Junya Arai

Dr. Junya Arai

orcid

Research Focus & Metrics

Academic Career Length

7Years (2020-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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5 January 2022 in Gastrointestinal Endoscopy
Verified
Journal Article
Closed access
Junya AraiJunya Arai
Junya Arai
TATomonori Aoki
Tomonori Aoki
MSMasaya Sato
Masaya Sato
RNRyota Niikura
Ryota Niikura
NSNobumi Suzuki
Nobumi Suzuki
MFMitsuhiro Fujishiro
Mitsuhiro Fujishiro

13 February 2024 in Clinical Gastroenterology and Hepatology
Verified
Journal Article
Closed access
Junya AraiJunya Arai
Junya Arai
AMAtsushi Miyawaki
Atsushi Miyawaki
TATomonori Aoki
Tomonori Aoki
RNRyota Niikura
Ryota Niikura
YHYoku Hayakawa
Yoku Hayakawa
MKMasato Kasuga
Masato Kasuga

19 July 2024 in Cancer Science
Verified
Journal Article
Open access
Junya AraiJunya Arai
Junya Arai
YHYoku Hayakawa
Yoku Hayakawa
HTHiroaki Tateno
Hiroaki Tateno
HFHiroaki Fujiwara
Hiroaki Fujiwara
MKMasato Kasuga
Masato Kasuga
MFMitsuhiro Fujishiro
Mitsuhiro Fujishiro
Gastric mucins serve as a protective barrier on the stomach's surface, protecting from external stimuli including gastric acid and gut microbiota. Their composition typically changes in response to the metaplastic sequence triggered by Helicobacter pylori infection. This alteration in gastric mucins is also observed in cases of gastric cancer, although the precise connection between mucin expressions and gastric carcinogenesis remains uncertain. This review first introduces the relationship between mucin expressions and gastric metaplasia or cancer observed in humans and mice. Additionally, we discuss potential pathogenic mechanisms of how aberrant mucins and their glycans affect gastric carcinogenesis. Finally, we summarize challenges to target tumor‐specific glycans by utilizing lectin‐drug conjugates that can bind to specific glycans. Understanding the correlation and mechanism between these mucin expressions and gastric carcinogenesis could pave the way for new strategies in gastric cancer treatment.

20 December 2021 in Digestion
Verified
Journal Article
Open access
PDF file
Junya AraiJunya Arai
Junya Arai
RNRyota Niikura
Ryota Niikura
YHYoku Hayakawa
Yoku Hayakawa
TKTakuya Kawahara
Takuya Kawahara
THTetsuro Honda
Tetsuro Honda
KKKazuhiko Koike
Kazuhiko Koike
Background: Oesophageal cancer comprises 2 different histological variants: oesophageal squamous-cell carcinoma (ESCC) and adenocarcinoma (EAC). While there are multiple therapeutic options for both types, patients with advanced or metastatic oesophageal cancer still suffer from poor prognosis. Aims: The study aimed to examine the association between the risk of oesophageal cancer and medications and to estimate the chemopreventive effects of commonly used drugs. Methods: A multicentre retrospective cohort study was conducted using data from 9 hospital databases of hospitalized patients between 2014 and 2019. The primary outcomes were ESCC and EAC. The association of oesophageal cancer with drug use and clinical factors was evaluated. Odds ratios (ORs) were adjusted for age, sex, Charlson comorbidity index scores, and smoking with/without gastro-oesophageal reflux disease. Results: The use of proton pump inhibitors (PPIs) (adjusted OR [aOR] 0.48, p < 0.0001), aspirin (aOR 0.32, p < 0.0001), cyclooxygenase-2 inhibitor (COX2I) (aOR 0.70, p = 0.0005), steroid (aOR 0.19, p < 0.0001), statin (aOR 0.43, p < 0.0001), and metformin (aOR 0.42, p < 0.0001) was associated with a lower risk of ESCC than that in non-use. The use of aspirin (aOR 0.33, p = 0.0006) and steroids (aOR 0.54, p = 0.022) was associated with a lower risk of EAC than that in non-use. Conclusion: COX2Is, statins, metformin, and PPIs could help in prevention of ESCC, and aspirin and steroids may be chemopreventive for both types of oesophageal cancer.

