Evidence map›Paper›PMID 26779377›Full record

ArticleCancer biology & medicine2015

Synergistic suppression of the PI3K inhibitor CAL-101 with bortezomib on mantle cell lymphoma growth.

Fu-Lian Qu, Bing Xia, Su-Xia Li, Chen Tian, Hong-Liang Yang, Qian Li, Ya-Fei Wang, Yong Yu, Yi-Zhuo Zhang

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

Article in Cancer biology & medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Therapeutic Targeting of Notch Signaling Pathway in Hematological Malignancies.Mediterranean journal of hematology and infectious diseases · 2019
    Review
  4. Article
  5. 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

9 authors at 1 institution in 1 country.

Fu-Lian Qu1 Department of Hematology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China ; 2 Department of Medical Oncology, Kaifeng Central Hospital, Kaifeng 475000, China ; 3 Department of Geriatric Hematology, Chinese PLA General Hospital, Beijing 100853, China.
Bing Xia1 Department of Hematology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China ; 2 Department of Medical Oncology, Kaifeng Central Hospital, Kaifeng 475000, China ; 3 Department of Geriatric Hematology, Chinese PLA General Hospital, Beijing 100853, China.
Su-Xia Li1 Department of Hematology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China ; 2 Department of Medical Oncology, Kaifeng Central Hospital, Kaifeng 475000, China ; 3 Department of Geriatric Hematology, Chinese PLA General Hospital, Beijing 100853, China.
Chen Tian1 Department of Hematology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China ; 2 Department of Medical Oncology, Kaifeng Central Hospital, Kaifeng 475000, China ; 3 Department of Geriatric Hematology, Chinese PLA General Hospital, Beijing 100853, China.
Hong-Liang Yang1 Department of Hematology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China ; 2 Department of Medical Oncology, Kaifeng Central Hospital, Kaifeng 475000, China ; 3 Department of Geriatric Hematology, Chinese PLA General Hospital, Beijing 100853, China.
Qian Li1 Department of Hematology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China ; 2 Department of Medical Oncology, Kaifeng Central Hospital, Kaifeng 475000, China ; 3 Department of Geriatric Hematology, Chinese PLA General Hospital, Beijing 100853, China.
Ya-Fei Wang1 Department of Hematology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China ; 2 Department of Medical Oncology, Kaifeng Central Hospital, Kaifeng 475000, China ; 3 Department of Geriatric Hematology, Chinese PLA General Hospital, Beijing 100853, China.
Yong Yu1 Department of Hematology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China ; 2 Department of Medical Oncology, Kaifeng Central Hospital, Kaifeng 475000, China ; 3 Department of Geriatric Hematology, Chinese PLA General Hospital, Beijing 100853, China.
Yi-Zhuo Zhang1 Department of Hematology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China ; 2 Department of Medical Oncology, Kaifeng Central Hospital, Kaifeng 475000, China ; 3 Department of Geriatric Hematology, Chinese PLA General Hospital, Beijing 100853, China.
Tianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the effects of CAL-101, particularly when combined with bortezomib (BTZ) on mantle cell lymphoma (MCL) cells, and to explore its relative mechanisms.

methodsMTT assay was applied to detect the inhibitory effects of different concentrations of CAL-101. MCL cells were divided into four groups: control group, CAL-101 group, BTZ group, and CAL-101/BTZ group. The expression of PI3K-p110σ, AKT, ERK, p-AKT and p-ERK were detected by Western blot. The apoptosis rates of CAL-101 group, BTZ group, and combination group were detected by flow cytometry. The location changes of nuclear factor kappa-B (NF-κB) of 4 groups was investigated by NF-κB Kit exploring. Western blot was applied to detect the levels of caspase-3 and the phosphorylation of AKT in different groups.

resultsCAL-101 dose- and time-dependently induced reduction in MCL cell viability. CAL-101 combined with BTZ enhanced the reduction in cell viability and apoptosis. Western blot analysis showed that CAL-101 significantly blocked the PI3K/AKT and ERK signaling pathway in MCL cells. The combination therapy contributed to the inactivation of NF-κB and AKT in MCL cell lines. However, cleaved caspase-3 was up-regulated after combined treatment.

conclusionOur study showed that PI3K/p110σ is a novel therapeutic target in MCL, and the underlying mechanism could be the blocking of the PI3K/AKT and ERK signaling pathways. These findings provided a basis for clinical evaluation of CAL-101 and a rationale for its application in combination therapy, particularly with BTZ.

Indexed as

bortezomib (BTZ)CAL-101mantle cell lymphoma (MCL)phosphatidylinositol-3-kinase (PI3K)

Identifiers

PMID26779377
PMCPMC4706520
OpenAlexW2204992708

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Registered trials

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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.