Evidence map›Paper›PMID 26762407›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

Inhibition of carbonic anhydrase potentiates bevacizumab treatment in cholangiocarcinoma.

Kulthida Vaeteewoottacharn, Ryusho Kariya, Paweena Dana, Sawako Fujikawa, Kouki Matsuda, Koichi Ohkuma, Eriko Kudo, Ratthaphol Kraiklang, Chaisiri Wongkham, Sopit Wongkham and 1 more

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Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 45 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

11 authors at 2 institutions in 2 countries.

Kulthida VaeteewoottacharnDivision of Hematopoiesis, Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Kumamoto, 860-0811, Japan.
Ryusho KariyaDivision of Hematopoiesis, Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Kumamoto, 860-0811, Japan.
Paweena DanaDepartment of Biochemistry, Khon Kaen University, Khon Kaen, Thailand.
Sawako FujikawaDivision of Hematopoiesis, Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Kumamoto, 860-0811, Japan.
Kouki MatsudaDivision of Hematopoiesis, Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Kumamoto, 860-0811, Japan.
Koichi OhkumaDivision of Hematopoiesis, Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Kumamoto, 860-0811, Japan.
Eriko KudoDivision of Hematopoiesis, Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Kumamoto, 860-0811, Japan.
Ratthaphol KraiklangLiver Fluke and Cholangiocarcinoma Research Center, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Chaisiri WongkhamDepartment of Biochemistry, Khon Kaen University, Khon Kaen, Thailand.
Sopit WongkhamDepartment of Biochemistry, Khon Kaen University, Khon Kaen, Thailand.
Seiji OkadaDivision of Hematopoiesis, Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Kumamoto, 860-0811, Japan. okadas@kumamoto-u.ac.jp.
Kumamoto University · JPKhon Kaen University · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholangiocarcinoma (CCA) is a unique liver cancer subtype with an increasing incidence globally. The lack of specific symptoms and definite diagnostic markers results in a delayed diagnosis and disease progression. Systemic chemotherapy is commonly selected for advanced CCA even though its advantages remain unknown. Targeted therapy, especially anti-vascular endothelial growth factor (VEGF) therapy, is promising for CCA; however, improvements in the therapeutic regimen are necessary to overcome subsequent resistance. We demonstrated VEGF expression was higher in CCA cell lines than in other liver cancer cells. Secreted VEGFs played roles in the induction of peri- and intra-tumoral vascularization. VEGF neutralization by bevacizumab effectively reduced tumor growth, mainly through the suppression of angiogenesis; however, increases in the expression of hypoxia-inducible factor 1α (HIF1α) and HIF1α-responsive genes (such as VEGF, VEGFR1, VEGFR2, carbonic anhydrase (CA) IX and CAXII) indicated the potential for subsequent therapeutic resistance. Supplementation with a carbonic anhydrase inhibitor, acetazolamide, enhanced the anti-CCA effects of bevacizumab. Anti-angiogenesis and anti-proliferation were observed with the combination treatment. These results suggested a novel treatment strategy to overcome anti-angiogenesis resistance and the importance of "induced essentiality" in the treatment of CCA.

Indexed as

AcetazolamideAngiogenesis InhibitorsBevacizumabBile Duct NeoplasmsCarbonic Anhydrase InhibitorsCarbonic AnhydrasesCell Line, TumorCell ProliferationCholangiocarcinomaDrug Resistance, NeoplasmHep G2 CellsHumansHypoxia-Inducible Factor 1, alpha SubunitNeovascularization, PathologicVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1AcetazolamideAngiogenesis InhibitorsBevacizumabCarbonic Anhydrase InhibitorsCarbonic AnhydrasesHypoxia-Inducible Factor 1, alpha SubunitVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2VEGFA protein, humanAnti-angiogenic treatmentCarbonic anhydraseCholangiocarcinomaHypoxia-inducible factor 1αVascular endothelial growth factor

Identifiers

PMID26762407
OpenAlexW2238301302

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.