ArticleScientific reports2019
A FAM83A Positive Feed-back Loop Drives Survival and Tumorigenicity of Pancreatic Ductal Adenocarcinomas.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 59 citations in OpenAlex.
- ARHGAP11A affects lung adenocarcinoma (LUAD) and pancreatic adenocarcinoma (PAAD) progression by regulating FAM83A.Translational cancer research · 2026Article
- FAM83A may serve as a potential prognostic indicator for stomach adenocarcinoma.Translational cancer research · 2025Article
- The complex role and molecular mechanism of family with sequence similarity genes in cancer: a comprehensive review.Discover oncology · 2025Review
- Multi-omics integration and machine learning uncover molecular basal-like subtype of pancreatic cancer and implicate A2ML1 in promoting tumor epithelial-mesenchymal transition.Journal of translational medicine · 2025Article
- Application of integrin subunit genes in pancreatic cancer and the construction of a prognosis model.Journal of gastrointestinal oncology · 2024Article
- Diagnostic value of immune-related biomarker FAM83A in differentiating malignant from benign pleural effusion in lung adenocarcinoma.Discover oncology · 2024Article
- Integrated whole-exome and bulk transcriptome sequencing delineates the dynamic evolution from preneoplasia to invasive lung adenocarcinoma featured with ground-glass nodules.Cancer medicine · 2024Article
- Multi-modal domain adaptation for revealing spatial functional landscape from spatially resolved transcriptomics.Briefings in bioinformatics · 2024Article
- Reconstitution of human PDAC using primary cells reveals oncogenic transcriptomic features at tumor onset.Nature communications · 2024Article
- Lovastatin inhibits erythroleukemia progression through KLF2-mediated suppression of MAPK/ERK signaling.BMC cancer · 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
- Article
- 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
- The Role of Feedback Loops in Targeted Therapy for Pancreatic Cancer.Frontiers in oncology · 2022Review
- Machine learning and BP neural network revealed abnormal B cell infiltration predicts the survival of lung cancer patients.Frontiers in oncology · 2022Article
- LncRNA FAM83A-AS1 promotes lung adenocarcinoma progression by enhancing the pre-mRNA stability of FAM83A.Thoracic cancer · 2021Article
- FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma.Oncology letters · 2021Article
- A Cancer Cell Cluster Marked by LincRNAFrontiers in oncology · 2021Article
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
Pancreatic ductal adenocarcinomas (PDAC) are deadly on account of the delay in diagnosis and dearth of effective treatment options for advanced disease. The insurmountable hurdle of targeting oncogene KRAS, the most prevalent genetic mutation in PDAC, has delayed the availability of targeted therapy for PDAC patients. An alternate approach is to target other tumour-exclusive effector proteins important in RAS signalling. The Family with Sequence Similarity 83 (FAM83) proteins are oncogenic, tumour-exclusive and function similarly to RAS, by driving the activation of PI3K and MAPK signalling. In this study we show that FAM83A expression is significantly elevated in human and murine pancreatic cancers and is essential for the growth and tumorigenesis of pancreatic cancer cells. Elevated FAM83A expression maintains essential MEK/ERK survival signalling, preventing cell death in pancreatic cancer cells. Moreover, we identified a positive feed-forward loop mediated by the MEK/ERK-activated AP-1 transcription factors, JUNB and FOSB, which is responsible for the elevated expression of oncogenic FAM83A. Our data indicates that targeting the MEK/ERK-FAM83A feed-forward loop opens up additional avenues for clinical therapy that bypass targeting of oncogenic KRAS in aggressive pancreatic cancers.
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.