12 April 2022 in Biomedicines
Verified
Journal Article
Open access
PDF file
Junya AraiJunya Arai
Junya Arai
RNRyota Niikura
Ryota Niikura
YHYoku Hayakawa
Yoku Hayakawa
NSNobumi Suzuki
Nobumi Suzuki
YHYoshihiro Hirata
Yoshihiro Hirata
MFMitsuhiro Fujishiro
Mitsuhiro Fujishiro
Most gastric cancers develop in patients with chronic gastritis. Chronic gastritis can be classified into two major subtypes: Helicobacter pylori (H. pylori)-induced gastritis and autoimmune gastritis (AIG). Whereas H. pylori-related gastric cancers are more common and have been extensively investigated, the clinicopathological features of gastric cancer with autoimmune gastritis are unclear. Patients diagnosed with gastric cancer and hospitalized in the University Tokyo Hospital from 1998 to 2017 were enrolled. Diagnosis of autoimmune gastritis was based on positivity for serum anti-parietal cell antibody (APCA). We evaluated mucin expression and immune cell infiltration by immunohistochemical staining for MUC5AC, MUC6, PD-L1, CD3, CD11, Foxp3, and PD1. We also examined the presence of bacterial taxa that are reportedly enriched in AIG. Survival analyses of recurrence and 5-year mortality were also performed. In total, 261 patients (76 APCA-positive and 185 APCA-negative) were analyzed. Immunohistochemical staining in the matched cohort showed that AIG-related gastric cancer had higher MUC5AC expression (p = 0.0007) and MUC6 expression (p = 0.0007). Greater infiltration of CD3-positive (p = 0.001), Foxp3-positive (p < 0.001), and PD1-positive cells (p = 0.001); lesser infiltration of CD11b-positive (p = 0.005) cells; and a higher prevalence of Bacillus cereus (p = 0.006) were found in AIG-related gastric cancer patients. The cumulative incidences of gastric cancer recurrence were 2.99% at 2 years, 15.68% at 6 years, and 18.81% at 10 years in APCA-positive patients; they were 12.79% at 2 years, 21.35% at 6 years, and 31.85% at 10 years in APCA-negative patients. The cumulative incidences of mortality were 0% at 3 years and 0% at 5 years in APCA-positive patients; they were 1.52% at 3 years and 2.56% at 5 years in APCA-negative patients. We identified molecular differences between AIG and non-AIG gastric cancer. Differences in T-cell populations and the gastric microbiota may contribute to the pathogenesis of gastric cancers and potentially affect the response to immunotherapy.

3 August 2021 in Gut
Verified
Journal Article
Closed access
PDF file
Junya AraiJunya Arai
Junya Arai
RNRyota Niikura
Ryota Niikura
YHYoku Hayakawa
Yoku Hayakawa
TATomonori Aoki
Tomonori Aoki
AYAtsuo Yamada
Atsuo Yamada
MFMitsuhiro Fujishiro
Mitsuhiro Fujishiro
OBJECTIVE To describe the mode of presentation and the clinical course of patients with ventricular pre-excitation (Wolff-Parkinson-White (WPW) syndrome), with special emphasis on asymptomatic cases in the general population. METHODS Over an eight year period (1990–97) a prospective population based survey of cases with WPW pattern was conducted in a defined population in north west Greece (340 000 inhabitants). ECGs with WPW pattern were obtained from a widespread pool of ECGs within the health system. RESULTS During the study period, 157 cases with WPW pattern were identified (49 female, 108 male). Ages ranged from infants to 84 years, mean (SD) 49.1 (21.0) years in female and 39.6 (20.6) years in male subjects (p < 0.01); 78 (49%) had no history of syndrome related symptoms. Asymptomatic subjects (n = 77; 24 female, 53 male) were older than symptomatic subjects (mean age 46.7 (21.0)v 38.5 (20.6) years, p < 0.03). Documented supraventricular tachycardia was recorded in 27 patients (17%) and atrial fibrillation in 12 (8%) (mean age at first episode 31.2 (18.3) and 51.6 (20.7) years, respectively, p < 0.01). During follow up (mean 55 months) no case of sudden death occurred. Three asymptomatic subjects reported episodes of brief palpitation. CONCLUSIONS WPW pattern is more common, and diagnosed at a younger age, in men than in women. About half the patients with WPW pattern on ECG are asymptomatic at diagnosis and tend to remain so thereafter. No sudden cardiac death occurred during the study period.