Scholarlink

Background <p>The neurotrophic TRK family, which includes NTRK1, 2, and 3, could be the oncogenic driving force in various cancers, when they undergo fusion mutations with other genes and form a chimeric oncoprotein. In our study, we aimed to explore the expression and gene alterations of NTRK in pancreatic neuroendocrine tumors (pNETs).</p> Methods <p>Immunohistochemistry (IHC) staining was utilized to assess NTRK expression in pNETs, using pan-TRK cocktail (clone LBP2-NTRK). Any intensity of staining in ≥ 1% of tumor cells was classified as positive. IHC-positive specimens then underwent Fluorescence In Situ Hybridization (FISH) analysis, using the NTRK1-3 gene fragmentation probe. Clinical data were obtained through retrospective chart review.</p> Results <p>NTRK expression was observed in 16.7% (7/42) of pNETs: 4 patients were females and 3 were males; 6 were over 50 years old, with only one patient aged 29 years; 3 tumors were WHO G1, 3 were G2 and 1 was G3. Lymphovascular invasion was identified in 3 cases. No NTRK expression was detected in any of the 8 cases with liver-metastatic pNETs. No statistically significant difference was identified between the NTRK-expression and the clinicopathological parameters, such as the age, tumor location, tumor size, tumor grade, lymphovascular invasion, metastatic disease, and the expression of MGMT and SSTR2. Furthermore, no NTRK fusions were identified in any of the 7 cases by FISH analysis.</p> Conclusions <p>Our data suggest that NTRK expression could be present in some pNETs, but not associated with its gene translocation. The pathophysiology of this phenotype is discussed.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

NTRK expression and its clinical significance in pancreatic neuroendocrine tumors

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年8月28日

查看全文
  • Pingping Yan,
  • Xiaoqin Dai,
  • Fenfen Zhang,
  • Yu Dong,
  • Huijuan Shi,
  • Anjia Han

摘要

Background

The neurotrophic TRK family, which includes NTRK1, 2, and 3, could be the oncogenic driving force in various cancers, when they undergo fusion mutations with other genes and form a chimeric oncoprotein. In our study, we aimed to explore the expression and gene alterations of NTRK in pancreatic neuroendocrine tumors (pNETs).

Methods

Immunohistochemistry (IHC) staining was utilized to assess NTRK expression in pNETs, using pan-TRK cocktail (clone LBP2-NTRK). Any intensity of staining in ≥ 1% of tumor cells was classified as positive. IHC-positive specimens then underwent Fluorescence In Situ Hybridization (FISH) analysis, using the NTRK1-3 gene fragmentation probe. Clinical data were obtained through retrospective chart review.

Results

NTRK expression was observed in 16.7% (7/42) of pNETs: 4 patients were females and 3 were males; 6 were over 50 years old, with only one patient aged 29 years; 3 tumors were WHO G1, 3 were G2 and 1 was G3. Lymphovascular invasion was identified in 3 cases. No NTRK expression was detected in any of the 8 cases with liver-metastatic pNETs. No statistically significant difference was identified between the NTRK-expression and the clinicopathological parameters, such as the age, tumor location, tumor size, tumor grade, lymphovascular invasion, metastatic disease, and the expression of MGMT and SSTR2. Furthermore, no NTRK fusions were identified in any of the 7 cases by FISH analysis.

Conclusions

Our data suggest that NTRK expression could be present in some pNETs, but not associated with its gene translocation. The pathophysiology of this phenotype is discussed.