Evidence map›Paper›PMID 27308315›Full record

ReviewMolecular & cellular oncology2014

Noxa and cancer therapy: Tuning up the mitochondrial death machinery in response to chemotherapy.

Marie-Christine Albert, Kerstin Brinkmann, Hamid Kashkar

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular & cellular oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 29% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

Marie-Christine AlbertCentre for Molecular Medicine Cologne (CMMC); Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD); University of Cologne, Köln, Germany; Institute for Medical Microbiology, Immunology and Hygiene (IMMIH); University of Cologne, Köln, Germany.
Kerstin BrinkmannCentre for Molecular Medicine Cologne (CMMC); Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD); University of Cologne, Köln, Germany; Institute for Medical Microbiology, Immunology and Hygiene (IMMIH); University of Cologne, Köln, Germany.
Hamid KashkarCentre for Molecular Medicine Cologne (CMMC); Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD); University of Cologne, Köln, Germany; Institute for Medical Microbiology, Immunology and Hygiene (IMMIH); University of Cologne, Köln, Germany.
University of Cologne · DEInstitute of Medical Microbiology and Hygiene · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Biochemical analyses have characterized the BH3-only protein family member Noxa as a "sensitizer" with weak pro-apoptotic activity. Investigations into cancer cell responses to chemotherapeutic agents have identified Noxa as a pivotal factor mediating the cytotoxic effect of a plethora of anticancer treatments independent of its own pro-apoptotic activity. Accumulating evidence now suggests that tumor cells exert a number of strategies to counteract Noxa function by exploiting diverse cellular regulatory circuits that normally govern Noxa expression during cellular stress responses. Here, we summarize data concerning the role of Noxa in cancer chemosensitivity and highlight the potential of this enigmatic BH3-only protein family member in current and novel anticancer therapies.

Indexed as

apoptosisbcl-2cancercell deathnoxatherapy

Identifiers

PMID27308315
PMCPMC4905168
OpenAlexW2333760797

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.