A truncated splice variant of human lysyl oxidase-like 2 promotes migration and invasion in esophageal squamous cell carcinoma

Specific gene expression profiles are associated with a pathologic complete response to neoadjuvant therapy in esophageal adenocarcinoma

“…For example the pCR rate for SCC tumors has been as high as 49% compared to 23% for EAC. (9) Overexpression of CCL28 has been shown to be associated with tumor progression in other studies of SCC, (26) but to our knowledge, this gene has not been studied exclusively in EAC tumors. In addition, all patients in the 2009 study received the older chemotherapy regimen of Cisplatinum and 5-FU, (20) while the vast majority of patients in our study received Carboplatin and Paclitaxel based on the results of the 2012 CROSS trial.…”

“…(26) It is recognized that tumor microenvironment and systemic inflammation play an important role in tumor behavior. Accordingly, CCL28 seems like a rational candidate gene for our investigations.…”

“…Accordingly, CCL28 seems like a rational candidate gene for our investigations. (26, 27) An association between CCL28 and pCR in esophageal cancer was first shown in a 2009 study, that carried out microarray analyses of over 27,000 individual human genes on 27 patients with both EAC and SCC of the esophagus. (20) From the microarray analysis the authors able to create a panel of 5 genes, including CCL28, which could predict response to therapy with 95% accuracy in 74% of their patients.…”

Increased lysyl oxidase‐like 2 associates with a poor prognosis in non‐small cell lung cancer

“…Overexpression of cytoplasmic and nuclear LOXL2 has also been reported in gastric cancer tissues compared to matched adjacent normal tissues, and this overexpression was associated with depth of tumor invasion, lymph node metastasis, and shorter overall survival. 12,24 It is possible that storage of LOXL2 in the cytoplasm may prevent GSK3induced Snail degradation, which in turn may trigger epithelial-mesenchymal transition. 22 The same group also explored the biological functions of LOXL2 in ESCC and identified a new LOLX2 splice variant (lacking 72 nucleotides) that promotes cell migration and invasion to a greater extent than wild-type LOXL2.…”

A novel splice variant of LOXL2 promotes progression of human papillomavirus–negative head and neck squamous cell carcinoma

“…17,18 In patients with esophageal squamous cell carcinoma, several alternative splicing isoforms of LOXL2 also have been discovered to exert cell functions distinct from those of canonical-type LOXL2. [19][20][21][22] In our previous study, a total of 580 significant ASEs related to HPV-negative HNSCC have been identified using outlier analysis, including a novel splice variant of LOXL2 with a unique inserted exon. 16 However, to the best of our knowledge, the function and downstream effects of this specific LOXL2 variant have not been described to date.…”