ArticleThe Journal of clinical investigation2012
FAM83B mediates EGFR- and RAS-driven oncogenic transformation.
Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 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
76 citing papers in PubMed, 133 citations in OpenAlex.
- Nucleoporin TPR integrates MAPK signaling with mitogen-induced transcriptional programs.Cell death & disease · 2026Article
- FAM83A is a prognostic biomarker for lung squamous cell carcinoma and correlated with immunoregulation.Scientific reports · 2025Article
- The complex role and molecular mechanism of family with sequence similarity genes in cancer: a comprehensive review.Discover oncology · 2025Review
- Comprehensive analysis of FAM83B in pan-cancer and preliminary exploration in esophageal squamous cell carcinoma.Journal of molecular histology · 2025Article
- Construction of a Prognostic Model for Cervical Cancer Related to lncRNA Based on Differential Co-expression Network and Functional Study of Key Gene EGFR-AS1.Journal of Cancer · 2025Article
- Zebrafish reveal new roles for Fam83f in hatching and the DNA damage-mediated autophagic response.Open biology · 2024Article
- FAM83B regulates mitochondrial metabolism and anti-apoptotic activity in pulmonary adenocarcinoma.Apoptosis : an international journal on programmed cell death · 2024Article
- Advances in research on autophagy mechanisms in resistance to endometrial cancer treatment.Frontiers in oncology · 2024Review
- Consensus clustering methodology to improve molecular stratification of non-small cell lung cancer.Scientific reports · 2023Article
- Lovastatin inhibits erythroleukemia progression through KLF2-mediated suppression of MAPK/ERK signaling.BMC cancer · 2023Article
- B-lymphoid tyrosine kinase-mediated FAM83A phosphorylation elevates pancreatic tumorigenesis through interacting with β-catenin.Signal transduction and targeted therapy · 2023Article
- FAM83B promotes the invasion of primary lung adenocarcinoma via PI3K/AKT/NF-κB pathway.BMC pulmonary medicine · 2023Article
- Involvement of FAM83 Family Proteins in the Development of Solid Tumors: An Update Review.Journal of Cancer · 2023Review
- Comprehensive analysis of the expression, prognostic significance, and function of FAM83 family members in breast cancer.World journal of surgical oncology · 2022Article
- FAM83B is involved in thyroid cancer cell differentiation and migration.Scientific reports · 2022Article
- Validation-Based Insertional Mutagenesis (VBIM), A Powerful Forward Genetic Screening Strategy.Current protocols · 2022Review
- FAM83A is a potential biomarker for breast cancer initiation.Biomarker research · 2022Article
- Aberrant epigenetic and transcriptional events associated with breast cancer risk.Clinical epigenetics · 2022Article
- Pan-cancer analysis of the FAM83 family and its association with prognosis and tumor microenvironment.Frontiers in genetics · 2022Article
- Pan-cancer and single-cell analysis revealsFrontiers in genetics · 2022Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Aberrant regulation of growth signaling is a hallmark of cancer development that often occurs through the constitutive activation of growth factor receptors or their downstream effectors. Using validation-based insertional mutagenesis (VBIM), we identified family with sequence similarity 83, member B (FAM83B), based on its ability to substitute for RAS in the transformation of immortalized human mammary epithelial cells (HMECs). We found that FAM83B coprecipitated with a downstream effector of RAS, CRAF. Binding of FAM83B with CRAF disrupted CRAF/14-3-3 interactions and increased CRAF membrane localization, resulting in elevated MAPK and mammalian target of rapamycin (mTOR) signaling. Ablation of FAM83B inhibited the proliferation and malignant phenotype of tumor-derived cells or RAS-transformed HMECs, implicating FAM83B as a key intermediary in EGFR/RAS/MAPK signaling. Analysis of human tumor specimens revealed that FAM83B expression was significantly elevated in cancer and was associated with specific cancer subtypes, increased tumor grade, and decreased overall survival. Cumulatively, these results suggest that FAM83B is an oncogene and potentially represents a new target for therapeutic intervention.
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.