Evidence map›Paper›PMID 27499639›Full record

ArticleOncoTargets and therapy2016

Lapatinib induces autophagic cell death and differentiation in acute myeloblastic leukemia.

Yu-Jen Chen, Li-Wen Fang, Wen-Chi Su, Wen-Yi Hsu, Kai-Chien Yang, Huey-Lan Huang

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

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  6. The Interplay between Autophagy and Mitochondria in Cancer.International journal of molecular sciences · 2024
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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

6 authors at 2 institutions in 1 country.

Yu-Jen ChenDepartment of Medical Research; Department of Radiation Oncology, Mackay Memorial Hospital; Institute of Traditional Medicine, School of Medicine, National Yang-Ming University; Institute of Pharmacology, Taipei Medical University, Taipei.
Li-Wen FangDepartment of Nutrition, I-Shou University, Kaohsiung.
Wen-Chi SuResearch Center for Emerging Viruses, China Medical University Hospital; Graduate Institute of Clinical Medical Science, China Medical University, Taichung.
Wen-Yi HsuDepartment of Medical Research.
Kai-Chien YangDepartment of Medical Research.
Huey-Lan HuangDepartment of Bioscience Technology, College of Health Science, Chang Jung Christian University, Tainan, Taiwan, Republic of China.
Chang Jung Christian University · TWI-Shou University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lapatinib is an oral-form dual tyrosine kinase inhibitor of epidermal growth factor receptor (EGFR or ErbB/Her) superfamily members with anticancer activity. In this study, we examined the effects and mechanism of action of lapatinib on several human leukemia cells lines, including acute myeloid leukemia (AML), chronic myeloid leukemia (CML), and acute lymphoblastic leukemia (ALL) cells. We found that lapatinib inhibited the growth of human AML U937, HL-60, NB4, CML KU812, MEG-01, and ALL Jurkat T cells. Among these leukemia cell lines, lapatinib induced apoptosis in HL-60, NB4, and Jurkat cells, but induced nonapoptotic cell death in U937, K562, and MEG-01 cells. Moreover, lapatinib treatment caused autophagic cell death as shown by positive acridine orange staining, the massive formation of vacuoles as seen by electronic microscopy, and the upregulation of LC3-II, ATG5, and ATG7 in AML U937 cells. Furthermore, autophagy inhibitor 3-methyladenine and knockdown of ATG5, ATG7, and Beclin-1 using short hairpin RNA (shRNA) partially rescued lapatinib-induced cell death. In addition, the induction of phagocytosis and ROS production as well as the upregulation of surface markers CD14 and CD68 was detected in lapatinib-treated U937 cells, suggesting the induction of macrophagic differentiation in AML U937 cells by lapatinib. We also noted the synergistic effects of the use of lapatinib and cytotoxic drugs in U937 leukemia cells. These results indicate that lapatinib may have potential for development as a novel antileukemia agent.

Indexed as

AMLautophagic cell deathdifferentiationlapatinibleukemia

Identifiers

PMID27499639
PMCPMC4959590
OpenAlexW2475598855

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.