changes in expression patterns of serum carcinoembryonic antigen at initial diagnosis (ceA in) and disease progression (ceA pd) in lung cancer patients under eGfR-tyrosine kinase inhibitors (tKi) treatment may reflect different tumor progression profiles. Of the 1736 lung cancer patients identified from the cancer registry group between 2011 to 2016, we selected 517 patients with advanced stage adenocarcinoma, data on eGfR mutation status and ceA in , among whom were 288 patients with data on ceA pd , eligible for inclusion in the correlation analysis of clinical characteristics and survival. Multivariable analysis revealed that ceA in expression was associated with poor progression-free survival in patients harboring mutant EGFR. Moreover, CEA in and ceA pd were associated with the good and poor post-progression survival, respectively, in the EGFR-mutant group. Cell line experiments revealed that CEA expression and cancer dissemination can be affected by EGFR-TKI selection. EGFR-mutant patients, exhibiting high ceA in (≥5 ng/mL) and low CEA pd (<5 ng/mL), showed a potential toward displaying new metastasis. Taken together, these findings support the conclusion that EGFR mutation status is a critical factor in determining prognostic potential of ceA in and ceA pd in patients under eGfR-tKi treatment, and ceA in and ceA pd are associated with distinct cancer progression profiles. Carcinoembryonic antigen (CEA) is one of the most commonly used tumor markers whose overexpression was first discovered in colorectal cancer and followed by cancers in the aerodigestive tract and other organs 1,2. Serum CEA is used as a marker along with imaging for monitoring tumor progression and predicting survival outcomes in colorectal cancer 3,4. Although the suitability of CEA as an effective marker for lung cancer remains debatable, characteristics such as lower cost, noninvasiveness, and lack of other reliable markers, make CEA an attractive option in lung cancer 5,6. Additionally, CEA measurements before and after surgery have been suggested to provide valuable information for predicting disease progression and for determining the need for adjuvant treatment during early stage lung cancer 7,8. As proven by several large-scale clinical trials, epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKI) are highly effective in lung cancer patients harboring EGFR activating mutations, mainly, deletions in exon 19 (Del19) and a L858R mutation in exon 21 9-13. However, despite an initial positive response, patients harboring the activating EGFR mutations ultimately develop resistance to EGFR-TKI by different mechanisms 14-18. Thus, the utility of CEA as a predictive or prognostic marker of EGFR-TKI treatment response remains controversial. Several studies have reported that serum CEA levels are closely associated with EGFR-TKI treatment outcomes, and that high CEA expression after EGFR-TKI treatment predicts poor survival in patients with EGFR-mutant lung cancer 19,20. In contrast, some reports have shown that CEA levels...
Inhibitors of DNA binding and cell differentiation (ID) proteins regulate cellular differentiation and tumor progression. Whether ID family proteins serve as a linkage between pathological differentiation and cancer stemness in colorectal cancer is largely unknown. Here, the expression of ID4, but not other ID family proteins, was enriched in LGR5-high colon cancer stem cells. Its high expression was associated with poor pathological differentiation of colorectal tumors and shorter survival in patients. Knockdown of ID4 inhibited the growth and dissemination of colon cancer cells, while enhancing chemosensitivity. Through gene expression profiling analysis, brain-derived neurotrophic factor (BDNF) was identified as a downstream target of ID4 expression in colorectal cancer. BDNF knockdown decreased the growth and migration of colon cancer cells, and its expression enhanced dissemination, anoikis resistance, and chemoresistance. ID4 silencing attenuated the epithelial-to-mesenchymal transition (EMT) pattern in colon cancer cells. Gene cluster analysis revealed that ID4 and BDNF expression was clustered with mesenchymal markers and distant from epithelial genes. BDNF silencing decreased the expression of mesenchymal markers Vimentin, CDH2 and SNAI1. These findings demonstrated that ID4-BDNF signaling regulates colorectal cancer survival, with the potential to serve as a prognostic marker in colorectal cancer.
Carcinoembryonic antigen (CEA) is one of the most commonly used tumor markers. Although the suitability of CEA as an effective marker for lung cancer remains debatable, characteristics such as noninvasiveness and lack of other reliable markers make CEA an attractive option in lung cancer. Divergent CEA expression patterns before and after EGFR-tyrosine kinase inhibitor (TKI) treatment have been reported. However, whether these patterns are associated with tumor progression remain elusive. We hypothesized that divergent patterns of serum carcinoembryonic antigen at initial diagnosis (CEAIn) and disease progression (CEAPd) may reflect the diversity of lung cancer cells selected by TKI, conferring distinct progression profiles in patients. Our objective was to verify the prognostic potential of divergent CEA patterns before and after TKI treatment in lung cancer patients with wild-type or mutant EGFR. Of the 1736 lung cancer patients identified from the cancer registry group between 2011 to 2016, we selected 517 patients with advanced stage adenocarcinoma, data on EGFR mutation status and CEAIn, among whom were 288 patients with data on CEAPd, eligible for inclusion in the correlation analysis of clinical characteristics and survival. EGFR wild-type lung adenocarcinoma patients displayed lower CEAIn level than those with EGFR mutations. Multivariable analysis revealed that CEAIn expression was associated with poor progression-free survival in patients harboring mutant EGFR but not in those with wild-type EGFR. Moreover, CEAIn and CEAPd were associated with the good and poor post-progression survival, respectively, only in the EGFR-mutant and not in the wild-type group. In vitro cell line experiments revealed that CEA expression, cancer dissemination, and chemoresistant properties can be affected by EGFR-TKI selection. EGFR-mutant patients, exhibiting high CEAIn (≥ 5 ng/mL) and low CEAPd (< 5 ng/mL), showed a potential toward displaying new metastasis. Our findings support the notion that EGFR mutation status is a critical factor in determining prognostic potential of CEAIn and CEAPd in patients under EGFR-TKI treatment, and divergent CEAIn and CEAPd patterns are associated with distinct cancer progression profiles. Citation Format: Ming-Yi Zheng, Yen-Shou Kuo, Yu-Ting Chou. Prognostic potential of carcinoembryonic antigen expression patterns in lung adenocarcinoma [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 6491.
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