Evidence map›Paper›PMID 36291856›Full record

ReviewCancers2022

Autophagy in Hematological Malignancies.

Olga García Ruiz, José Manuel Sánchez-Maldonado, Miguel Ángel López-Nevot, Paloma García, Angelica Macauda, Francisca Hernández-Mohedo, Pedro Antonio González-Sierra, Manuel Martínez-Bueno, Eva Pérez, Fernando Jesús Reyes-Zurita and 5 more

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. The Comparative Effect of Plasma Exosomes of Young and Old People on the Expression ofIndian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2024
    Article
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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

15 authors at 6 institutions in 3 countries.

Olga García RuizGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS Granada, 18016 Granada, Spain.ORCID 0000-0002-7924-8273
José Manuel Sánchez-MaldonadoGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS Granada, 18016 Granada, Spain.
Miguel Ángel López-NevotInstituto de Investigación Biosanitaria de Granada (ibs.GRANADA), Complejo Hospitales Universitarios de Granada, Universidad de Granada, 18016 Granada, Spain.ORCID 0000-0002-3465-6062
Paloma GarcíaCampus de la Salud Hospital, PTS Granada, 18007 Granada, Spain.
Angelica MacaudaGenomic Epidemiology Group, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Francisca Hernández-MohedoInstituto de Investigación Biosanitaria de Granada (ibs.GRANADA), Complejo Hospitales Universitarios de Granada, Universidad de Granada, 18016 Granada, Spain.
Pedro Antonio González-SierraInstituto de Investigación Biosanitaria de Granada (ibs.GRANADA), Complejo Hospitales Universitarios de Granada, Universidad de Granada, 18016 Granada, Spain.
Manuel Martínez-BuenoGenomic Medicine Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS Granada, 18016 Granada, Spain.ORCID 0000-0002-4333-4487
Eva PérezCampus de la Salud Hospital, PTS Granada, 18007 Granada, Spain.
Fernando Jesús Reyes-ZuritaDepartment of Biochemistry and Molecular Biology I, University of Granada, 18071 Granada, Spain.
Daniele CampaDepartment of Biology, University of Pisa, 56126 Pisa, Italy.
Federico CanzianGenomic Epidemiology Group, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.ORCID 0000-0002-4261-4583
Manuel JuradoGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS Granada, 18016 Granada, Spain.
Juan José Rodríguez-SevillaDepartment of Hematology, Hospital del Mar, 08003 Barcelona, Spain.ORCID 0000-0002-4741-7925
Juan SainzGenomic Oncology Area, GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS Granada, 18016 Granada, Spain.ORCID 0000-0002-9355-2423
Universidad de Granada · ESGerman Cancer Research Center · DEParque Tecnológico de la Salud · ESPfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research · ESHospital Del Mar · ESUniversity of Pisa · IT

Funding

Instituto de Salud Carlos III PI17/02256Instituto de Salud Carlos III PI20/01845Junta de Andalucía PY20/01282
6 · The paper itself

Abstract

Autophagy is a highly conserved metabolic pathway via which unwanted intracellular materials, such as unfolded proteins or damaged organelles, are digested. It is activated in response to conditions of oxidative stress or starvation, and is essential for the maintenance of cellular homeostasis and other vital functions, such as differentiation, cell death, and the cell cycle. Therefore, autophagy plays an important role in the initiation and progression of tumors, including hematological malignancies, where damaged autophagy during hematopoiesis can cause malignant transformation and increase cell proliferation. Over the last decade, the importance of autophagy in response to standard pharmacological treatment of hematological tumors has been observed, revealing completely opposite roles depending on the tumor type and stage. Thus, autophagy can promote tumor survival by attenuating the cellular damage caused by drugs and/or stabilizing oncogenic proteins, but can also have an antitumoral effect due to autophagic cell death. Therefore, autophagy-based strategies must depend on the context to create specific and safe combination therapies that could contribute to improved clinical outcomes. In this review, we describe the process of autophagy and its role on hematopoiesis, and we highlight recent research investigating its role as a potential therapeutic target in hematological malignancies. The findings suggest that genetic variants within autophagy-related genes modulate the risk of developing hemopathies, as well as patient survival.

Indexed as

autophagyautophagy-related variantsclinical outcomesdisease progressionhematological malignancieshematopoiesispatient survivaltherapeutic target

Identifiers

PMID36291856
PMCPMC9600546
OpenAlexW4306651517

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.