Evidence map›Paper›PMID 41235687›Full record

ArticleOncology reports2026

C‑terminal HSP90 inhibitor NCT‑58 impairs the cancer stem‑like phenotype and enhances chemotherapy efficacy in TNBC.

Eunsun Jung, Yoon-Jae Kim, Kyoungmin Lee, Seojin Jang, Soeun Park, Eunhye Oh, Minsu Park, Seongjae Kim, Dongmi Ko, Yong Koo Kang and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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.

No citing paper in PubMed yet.

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

18 authors.

Eunsun Jung *Division of Medical Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul 152‑703, Republic of Korea.
Yoon-Jae Kim *Division of Medical Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul 152‑703, Republic of Korea.
Kyoungmin Lee *Division of Medical Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul 152‑703, Republic of Korea.
Seojin Jang *Division of Medical Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul 152‑703, Republic of Korea.
Soeun ParkDivision of Medical Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul 152‑703, Republic of Korea.
Eunhye OhDivision of Medical Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul 152‑703, Republic of Korea.
Minsu ParkDivision of Medical Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul 152‑703, Republic of Korea.
Seongjae KimDivision of Medical Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul 152‑703, Republic of Korea.
Dongmi KoDivision of Medical Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul 152‑703, Republic of Korea.
Yong Koo KangDivision of Medical Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul 152‑703, Republic of Kore.
Kee Dal NamDivision of Medical Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul 152‑703, Republic of Korea.
Lee FarrandAdelaide Medical School, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia 5000, Australia.
Cong-Truong NguyenLaboratory of Medicinal Chemistry, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.
Minh Thanh LaLaboratory of Medicinal Chemistry, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.
Jihyae AnnLaboratory of Medicinal Chemistry, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.
Jeewoo LeeLaboratory of Medicinal Chemistry, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.
Ji Young KimDivision of Medical Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul 152‑703, Republic of Korea.
Jae Hong SeoDivision of Medical Oncology, Department of Internal Medicine, Korea University College of Medicine, Korea University, Seoul 152‑703, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Treatment options for triple‑negative breast cancer (TNBC) are limited because they typically harbor a high cancer stem‑like population and exhibit a relatively aggressive metastatic phenotype. Heat shock protein 90 (HSP90), a molecular chaperone that regulates diverse oncogenic client proteins, has emerged as a compelling therapeutic target owing to its involvement in key tumor‑promoting processes, such as uncontrolled proliferation, angiogenesis and metastasis. Owing to the undesirable induction of a compensatory heat shock response (HSR) and systemic toxicity, classical N‑terminal inhibitors of HSP90 have failed in clinical trials. The impact of a rationally designed novel inhibitor of the HSP90 C‑terminus in TNBC cells was investigated. NCT‑58 eliminates rapidly proliferating tumor cells accompanied by simultaneous degradation of AKT, MEK and STAT3, and effectively eradicates the cancer stem‑like population (breast cancer stem cells) in both human MDA‑MB‑231 and murine 4T1 cells. The latter phenomenon is accompanied by reductions in the activity of ALDH1 and the CD44

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsHSP90 Heat-Shock ProteinsNeoplastic Stem CellsTriple Negative Breast NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationDrug SynergismFemaleHumansMicePhenotypeXenograft Model Antitumor AssaysHSP90 Heat-Shock Proteinscancer stem cellsheat shock responseHSP90 inhibitorNCT‑58triple‑negative breast cancer

Identifiers

PMID41235687
PMCPMC12635604

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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.