Evidence map›Paper›PMID 36864513›Full record

ArticleClinical epigenetics2023

Selenite as a dual apoptotic and ferroptotic agent synergizes with EGFR and KRAS inhibitors with epigenetic interference.

Lok Seng Chan, Johnson Liu, Molly S C Li, Lili Li, Qian Tao, Tony S K Mok

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical epigenetics, 2023. 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
3.1field-weighted citation impact, top 8% 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, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Regulation of Ferroptosis in Lung Adenocarcinoma.International journal of molecular sciences · 2023
    Review
  6. Article
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

6 authors at 2 institutions in 2 countries.

Lok Seng ChanCancer Epigenetics Laboratory, Department of Clinical Oncology, State Key Laboratory of Translational Oncology, Sir YK Pao Center for Cancer and Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Prince of Wales Hospital, Room 315, Sir Yue-Kong Pao Center for Cancer, Shatin, Hong Kong.
Johnson LiuCancer Epigenetics Laboratory, Department of Clinical Oncology, State Key Laboratory of Translational Oncology, Sir YK Pao Center for Cancer and Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Prince of Wales Hospital, Room 315, Sir Yue-Kong Pao Center for Cancer, Shatin, Hong Kong.
Molly S C LiCancer Epigenetics Laboratory, Department of Clinical Oncology, State Key Laboratory of Translational Oncology, Sir YK Pao Center for Cancer and Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Prince of Wales Hospital, Room 315, Sir Yue-Kong Pao Center for Cancer, Shatin, Hong Kong.
Lili LiCancer Epigenetics Laboratory, Department of Clinical Oncology, State Key Laboratory of Translational Oncology, Sir YK Pao Center for Cancer and Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Prince of Wales Hospital, Room 315, Sir Yue-Kong Pao Center for Cancer, Shatin, Hong Kong.
Qian TaoCancer Epigenetics Laboratory, Department of Clinical Oncology, State Key Laboratory of Translational Oncology, Sir YK Pao Center for Cancer and Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Prince of Wales Hospital, Room 315, Sir Yue-Kong Pao Center for Cancer, Shatin, Hong Kong. qtao@cuhk.edu.hk.
Tony S K MokCancer Epigenetics Laboratory, Department of Clinical Oncology, State Key Laboratory of Translational Oncology, Sir YK Pao Center for Cancer and Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Prince of Wales Hospital, Room 315, Sir Yue-Kong Pao Center for Cancer, Shatin, Hong Kong.
Chinese University of Hong Kong · HKPrince of Wales Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSelenium, an essential trace element, has previously been investigated as a pro-apoptotic and DNA demethylation agent. It sensitizes the response to chemotherapy in patients who were refractory to cytotoxic agents. Meanwhile, ferroptosis is a novel approach to cancer treatment by triggering cell death and reversing drug resistance. The role of selenium in treating cancer cells harboring druggable oncogenic alterations and its underlying mechanism are largely unknown.

resultsWe treated lung adenocarcinoma cell lines-EGFR-mutant H1975 (H1975

conclusionThese results suggest that selenite is a potential apoptotic and ferroptotic drug candidate for the treatment of especially EGFR- and potentially KRAS-mutant lung cancer.

Indexed as

Lung NeoplasmsSeleniumAcetonitrilesAcrylamidesAniline CompoundsDNA MethylationEpigenesis, GeneticErbB ReceptorsHumansIndolesMixed Function OxygenasesMutationPiperazinesProtein Kinase InhibitorsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)AcetonitrilesAcrylamidesadagrasibAniline CompoundsEGFR protein, humanErbB ReceptorsIndolesKRAS protein, humanMixed Function OxygenasesosimertinibPiperazinesProtein Kinase InhibitorsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)PyrimidinesSelenious AcidSeleniumTET1 protein, humanFerroptosisLung adenocarcinomaOsimertinibSeleniteUnfolded protein response

Identifiers

PMID36864513
PMCPMC9983273
OpenAlexW4322764004

What OpenQuestion holds

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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.