PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.




PMID- 28422979
OWN - NLM
STAT- MEDLINE
DA  - 20170419
DCOM- 20170427
LR  - 20170427
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 4
DP  - 2017
TI  - Correlation of EGFR or KRAS mutation status with 18F-FDG uptake on PET-CT scan in
      lung adenocarcinoma.
PG  - e0175622
LID - 10.1371/journal.pone.0175622 [doi]
AB  - BACKGROUND: 18F-fluoro-2-deoxy-glucose (18F-FDG) positron emission tomography
      (PET) is a functional imaging modality based on glucose metabolism. The
      correlation between EGFR or KRAS mutation status and the standardized uptake
      value (SUV) of 18F-FDG PET scanning has not been fully elucidated. METHODS:
      Correlations between EGFR or KRAS mutation status and clinicopathological factors
      including SUVmax were statistically analyzed in 734 surgically resected lung
      adenocarcinoma patients. Molecular causal relationships between EGFR or KRAS
      mutation status and glucose metabolism were then elucidated in 62 lung
      adenocarcinomas using cap analysis of gene expression (CAGE), a method to
      determine and quantify the transcription initiation activities of mRNA across the
      genome. RESULTS: EGFR and KRAS mutations were detected in 334 (46%) and 83 (11%) 
      of the 734 lung adenocarcinomas, respectively. The remaining 317 (43%) patients
      had wild-type tumors for both genes. EGFR mutations were more frequent in tumors 
      with lower SUVmax. In contrast, no relationship was noted between KRAS mutation
      status and SUVmax. CAGE revealed that 4 genes associated with glucose metabolism 
      (GPI, G6PD, PKM2, and GAPDH) and 5 associated with the cell cycle (ANLN, PTTG1,
      CIT, KPNA2, and CDC25A) were positively correlated with SUVmax, although
      expression levels were lower in EGFR-mutated than in wild-type tumors. No similar
      relationships were noted with KRAS mutations. CONCLUSIONS: EGFR-mutated
      adenocarcinomas are biologically indolent with potentially lower levels of
      glucose metabolism than wild-type tumors. Several genes associated with glucose
      metabolism and the cell cycle were specifically down-regulated in EGFR-mutated
      adenocarcinomas.
FAU - Takamochi, Kazuya
AU  - Takamochi K
AD  - Department of General Thoracic Surgery, Juntendo University School of Medicine,
      Tokyo, Japan.
FAU - Mogushi, Kaoru
AU  - Mogushi K
AD  - Center for Genomic and Regenerative Medicine, Juntendo University School of
      Medicine, Tokyo, Japan.
FAU - Kawaji, Hideya
AU  - Kawaji H
AD  - Preventive Medicine and Applied Genomics Unit, RIKEN Advanced Center for
      Computing and Communication, Yokohama, Kanagawa, Japan.
AD  - RIKEN Preventive Medicine and Diagnosis Innovation Program, Wako, Saitama, Japan.
FAU - Imashimizu, Kota
AU  - Imashimizu K
AD  - Department of General Thoracic Surgery, Juntendo University School of Medicine,
      Tokyo, Japan.
FAU - Fukui, Mariko
AU  - Fukui M
AD  - Department of General Thoracic Surgery, Juntendo University School of Medicine,
      Tokyo, Japan.
FAU - Oh, Shiaki
AU  - Oh S
AD  - Department of General Thoracic Surgery, Juntendo University School of Medicine,
      Tokyo, Japan.
FAU - Itoh, Masayoshi
AU  - Itoh M
AD  - Preventive Medicine and Applied Genomics Unit, RIKEN Advanced Center for
      Computing and Communication, Yokohama, Kanagawa, Japan.
FAU - Hayashizaki, Yoshihide
AU  - Hayashizaki Y
AD  - Preventive Medicine and Applied Genomics Unit, RIKEN Advanced Center for
      Computing and Communication, Yokohama, Kanagawa, Japan.
FAU - Ko, Weijey
AU  - Ko W
AD  - Diagnostic Imaging Center, Yotsuya Medical Cube, Tokyo, Japan.
FAU - Akeboshi, Masao
AU  - Akeboshi M
AD  - Diagnostic Imaging Center, Yotsuya Medical Cube, Tokyo, Japan.
FAU - Suzuki, Kenji
AU  - Suzuki K
AD  - Department of General Thoracic Surgery, Juntendo University School of Medicine,
      Tokyo, Japan.
LA  - eng
PT  - Journal Article
DEP - 20170419
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (KRAS protein, human)
RN  - 0 (Radiopharmaceuticals)
RN  - 0Z5B2CJX4D (Fluorodeoxyglucose F18)
RN  - EC 2.7.10.1 (EGFR protein, human)
RN  - EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
RN  - EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
RN  - Adenocarcinoma of lung
SB  - IM
MH  - Adenocarcinoma/diagnostic imaging/*genetics/surgery
MH  - Aged
MH  - Biological Transport
MH  - Female
MH  - Fluorodeoxyglucose F18/*metabolism
MH  - Gene Expression Profiling
MH  - *Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Lung/diagnostic imaging/metabolism/surgery
MH  - Lung Neoplasms/diagnostic imaging/*genetics/surgery
MH  - Male
MH  - Middle Aged
MH  - *Mutation
MH  - Positron-Emission Tomography
MH  - Proto-Oncogene Proteins p21(ras)/*genetics/metabolism
MH  - ROC Curve
MH  - Radiopharmaceuticals/metabolism
MH  - Receptor, Epidermal Growth Factor/*genetics/metabolism
MH  - Transcription Initiation, Genetic
EDAT- 2017/04/20 06:00
MHDA- 2017/04/28 06:00
CRDT- 2017/04/20 06:00
PHST- 2016/03/02 [received]
PHST- 2017/03/27 [accepted]
AID - 10.1371/journal.pone.0175622 [doi]
AID - PONE-D-16-07861 [pii]
PST - epublish
SO  - PLoS One. 2017 Apr 19;12(4):e0175622. doi: 10.1371/journal.pone.0175622.
      eCollection 2017.

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