Evidence map›Paper›PMID 24736947›Full record

ArticleMolecular cancer research : MCR2014

Conserved oncogenic behavior of the FAM83 family regulates MAPK signaling in human cancer.

Rocky Cipriano, Kristy L S Miskimen, Benjamin L Bryson, Chase R Foy, Courtney A Bartel, Mark W Jackson

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

80 citing papers in PubMed, 144 citations in OpenAlex.

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  16. ncRNA-mediated upregulation ofFrontiers in endocrinology · 2023
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20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Rocky CiprianoDepartment of Pathology, and.
Kristy L S MiskimenDepartment of Pathology, and.
Benjamin L BrysonDepartment of Pathology, and.
Chase R FoyDepartment of Pathology, and.
Courtney A BartelDepartment of Pathology, and.
Mark W JacksonDepartment of Pathology, and Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio mwj7@cwru.edu.
Case Western Reserve University · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI Drew James Adams · 1987 to 2026
$142.3M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007250 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI HUANG, ALEX YEE-CHEN · 1985 to 2023
$33.4M
RESEARCH ONCOLOGY TRAINING GRANTT32CA059366 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI JACKSON, MARK W. · 1993 to 2025
$5.5M
Identification of a noval oncogene using validation-based insertional mutagenesisR01CA138421 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI JACKSON, MARK W. · 2010 to 2020
$3.2M
A RAS-FAM83A Regulatory Loop as a Novel Therapeutic Target for Pancreatic CancerR21CA178651 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI JACKSON, MARK W. · 2013 to 2014
$374k
NCI NIH HHS P30 CA043703NCI NIH HHS P30 CA43703NCI NIH HHS R01 CA138421NCI NIH HHS R01CA138421NCI NIH HHS R21 CA178651NCI NIH HHS T32 CA059366NCI NIH HHS T32CA059366NIGMS NIH HHS T32 GM007250
6 · The paper itself

Abstract

unlabelledFAM83B (family with sequence similarity 83, member B) was recently identified as a novel oncogene involved in activating CRAF/MAPK signaling and driving epithelial cell transformation. FAM83B is one of eight members of a protein family (FAM83) characterized by a highly conserved domain of unknown function (DUF1669), which is necessary and sufficient to drive transformation. Here, it is demonstrated that additional FAM83 members also exhibit oncogenic properties and have significantly elevated levels of expression in multiple human tumor types using a TissueScan Cancer Survey Panel PCR array and database mining. Furthermore, modeling the observed tumor expression of FAM83A, FAM83C, FAM83D, or FAM83E promoted human mammary epithelial cell (HMEC) transformation, which correlated with the ability of each FAM83 member to bind CRAF (RAF1) and promote CRAF membrane localization. Conversely, ablation of FAM83A or FAM83D from breast cancer cells resulted in diminished MAPK signaling with marked suppression of growth in vitro and tumorigenicity in vivo. Importantly, each FAM83 member was determined to be elevated in at least one of 17 distinct tumor types examined, with FAM83A, FAM83B, and FAM83D most frequently overexpressed in several diverse tissue types. Finally, evidence suggests that elevated expression of FAM83 members is associated with elevated tumor grade and decreased overall survival. IMPLICATIONS: FAM83 proteins represent a novel family of oncogenes suitable for the development of cancer therapies aimed at suppressing MAPK signaling.

Indexed as

AnimalsBreast NeoplasmsCarcinogenesisCell Line, TumorCell Transformation, NeoplasticEpithelial CellsFemaleHumansMammary Glands, HumanMiceMice, NudeMitogen-Activated Protein KinasesNeoplasm ProteinsOncogenesSignal TransductionMitogen-Activated Protein KinasesNeoplasm Proteins

Identifiers

PMID24736947
PMCPMC4135001
OpenAlexW2053631236

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.