Evidence map›Paper›PMID 31488583›Full record

ArticleThe Journal of cell biology2019

Hair follicle regeneration suppresses Ras-driven oncogenic growth.

Cristiana M Pineda, David G Gonzalez, Catherine Matte-Martone, Jonathan Boucher, Elizabeth Lathrop, Sara Gallini, Nathan R Fons, Tianchi Xin, Karen Tai, Edward Marsh and 4 more

Abstract read
In one paragraph

Article in The Journal of cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Cristiana M PinedaDepartment of Genetics, Yale School of Medicine, New Haven, CT.
David G GonzalezDepartment of Genetics, Yale School of Medicine, New Haven, CT.ORCID 0000-0002-0106-6461
Catherine Matte-MartoneDepartment of Genetics, Yale School of Medicine, New Haven, CT.
Jonathan BoucherDepartment of Genetics, Yale School of Medicine, New Haven, CT.
Elizabeth LathropDepartment of Genetics, Yale School of Medicine, New Haven, CT.
Sara GalliniDepartment of Genetics, Yale School of Medicine, New Haven, CT.ORCID 0000-0001-6945-093X
Nathan R FonsDepartment of Therapeutic Radiology, Yale School of Medicine, New Haven, CT.
Tianchi XinDepartment of Genetics, Yale School of Medicine, New Haven, CT.
Karen TaiDepartment of Genetics, Yale School of Medicine, New Haven, CT.ORCID 0000-0001-6182-9718
Edward MarshDepartment of Genetics, Yale School of Medicine, New Haven, CT.
Don X NguyenDepatment of Pathology, Yale School of Medicine, New Haven, CT.
Kathleen C SuozziDepartment of Genetics, Yale School of Medicine, New Haven, CT.
Slobodan BeronjaDivision of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA.
Valentina GrecoDepartment of Genetics, Yale School of Medicine, New Haven, CT valentina.greco@yale.edu.ORCID 0000-0002-6492-4603

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM007499 · NIGMS · YALE UNIVERSITY · PI CARLSON, JOHN R, REINKE, VALERIE J · 1985 to 2022
$13.9M
Live Imaging of Skin RegenerationR01AR063663 · NIAMS · YALE UNIVERSITY · PI Valentina Greco · 2012 to 2026
$7.7M
Understanding Skin Tissue Repair in Live MammalsR01AR072668 · NIAMS · YALE UNIVERSITY · PI Valentina Greco · 2018 to 2026
$6.2M
Normal stem cells and their transition to disease in the skinR01AR067755 · NIAMS · YALE UNIVERSITY · PI GRECO, VALENTINA · 2016 to 2020
$2.2M
A novel lineage pathway controls metabolic adaptation by metastatic lung cancersR01CA191489 · NCI · YALE UNIVERSITY · PI NGUYEN, DON X · 2015 to 2019
$1.9M
Live-imaging the interface between homeostasis and cancerF31CA206419 · NCI · YALE UNIVERSITY · PI PINEDA, CRISTIANA · 2017 to 2018
$33k
NCI NIH HHS F31 CA206419NCI NIH HHS R01 CA191489NIAMS NIH HHS R01 AR063663NIAMS NIH HHS R01 AR067755NIAMS NIH HHS R01 AR072668NIGMS NIH HHS T32 GM007499
6 · The paper itself

Abstract

Mutations associated with tumor development in certain tissues can be nontumorigenic in others, yet the mechanisms underlying these different outcomes remains poorly understood. To address this, we targeted an activating Hras mutation to hair follicle stem cells and discovered that Hras mutant cells outcompete wild-type neighbors yet are integrated into clinically normal skin hair follicles. In contrast, targeting the Hras mutation to the upper noncycling region of the skin epithelium leads to benign outgrowths. Follicular Hras mutant cells autonomously and nonautonomously enhance regeneration, which directs mutant cells into continuous tissue cycling to promote integration rather than aberrancy. This follicular tolerance is maintained under additional challenges that promote tumorigenesis in the epidermis, including aging, injury, and a secondary mutation. Thus, the hair follicle possesses a unique, enhanced capacity to integrate and contain Hras mutant cells within both homeostatic and perturbed tissue, demonstrating that in the skin, multiple, distinct mechanisms exist to suppress oncogenic growth.

Indexed as

CarcinogenesisRegenerationAnimalsHair FollicleMiceMice, TransgenicNeoplasmsras Proteinsras Proteins

Identifiers

PMID31488583
PMCPMC6781447

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.