Evidence map›Paper›PMID 34376983›Full record

ArticleBreast cancer : basic and clinical research2021

An Extract of Taro (

Namita Kundu, Xinrong Ma, Stephen Hoag, Fang Wang, Ahmed Ibrahim, Raquel Godoy-Ruiz, David J Weber, Amy M Fulton

Open access · goldAbstract read
In one paragraph

Article in Breast cancer : basic and clinical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Journal of experimental pharmacology · 2025
    Review
  3. Activity ofInternational journal of molecular sciences · 2023
    Article
  4. Review
  5. Article
  6. Review
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

8 authors at 1 institution in 1 country.

Namita KunduDepartment of Pathology, University of Maryland School of Medicine, Baltimore, MD, USA.
Xinrong MaUniversity of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center, Baltimore, MD, USA.
Stephen HoagUniversity of Maryland School of Pharmacy, Baltimore, MD, USA.ORCID https://orcid.org/0000-0003-0657-6951
Fang WangUniversity of Maryland School of Pharmacy, Baltimore, MD, USA.
Ahmed IbrahimUniversity of Maryland School of Pharmacy, Baltimore, MD, USA.ORCID https://orcid.org/0000-0003-1513-1014
Raquel Godoy-RuizUniversity of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center, Baltimore, MD, USA.
David J WeberUniversity of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center, Baltimore, MD, USA.
Amy M FultonDepartment of Pathology, University of Maryland School of Medicine, Baltimore, MD, USA.ORCID https://orcid.org/0000-0002-7657-9683
University of Maryland, Baltimore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The taro plant, PURPOSE: We sought to confirm our earlier studies in additional models and to identify novel mechanisms by which efficacy is achieved.

methodsWe employed a panel of murine and human breast and ovarian cancer cell lines to determine the effect of TE on tumor cell viability, migration, and the ability to support cancer stem cells. Two syngeneic models of TNBC were employed to confirm our earlier report that TE potently inhibits metastasis. Cancer stem cell assays were employed to determine the ability of TE to inhibit tumorsphere-forming ability and to inhibit aldehyde dehydrogenase activity. To determine if host immunity contributes to the mechanism of metastasis inhibition, efficacy was assessed in immune-compromised mice.

resultsWe demonstrate that viability of some, but not all cell lines is inhibited by TE. Likewise, tumor cell migration is inhibited by TE. Using 2 immune competent, syngeneic models of TNBC, we confirm our earlier findings that tumor metastasis is potently inhibited by TE. We also demonstrate, for the first time, that TE directly inhibits breast cancer stem cells. Administration of TE to mice elicits expansion of several spleen cell populations but it was not known if host immune cells contribute to the mechanism by which TE inhibits tumor cell dissemination. In novel findings, we now show that the ability of TE to inhibit metastasis relies on immune T-cell-dependent, but not B cell or Natural Killer (NK)-cell-dependent mechanisms. Thus, both tumor cell-autonomous and host immune factors contribute to the mechanisms underlying TE efficacy. Our long-term goal is to evaluate TE efficacy in clinical trials. Most of our past studies as well as many of the results reported in this report were carried out using an isolation protocol described earlier (TE). In preparation for a near future clinical trial, we have now developed a strategy to isolate an enriched taro fraction, TE-method 2, (TE-M2) as well as a more purified subfraction (TE-M2F1) which can be scaled up under Good Manufacturing Practice (GMP) conditions for evaluation in human subjects. We demonstrate that TE-M2 and TE-M2F1 retain the anti-metastatic properties of TE.

conclusionsThese studies provide further support for the continued examination of biologically active components of

Indexed as

cancer stem cellColocasia esculentaimmune-modulatorymetastasisTaro

Identifiers

PMID34376983
PMCPMC8320546
OpenAlexW3183376321

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.