ReviewBiochemical Society transactions2018
The role of Rac in tumor susceptibility and disease progression: from biochemistry to the clinic.
Review in Biochemical Society transactions, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 69 citations in OpenAlex.
- FARP1 mediates cMET-driven motility in androgen-independent prostate cancer cells.Endocrinology · 2026Article
- WNT signaling in cancer: molecular mechanisms and potential therapies.Molecular biomedicine · 2025Review
- VAV2 Drives EGFR-Mediated Rac1 Responses in Prostate Cancer.Molecular cancer research : MCR · 2025Article
- Morphological control of merlin-Rac antagonism in proliferation-promoting signaling.Science signaling · 2025Article
- RAC1 signaling in prostate cancer: VAV GEFs take center stage.Frontiers in cell and developmental biology · 2025Article
- Unveiling the role of RAC3 in the growth and invasion of cisplatin-resistant bladder cancer cells.Journal of cellular and molecular medicine · 2024Article
- The Rac inhibitor HV-107 as a potential therapeutic for metastatic breast cancer.Molecular medicine (Cambridge, Mass.) · 2023Article
- Rac and Cdc42 inhibitors reduce macrophage function in breast cancer preclinical models.Frontiers in oncology · 2023Article
- Rac1 as a Target to Treat Dysfunctions and Cancer of the Bladder.Biomedicines · 2022Review
- Detecting Blood Methylation Signatures in Response to Childhood Cancer Radiotherapy via Machine Learning Methods.Biology · 2022Article
- The emerging roles of srGAPs in cancer.Molecular biology reports · 2022Review
- FARP1, ARHGEF39, and TIAM2 are essential receptor tyrosine kinase effectors for Rac1-dependent cell motility in human lung adenocarcinoma.Cell reports · 2021Article
- Fermitin family member 2 promotes melanoma progression by enhancing the binding of p-α-Pix to Rac1 to activate the MAPK pathway.Oncogene · 2021Article
- Rac inhibition as a novel therapeutic strategy for EGFR/HER2 targeted therapy resistant breast cancer.BMC cancer · 2021Article
- β-Pix-dependent cellular protrusions propel collective mesoderm migration in the mouse embryo.Nature communications · 2020Article
- The Small GTPase RAC1B: A Potent Negative Regulator of-and Useful Tool to Study-TGFβ Signaling.Cancers · 2020Review
- Evaluation of active Rac1 levels in cancer cells: A case of misleading conclusions from immunofluorescence analysis.The Journal of biological chemistry · 2020Article
- Review
- Article
- Identification of a truncated β1-chimaerin variant that inactivates nuclear Rac1.The Journal of biological chemistry · 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
7 authors at 1 institution in 1 country.
Funding
Abstract
The family of Rho GTPases are involved in the dynamic control of cytoskeleton reorganization and other fundamental cellular functions, including growth, motility, and survival. Rac1, one of the best characterized Rho GTPases, is an established effector of receptors and an important node in signaling networks crucial for tumorigenesis and metastasis. Rac1 hyperactivation is common in human cancer and could be the consequence of overexpression, abnormal upstream inputs, deregulated degradation, and/or anomalous intracellular localization. More recently, cancer-associated gain-of-function mutations in Rac1 have been identified which contribute to tumor phenotypes and confer resistance to targeted therapies. Deregulated expression/activity of Rac guanine nucleotide exchange factors responsible for Rac activation has been largely associated with a metastatic phenotype and drug resistance. Translating our extensive knowledge in Rac pathway biochemistry into a clinical setting still remains a major challenge; nonetheless, remarkable opportunities for cancer therapeutics arise from promising lead compounds targeting Rac and its effectors.
Indexed as
Identifiers
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.