Evidence map›Paper›PMID 29720727›Full record

ArticleOncogene2018

Recapitulation of pharmacogenomic data reveals that invalidation of SULF2 enhance sorafenib susceptibility in liver cancer.

Sarah Yoon, Eun-Ju Lee, Ji-Hye Choi, Taek Chung, Do Young Kim, Jong-Yeop Im, Myung-Ho Bae, Jung-Hee Kwon, Hyuk-Hoon Kim, Hyung Chul Kim and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. 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
1.5field-weighted citation impact, top 17% 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, 18 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

13 authors at 3 institutions in 2 countries.

Sarah YoonDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea.
Eun-Ju LeeDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea.
Ji-Hye ChoiDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea.
Taek ChungDepartment of Pathology and BK21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Republic of Korea.
Do Young KimDepartment of Gastroenterology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jong-Yeop ImDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea.
Myung-Ho BaeCbsBioscience, Inc, Daejeon, Republic of Korea.
Jung-Hee KwonCbsBioscience, Inc, Daejeon, Republic of Korea.
Hyuk-Hoon KimDepartment of Emergency Medicine, Ajou University School of Medicine, Suwon, Republic of Korea.
Hyung Chul KimDevelopmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Young Nyun ParkDepartment of Pathology and BK21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Republic of Korea.
Hee-Jung WangDepartment of Surgery, Ajou University School of Medicine, Suwon, Republic of Korea.
Hyun Goo WooDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of Korea. hg@ajou.ac.kr.ORCID http://orcid.org/0000-0002-0916-893X
Ajou University · KRYonsei University · KRNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene mutations play critical roles during cancer development and progression, and therefore represent targets for precision medicine. Here we recapitulated the pharmacogenomic data to delineate novel candidates for actionable mutations and therapeutic target drugs. As a proof-of-concept, we demonstrated that the loss-of-function of SULF2 by mutation (N491K) or inhibition enhanced sorafenib sensitivity in liver cancer cells and in vivo mouse models. This effect was mediated by deregulation of EGFR signaling and downstream expression of LCN2. We also report that the liver cancer patients non-responding to sorafenib treatment exhibit higher expression of SULF2 and LCN2. In conclusion, we suggest that SULF2 plays a key role in sorafenib susceptibility and resistance in liver cancer via deregulation of LCN2. Diagnostic or therapeutic targeting of SULF2 (e.g., OKN-007) and/or LCN2 can be a novel precision strategy for sorafenib treatment in cancer patients.

Indexed as

AnimalsCell Line, TumorErbB ReceptorsHumansLipocalin-2Liver NeoplasmsMiceMutationPharmacogeneticsSignal TransductionSorafenibSulfatasesSulfotransferasesErbB ReceptorsLipocalin-2SorafenibSULF2 protein, humanSulfatasesSulfotransferases

Identifiers

PMID29720727
OpenAlexW2799574560

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.