ArticleCancer research2012
B-Raf activation cooperates with PTEN loss to drive c-Myc expression in advanced prostate cancer.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
What it found
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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
67 citing papers in PubMed, 92 citations in OpenAlex.
- Mapping prostate cancer pathobiology: A review of genetically engineered mouse models (GEMMs).Gene · 2026Review
- Metastatic hormone-naïve prostate cancer: a distinct biological entity.Trends in cancer · 2024Review
- Differential contribution for ERK1 and ERK2 kinases in BRAFCell death and differentiation · 2024Article
- OncoLoop: A Network-Based Precision Cancer Medicine Framework.Cancer discovery · 2023Article
- Strategies to target the cancer driver MYC in tumor cells.Frontiers in oncology · 2023Review
- In Vivo Models for Prostate Cancer Research.Cancers · 2022Review
- Elevated serum CEA is associated with liver metastasis and distinctive circulating tumor DNA alterations in patients with castration-resistant prostate cancer.The Prostate · 2022Article
- KMT2C methyltransferase domain regulated INK4A expression suppresses prostate cancer metastasis.Molecular cancer · 2022Article
- Early differential responses elicited by BRAFCell death & disease · 2022Article
- From Therapy Resistance to Targeted Therapies in Prostate Cancer.Frontiers in oncology · 2022Review
- Pancreatic Cancer and Cellular Senescence: Tumor Microenvironment under the Spotlight.International journal of molecular sciences · 2021Review
- Multiplexed functional genomic analysis of 5' untranslated region mutations across the spectrum of prostate cancer.Nature communications · 2021Observational
- Inflammation-Induced Tumorigenesis and Metastasis.International journal of molecular sciences · 2021Review
- A Review of the Pathophysiological Mechanisms Underlying Castration-resistant Prostate Cancer.Research and reports in urology · 2021Review
- Review
- Loss of RBMS1 as a regulatory target of miR-106b influences cell growth, gap closing and colony forming in prostate carcinoma.Scientific reports · 2020Article
- Prostate carcinogenesis: inflammatory storms.Nature reviews. Cancer · 2020Review
- The PI3K-AKT-mTOR Pathway and Prostate Cancer: At the Crossroads of AR, MAPK, and WNT Signaling.International journal of molecular sciences · 2020Review
- Sequential Ras/MAPK and PI3K/AKT/mTOR pathways recruitment drives basal extrusion in the prostate-like gland of Drosophila.Nature communications · 2020Article
- ZNFX1 anti-sense RNA 1 promotes the tumorigenesis of prostate cancer by regulating c-Myc expression via a regulatory network of competing endogenous RNAs.Cellular and molecular life sciences : CMLS · 2020Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Both the PI3K → Akt → mTOR and mitogen-activated protein kinase (MAPK) signaling pathways are often deregulated in prostate tumors with poor prognosis. Here we describe a new genetically engineered mouse model of prostate cancer in which PI3K-Akt-mTOR signaling is activated by inducible disruption of PTEN, and extracellular signal-regulated kinase 1/2 (ERK1/2) MAPK signaling is activated by inducible expression of a BRAF(V600E) oncogene. These tissue-specific compound mutant mice develop lethal prostate tumors that are inherently resistant to castration. These tumors bypass cellular senescence and disseminate to lymph nodes, bone marrow, and lungs where they form overt metastases in approximately 30% of the cases. Activation of PI3K → Akt → mTOR and MAPK signaling pathways in these prostate tumors cooperate to upregulate c-Myc. Accordingly, therapeutic treatments with rapamycin and PD0325901 to target these pathways, respectively, attenuate c-Myc levels and reduce tumor and metastatic burden. Together, our findings suggest a generalized therapeutic approach to target c-Myc activation in prostate cancer by combinatorial targeting of the PI3K → Akt → mTOR and ERK1/2 MAPK signaling pathways.
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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.