Evidence map›Paper›PMID 38594547›Full record

ReviewCell biochemistry and biophysics2024

Disable 2, A Versatile Tissue Matrix Multifunctional Scaffold Protein with Multifaceted Signaling: Unveiling Role in Breast Cancer for Therapeutic Revolution.

Nidhi N Shah, Bhavarth P Dave, Kashvi C Shah, Disha D Shah, Kunal G Maheshwari, Mehul R Chorawala

RetractedAbstract readReviewRetracted Publication
PubMed Publisher
In one paragraph

Review in Cell biochemistry and biophysics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Nidhi N Shah *Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Navrangpura, Ahmedabad, 380009, Gujarat, India.
Bhavarth P Dave *Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Navrangpura, Ahmedabad, 380009, Gujarat, India.
Kashvi C Shah *Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Navrangpura, Ahmedabad, 380009, Gujarat, India.
Disha D Shah *Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Navrangpura, Ahmedabad, 380009, Gujarat, India.
Kunal G Maheshwari *Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Navrangpura, Ahmedabad, 380009, Gujarat, India.
Mehul R ChorawalaDepartment of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Navrangpura, Ahmedabad, 380009, Gujarat, India. mehul.chorawala@lmcp.ac.in.ORCID http://orcid.org/0000-0002-3724-0986
Gujarat University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Disabled-2 (DAB2) protein, found in 80-90% of various tumors, including breast cancer, has been identified as a potential tumor suppressor protein. On the contrary, some hypothesis suggests that DAB2 is associated with the modulation of the Ras/MAPK pathway by endocytosing the Grb/Sos1 signaling complex, which produces oncogenes and chemoresistance to anticancer drugs, leading to increased tumor growth and metastasis. DAB2 has multiple functions in several disorders and is typically under-regulated in several cancers, making it a potential target for treatment of cancer therapy. The primary function of DAB2 is the modulation of transforming growth factor- β (TGF-β) mediated endocytosis, which is involved in several mechanisms of cancer development, including tumor suppression through promoting apoptosis and suppressing cell proliferation. In this review, we will discuss in detail the mechanisms through which DAB2 leads to breast cancer and various advancements in employing DAB2 in the treatment of breast cancer. Additionally, we outlined its role in other diseases. We propose that upregulating DAB2 could be a novel approach to the therapeutics of breast cancer.

Indexed as

Adaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsBreast NeoplasmsSignal TransductionAnimalsAntineoplastic AgentsEndocytosisFemaleHumansTransforming Growth Factor betaTumor Suppressor ProteinsAdaptor Proteins, Signal TransducingAntineoplastic AgentsApoptosis Regulatory ProteinsDAB2 protein, humanTransforming Growth Factor betaTumor Suppressor ProteinsAnti-tumorigenicBreast cancerDAB2Epithelial-mesenchymal transition (EMT)Pro-tumorigenicTransforming growth factor-β (TGF-β)

Identifiers

PMID38594547
OpenAlexW4394622230

What OpenQuestion holds

Textmetadata
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.