Evidence map›Paper›PMID 30993194›Full record

ArticleNPJ breast cancer2019

Simultaneous defeat of MCF7 and MDA-MB-231 resistances by a hypericin PDT-tamoxifen hybrid therapy.

Theodossis A Theodossiou, Muhammad Ali, Mantas Grigalavicius, Beata Grallert, Pierre Dillard, Kay Oliver Schink, Cathrine E Olsen, Sébastien Wälchli, Else Marit Inderberg, Andreas Kubin and 2 more

Open access · goldAbstract read
In one paragraph

Article in NPJ breast cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 139 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

Theodossis A Theodossiou1Department of Radiation Biology, Institute for Cancer Research, Radium Hospital, Oslo University Hospital, Montebello, 0379 Oslo, Norway.ORCID 0000-0002-1982-8372
Muhammad Ali2Department of Immunology, Institute for Cancer Research, Radium Hospital, Oslo University Hospital, Montebello, 0379 Oslo, Norway.
Mantas Grigalavicius1Department of Radiation Biology, Institute for Cancer Research, Radium Hospital, Oslo University Hospital, Montebello, 0379 Oslo, Norway.
Beata Grallert1Department of Radiation Biology, Institute for Cancer Research, Radium Hospital, Oslo University Hospital, Montebello, 0379 Oslo, Norway.
Pierre Dillard3Department of Cellular Therapy, Department of Oncology, Radium Hospital, Oslo University Hospital, Oslo, Norway.
Kay Oliver Schink4Department of Molecular Cell Biology, Institute for Cancer Research, Radium Hospital, Oslo University Hospital, Montebello, 0379 Oslo, Norway.ORCID 0000-0002-5903-4059
Cathrine E Olsen1Department of Radiation Biology, Institute for Cancer Research, Radium Hospital, Oslo University Hospital, Montebello, 0379 Oslo, Norway.
Sébastien Wälchli3Department of Cellular Therapy, Department of Oncology, Radium Hospital, Oslo University Hospital, Oslo, Norway.
Else Marit Inderberg3Department of Cellular Therapy, Department of Oncology, Radium Hospital, Oslo University Hospital, Oslo, Norway.
Andreas KubinPLANTA Naturstoffe Vertriebs GmbH, A-1120 Wien, Austria.
Qian Peng6Department of Pathology, Radium Hospital, Oslo University Hospital, Montebello, 0379 Oslo, Norway.
Kristian Berg1Department of Radiation Biology, Institute for Cancer Research, Radium Hospital, Oslo University Hospital, Montebello, 0379 Oslo, Norway.ORCID 0000-0002-7816-7543
Oslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Currently the greatest challenge in oncology is the lack of homogeneity of the lesions where different cell components respond differently to treatment. There is growing consensus that monotherapies are insufficient to eradicate the disease and there is an unmet need for more potent combinatorial treatments. We have previously shown that hypericin photodynamic therapy (HYP-PDT) triggers electron transport chain (ETC) inhibition in cell mitochondria. We have also shown that tamoxifen (TAM) enhances cytotoxicity in cells with high respiration, when combined with ETC inhibitors. Herein we introduce a synergistic treatment based on TAM chemotherapy and HYP-PDT. We tested this novel combinatorial treatment (HYPERTAM) in two metabolically different breast cancer cell lines, the triple-negative MDA-MB-231 and the estrogen-receptor-positive MCF7, the former being quite sensitive to HYP-PDT while the latter very responsive to TAM treatment. In addition, we investigated the mode of death, effect of lipid peroxidation, and the effect on cell metabolism. The results were quite astounding. HYPERTAM exhibited over 90% cytotoxicity in both cell lines. This cytotoxicity was in the form of both necrosis and autophagy, while high levels of lipid peroxidation were observed in both cell lines. We, consequently, translated our research to an in vivo pilot study encompassing the MDA-MB-231 and MCF7 tumor models in NOD SCID-γ immunocompromised mice. Both treatment cohorts responded very positively to HYPERTRAM, which significantly prolonged mice survival. HYPERTAM is a potent, synergistic modality, which may lay the foundations for a novel, composite anticancer treatment, effective in diverse tumor types.

Identifiers

PMID30993194
PMCPMC6458138
OpenAlexW2935962579

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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.