Evidence map›Paper›PMID 25216532›Full record

ArticleOncotarget2014

Mapping of apoptin-interaction with BCR-ABL1, and development of apoptin-based targeted therapy.

Jaganmohan R Jangamreddy, Soumya Panigrahi, Kourosh Lotfi, Manisha Yadav, Subbareddy Maddika, Anil Kumar Tripathi, Sabyasachi Sanyal, Marek J Łos

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.9field-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

12 citing papers in PubMed, 16 citations in OpenAlex.

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  3. Identification ofBiomarker research · 2019
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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

8 authors at 5 institutions in 4 countries.

Jaganmohan R JangamreddyDept. Clinical & Experimental Medicine, Integrative Regenerative Med. Center (IGEN), Linköping University, Sweden. Authors contributed equally.
Soumya PanigrahiDept. Medicine/ Infectious Diseases, Case Western Reserve University, Cleveland, OH 44106, USA. Authors contributed equally.
Kourosh LotfiDept. of Medical and Health Sciences, Linköping University, Department of Hematology, County Council of Östergötland, Linköping, Sweden.
Manisha YadavDivision of Biochemistry, CSIR-Central Drug Research Institute, 10, Janakipuram Extn, Sitapur Rd, Lucknow 226031, UP, India.
Subbareddy MaddikaLaboratory of Cell Death & Survival, Centre for DNA Fingerprinting and Diagnostics (CDFD), Hyderabad, India.
Anil Kumar TripathiDepartment of Clinical Hematology and Medical Oncology, King George's Medical University, Lucknow 226003, Uttar Pradesh, India.
Sabyasachi SanyalDivision of Biochemistry, CSIR-Central Drug Research Institute, 10, Janakipuram Extn, Sitapur Rd, Lucknow 226031, UP, India.
Marek J ŁosDept. Clinical & Experimental Medicine, Integrative Regenerative Med. Center (IGEN), Linköping University, Sweden. Department of Pathology, Pomeranian Medical University, Szczecin, Poland.
Linköping University · SECentral Drug Research Institute · INCase Western Reserve University · USCentre for DNA Fingerprinting and Diagnostics · INKing George's Medical University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Majority of chronic myeloid leukemia patients experience an adequate therapeutic effect from imatinib however, 26-37% of patients discontinue imatinib therapy due to a suboptimal response or intolerance. Here we investigated derivatives of apoptin, a chicken anemia viral protein with selective toxicity towards cancer cells, which can be directed towards inhibiting multiple hyperactive kinases including BCR-ABL1. Our earlier studies revealed that a proline-rich segment of apoptin interacts with the SH3 domain of fusion protein BCR-ABL1 (p210) and acts as a negative regulator of BCR-ABL1 kinase and its downstream targets. In this study we show for the first time, the therapeutic potential of apoptin-derived decapeptide for the treatment of CML by establishing the minimal region of apoptin interaction domain with BCR-ABL1. We further show that the apoptin decapeptide is able to inhibit BCR-ABL1 down stream target c-Myc with a comparable efficacy to full-length apoptin and Imatinib. The synthetic apoptin is able to inhibit cell proliferation in murine (32Dp210), human cell line (K562), and ex vivo in both imatinib-resistant and imatinib sensitive CML patient samples. The apoptin based single or combination therapy may be an additional option in CML treatment and eventually be feasible as curative therapy.

Indexed as

AnimalsCapsid ProteinsCell ProliferationDrug Resistance, NeoplasmFusion Proteins, bcr-ablHumansK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMiceMolecular Targeted TherapyPeptide FragmentsProtein Kinase InhibitorsBCR-ABL1 fusion protein, humanCapsid ProteinsFusion Proteins, bcr-ablPeptide FragmentsProtein Kinase InhibitorsVP3 protein, Chicken anemia virus

Identifiers

PMID25216532
PMCPMC4196195
OpenAlexW2122984568

What OpenQuestion holds

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LicenceCC BY
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.