Evidence map›Paper›PMID 28912868›Full record

ArticleExperimental and therapeutic medicine2017

Bax is involved in the anticancer activity of Velcade in colorectal cancer.

Liya Su, Qimuge Suyila, Ling Yang, Hong Li, Yaguang Xi, Xiulan Su

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

Article in Experimental and therapeutic medicine, 2017. 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
0.1field-weighted citation impact, top 49% 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, 7 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

6 authors at 2 institutions in 2 countries.

Liya SuClinical Medical Research Center of The Affiliated Hospital, Inner Mongolia Medical University, Hohhot, Inner Mongolia 010050, P.R. China.
Qimuge SuyilaClinical Medical Research Center of The Affiliated Hospital, Inner Mongolia Medical University, Hohhot, Inner Mongolia 010050, P.R. China.
Ling YangClinical Medical Research Center of The Affiliated Hospital, Inner Mongolia Medical University, Hohhot, Inner Mongolia 010050, P.R. China.
Hong LiDepartment of Oncology of The Affiliated People's Hospital, Inner Mongolia Medical University, Hohhot, Inner Mongolia 010050, P.R. China.
Yaguang XiDepartment of Genetics and Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
Xiulan SuClinical Medical Research Center of The Affiliated Hospital, Inner Mongolia Medical University, Hohhot, Inner Mongolia 010050, P.R. China.
Inner Mongolia Medical University · CNLouisiana State University Health Sciences Center New Orleans · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous chemotherapeutic agents promote tumor cell death by activating the intrinsic apoptosis signaling pathway. This pathway is regulated by mitochondrial dysfunction, which occurs through an intricate process controlled by complex interactions between B-cell lymphoma 2 (Bcl-2) family members and other cellular proteins. Bcl-2-associated X protein (Bax) is a proapoptotic protein that is an essential component of the intrinsic apoptosis signaling pathway. Patients lacking Bax may be less sensitive to chemotherapy due to an impaired intrinsic apoptosis signaling pathway. The present study demonstrated that Bax expression in colorectal cancer (CRC) tissues was typically increased compared with that in adjacent normal tissues. Furthermore, Bax

Indexed as

apoptosisBaxcolorectal cancerVelcade

Identifiers

PMID28912868
PMCPMC5585753
OpenAlexW2741679389

What OpenQuestion holds

Textmetadata
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.