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Published on: January 22, 2018
Clinicopathological significance of JAK2, STAT3, and STAT4 expression in patients with gastric solid-type poorly
Shinya Umekita1, Daisuke Kiyozawa1, Hitoshi Honma1
1Department of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-Ku, Fukuoka, 812-8582, Japan.
Background:
The role of janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling remains unclear in gastric solid-type poorly differentiated adenocarcinoma. The present study investigates the clinicopathological significance of JAK2, STAT3, and STAT4 expression in solid-type poorly differentiated adenocarcinoma.
Methods:
We retrospectively enrolled 102 participants with primary solid-type poorly differentiated adenocarcinoma. We categorized participants according to deficient or proficient mismatch repair status (46 and 56 participants, respectively). Expression of phosphorylated JAK2 (pJAK2), phosphorylated STAT3 (pSTAT3), and STAT4 were analyzed via immunohistochemistry. We analyzed differences in protein expression in relation to mismatch repair status, and associations of high/low protein expression with clinicopathological characteristics and prognoses.
Results:
Deficient mismatch repair was found to be associated with high pJAK2 (p = 0.038) and STAT4 (p = 0.023) expression in contrast to proficient mismatch repair. Log-rank analysis revealed high pSTAT3 and low STAT4 expression to be significantly correlated with reduced overall survival (p = 0.001). Multivariate analysis revealed high pSTAT3 and low STAT4 expression to be independent indicators of unfavorable prognosis (hazard ratio = 2.751, p = 0.030), as was proficient mismatch repair status (hazard ratio = 3.819, p = 0.012).
Conclusions:
High expression of pJAK2 and STAT4 is more frequent in deficient compared with proficient mismatch repair in solid-type poorly differentiated adenocarcinoma. High pSTAT3 and low STAT4 expression could be a useful prognostic indicator in solid-type poorly differentiated adenocarcinoma.
Insights
Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling is implicated in gastric cancer. High pSTAT3 and low STAT4 expression indicate poor prognosis in solid-type poorly differentiated adenocarcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- The role of Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling in gastric solid-type poorly differentiated adenocarcinoma is not fully understood.
- This study investigates the clinicopathological significance of JAK2, STAT3, and STAT4 expression in this cancer subtype.
Purpose of the Study:
- To determine the clinicopathological significance of JAK2, STAT3, and STAT4 expression in gastric solid-type poorly differentiated adenocarcinoma.
- To explore the association between these proteins, mismatch repair status, and patient prognosis.
Main Methods:
- Retrospective analysis of 102 patients with primary solid-type poorly differentiated adenocarcinoma.
- Immunohistochemical analysis of phosphorylated JAK2 (pJAK2), phosphorylated STAT3 (pSTAT3), and STAT4 expression.
- Correlation of protein expression with mismatch repair status, clinicopathological characteristics, and survival outcomes.
Main Results:
- Deficient mismatch repair was associated with higher pJAK2 and STAT4 expression compared to proficient mismatch repair.
- High pSTAT3 and low STAT4 expression significantly correlated with reduced overall survival.
- High pSTAT3 and low STAT4 expression, along with proficient mismatch repair status, were independent indicators of unfavorable prognosis.
Conclusions:
- Increased pJAK2 and STAT4 expression is more prevalent in gastric solid-type poorly differentiated adenocarcinoma with deficient mismatch repair.
- High pSTAT3 and low STAT4 expression may serve as valuable prognostic biomarkers for this cancer type.
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