Evidence map›Paper›PMID 34316328›Full record

ArticleOncotarget2021

Next-generation multimodality of nutrigenomic cancer therapy: sulforaphane in combination with acetazolamide actively target bronchial carcinoid cancer in disabling the PI3K/Akt/mTOR survival pathway and inducing apoptosis.

Reza Bayat Mokhtari, Bessi Qorri, Narges Baluch, Angelo Sparaneo, Federico Pio Fabrizio, Lucia Anna Muscarella, Albina Tyker, Sushil Kumar, Hai-Ling Margaret Cheng, Myron R Szewczuk and 2 more

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 19% 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, 23 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 6 institutions in 4 countries.

Reza Bayat MokhtariProgram in Developmental and Stem Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada.
Bessi QorriDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
Narges BaluchDepartment of Immunology and Allergy, The Hospital for Sick Children, Toronto, Ontario, Canada.
Angelo SparaneoLaboratory of Oncology, IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo FG, Italy.
Federico Pio FabrizioLaboratory of Oncology, IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo FG, Italy.
Lucia Anna MuscarellaLaboratory of Oncology, IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo FG, Italy.
Albina TykerDepartment of Internal Medicine, University of Chicago, Chicago, IL, USA.
Sushil KumarQ.P.S. Holdings LLC, Pencader Corporate Center, Newark, DE, USA.
Hai-Ling Margaret ChengInstitute of Biomedical Engineering, The Edward S. Rogers Sr. Department of Electrical & Computer Engineering, University of Toronto, Toronto, Canada.
Myron R SzewczukDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
Bikul DasDepartment of Experimental Therapeutics, Thoreau Laboratory for Global Health, M2D2, University of Massachusetts, Lowell, MA, USA.
Herman YegerProgram in Developmental and Stem Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada.
Hospital for Sick Children · CAIstituti di Ricovero e Cura a Carattere Scientifico · ITQueen's University · CAIndian Institute of Technology Guwahati · INUniversity of Chicago · USUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAberrations in the PI3K/AKT/mTOR survival pathway in many cancers are the most common genomic abnormalities. The phytochemical and bioactive agent sulforaphane (SFN) has nutrigenomic potential in activating the expression of several cellular protective genes via the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2). Nrf2 is primarily related to mechanisms of endogenous cellular defense and survival. The efficacy of SFN in combination with acetazolamide (AZ) was investigated in reducing typical H727 and atypical H720 BC survival, migration potential, and apoptosis MATERIALS AND

methodsMicroscopic imaging, immunocytochemistry, wound healing assay, caspase-cleaved cytokeratin 18 (M30, CCK18) CytoDeath ELISA assay, immunofluorescence labeling assays for apoptosis, hypoxia, Western Blotting, Tunnel assay, measurement of 5-HT secretion by carbon fiber amperometry assay, quantitative methylation-specific PCR (qMSP), morphologic changes, cell viability, apoptosis activity and the expression levels of phospho-Akt1, Akt1, HIF-1α, PI3K, p21, CAIX, 5-HT, phospho-mTOR, and mTOR in xenografts derived from typical H727 and atypical H720 BC cell lines.

resultsCombining AZ+SFN reduced tumor cell survival compared to each agent alone, both

conclusionsCombining SFN+AZ significantly inhibits the PI3K/Akt/mTOR pathway and significantly reducing 5-HT secretion in carcinoid syndrome.

Indexed as

acetazolamidebronchial carcinoid tumorscarbonic anhydraseserotoninsulforaphane

Identifiers

PMID34316328
PMCPMC8310668
OpenAlexW3177788168

What OpenQuestion holds

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Registered trials

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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.