Evidence map›Paper›PMID 33105796›Full record

ReviewInternational journal of molecular sciences2020

Targeting Autophagy in Breast Cancer.

Stefania Cocco, Alessandra Leone, Michela Piezzo, Roberta Caputo, Vincenzo Di Lauro, Francesca Di Rella, Giuseppina Fusco, Monica Capozzi, Germira di Gioia, Alfredo Budillon and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 109 citations in OpenAlex.

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2 more citing papers are in PubMed but not listed here.

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

11 authors at 1 institution in 1 country.

Stefania CoccoBreast Unit, Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale", Via Mariano Semmola 53, 80131 Napoli, Italy.ORCID 0000-0003-3169-1580
Alessandra LeoneExperimental Pharmacology Unit, Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale", Via Mariano Semmola 53, 80131 Napoli, Italy.ORCID 0000-0002-1051-2937
Michela PiezzoBreast Unit, Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale", Via Mariano Semmola 53, 80131 Napoli, Italy.ORCID 0000-0002-1730-3900
Roberta CaputoBreast Unit, Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale", Via Mariano Semmola 53, 80131 Napoli, Italy.
Vincenzo Di LauroBreast Unit, Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale", Via Mariano Semmola 53, 80131 Napoli, Italy.
Francesca Di RellaBreast Unit, Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale", Via Mariano Semmola 53, 80131 Napoli, Italy.
Giuseppina FuscoBreast Unit, Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale", Via Mariano Semmola 53, 80131 Napoli, Italy.
Monica CapozziBreast Unit, Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale", Via Mariano Semmola 53, 80131 Napoli, Italy.
Germira di GioiaBreast Unit, Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale", Via Mariano Semmola 53, 80131 Napoli, Italy.
Alfredo BudillonExperimental Pharmacology Unit, Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale", Via Mariano Semmola 53, 80131 Napoli, Italy.
Michelino De LaurentiisBreast Unit, Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale", Via Mariano Semmola 53, 80131 Napoli, Italy.ORCID 0000-0001-9009-1572
Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale" · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is a heterogeneous disease consisting of different biological subtypes, with differences in terms of incidence, response to diverse treatments, risk of disease progression, and sites of metastases. In the last years, several molecular targets have emerged and new drugs, targeting PI3K/Akt/mTOR and cyclinD/CDK/pRb pathways and tumor microenvironment have been integrated into clinical practice. However, it is clear now that breast cancer is able to develop resistance to these drugs and the identification of the underlying molecular mechanisms is paramount to drive further drug development. Autophagy is a highly conserved homeostatic process that can be activated in response to antineoplastic agents as a cytoprotective mechanism. Inhibition of autophagy could enhance tumor cell death by diverse anti-cancer therapies, representing an attractive approach to control mechanisms of drug resistance. In this manuscript, we present a review of autophagy focusing on its interplay with targeted drugs used for breast cancer treatment.

Indexed as

Antineoplastic AgentsAutophagyBreast NeoplasmsClinical Trials as TopicErb-b2 Receptor Tyrosine KinasesFemaleHumansMolecular Targeted TherapyPhosphatidylinositol 3-KinasesReceptors, EstrogenTOR Serine-Threonine KinasesTriple Negative Breast NeoplasmsTumor MicroenvironmentAntineoplastic AgentsERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesMTOR protein, humanPhosphatidylinositol 3-KinasesReceptors, EstrogenTOR Serine-Threonine KinasesACDATGautophagybreast cancerChloroquineHydroxychloroquine

Identifiers

PMID33105796
PMCPMC7660056
OpenAlexW3093798225

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.