH RePORTER's grant and paper linksPublic domain (NIH RePORTER)
  • Open TargetsCC0 1.0. Open Targets asks that users cite its latest paper: Buniello et al. 2025, Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery, Nucleic Acids Research 53(D1):D1467, PMID 39657122. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
  • PMC's ID fileNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
  • PubMedNLM's terms
  • PubTator 3Public domain
  • UniProtCC BY 4.0. UniProt's licence file: "All databases and documents in the UniProt FTP directory may be copied and redistributed freely, without advance permission, provided that this copyright statement is reproduced with each copy." UniProt asks that users cite its latest paper: The UniProt Consortium, UniProt: the Universal Protein Knowledgebase in 2025, Nucleic Acids Research 53:D609-D617, https://doi.org/10.1093/nar/gkae1010. Read on 9 Nov 2026 at https://www.uniprot.org/help/license

ClinicalTrials.gov's data carry an international copyright outside the United States: https://clinicaltrials.gov/about-site/terms-conditions.

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