Evidence map›Paper›PMID 28122581›Full record

ReviewCell communication and signaling : CCS2017

Acute myeloid leukemia - strategies and challenges for targeting oncogenic Hedgehog/GLI signaling.

Fritz Aberger, Evelyn Hutterer, Christina Sternberg, Pedro J Del Burgo, Tanja N Hartmann

Open access · goldAbstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.7field-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

36 citing papers in PubMed, 54 citations in OpenAlex.

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  13. High GLI-1 Expression is a Reliable Indicator of Bad Prognosis in Newly Diagnosed Acute Leukemia Patients.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2023
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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

5 authors at 2 institutions in 1 country.

Fritz AbergerCancer Cluster Salzburg, Department of Molecular Biology, Paris-Lodron University of Salzburg, Hellbrunner Strasse 34, 5020, Salzburg, Austria. fritz.aberger@sbg.ac.at.
Evelyn HuttererCancer Cluster Salzburg, Salzburg Cancer Research Institute (SCRI) - Laboratory for Immunological and Molecular Cancer Research (LIMCR), 5020, Salzburg, Austria.
Christina SternbergCancer Cluster Salzburg, Department of Molecular Biology, Paris-Lodron University of Salzburg, Hellbrunner Strasse 34, 5020, Salzburg, Austria.
Pedro J Del BurgoCancer Cluster Salzburg, Department of Molecular Biology, Paris-Lodron University of Salzburg, Hellbrunner Strasse 34, 5020, Salzburg, Austria.
Tanja N HartmannCancer Cluster Salzburg, Salzburg Cancer Research Institute (SCRI) - Laboratory for Immunological and Molecular Cancer Research (LIMCR), 5020, Salzburg, Austria. t.hartmann@salk.at.
University of Salzburg · ATParacelsus Medical University · AT

Funding

Austrian Science Fund FWF P 25629
6 · The paper itself

Abstract

Treatment of acute myeloid leukemia (AML), an aggressive and heterogeneous hematological malignancy, remains a challenge. Despite advances in our understanding of the complex genetics and biology of AML pathophysiology, these findings have been translated to the clinic with only limited success, and poor outcomes persist for the majority of patients. Thus, novel treatment strategies are clearly needed for achieving deeper and prolonged remissions and for avoiding the development of resistance. Due to its profound role in (cancer) stem cell biology and differentiation, the Hedgehog (HH)/Glioma-associated Oncogene Homolog (GLI) signaling pathway may be an attractive novel therapeutic target in AML. In this review, we aim to provide a critical and concise overview of the currently known potential and challenges of HH/GLI targeting. We describe the biological role of the HH/GLI pathway in AML pathophysiology. We specifically focus on ways of targeting non-canonical HH/GLI signaling in AML, particularly in combination with standard treatment regimens, which may overcome some hurdles observed with approved HH pathway inhibitors in solid tumors.

Indexed as

Molecular Targeted TherapySignal TransductionAnimalsHedgehog ProteinsHumansLeukemia, Myeloid, AcuteNeoplastic Stem CellsZinc Finger Protein GLI1Hedgehog ProteinsZinc Finger Protein GLI1Acute myeloid leukemiaCancer stem cellsCombination therapyGLI proteinsHedgehog (HH) signalingNon-canonical Hedgehog/GLI signaling

Identifiers

PMID28122581
PMCPMC5267446
OpenAlexW2582028225

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.