Evidence map›Paper›PMID 20515293›Full record

ReviewExpert opinion on therapeutic targets2010

Non-cell-autonomous signaling by Shh in tumors: challenges and opportunities for therapeutic targets.

Maarten F Bijlsma, Henk Roelink

Abstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
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

2 authors.

Maarten F BijlsmaUniversity of California Berkeley, Department of Molecular and Cell Biology, Berkeley, CA 94720-3204, USA.
Henk Roelink

Funding

The roles of Ptch1 and Disp1 in the formation of the Shh gradientR01GM097035 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI ROELINK, HENK · 2011 to 2014
$1.2M
NIGMS NIH HHS R01 GM097035
6 · The paper itself

Abstract

importance of the fieldThe Hedgehog (Hh) pathway is required during many developmental events; in adults the Hedgehog pathway is involved in the maintenance of several stem cell niches. It is therefore not surprising that aberrantly regulated Hh pathway activity can cause birth defects in the developing organism, as well as neoplastic disease later in life. AREAS COVERED IN THIS REVIEW: As a consequence of the involvement in pathogenesis, the Hh pathway components are subject to an intense scrutiny as potential targets for therapeutic agents. We aim to provide an overview of the biology of the Hh proteins and the cellular response, in conjunction with potential therapeutic interventions. WHAT THE READER WILL GAIN: Specifically, we focus on the recently discovered non-cell-autonomous Shh signaling used by tumors and the implications of this for the design of treatment strategies. This should provide the reader with up-to-date knowledge on the role of the Hh pathway in tumor progression and the options to treat these malignancies. TAKE HOME MESSAGE: An important concept that we advocate in this review is the need to recognize the need to target both the stromal and the tumor compartment in malignancies that rely on paracrine Shh signaling.

Indexed as

Paracrine CommunicationAcylationAnimalsAntineoplastic AgentsEndocytosisHedgehog ProteinsHumansIntercellular Signaling Peptides and ProteinsLigandsNeoplasmsProtein Processing, Post-TranslationalSecretory PathwayStem Cell NicheStromal CellsAntineoplastic AgentsHedgehog ProteinsIntercellular Signaling Peptides and ProteinsLigandsSHH protein, human

Identifiers

PMID20515293
PMCPMC8480204

What OpenQuestion holds

Textmetadata
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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.