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An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
Published on: July 20, 2014
Array-based comparative genomic hybridization of circulating esophageal tumor cells
Dal Ho Kim1, Manabu Muto, Yoshitaka Kuwahara
1Division of Genetics, National Cancer Center Research Institute, Chome, Tokyo 104-0045, Japan.
Oncology Reports
|October 4, 2006
Summary
Genetic alterations in circulating esophageal tumor cells were analyzed. P16 deletion and CCND1 amplification are linked to esophageal squamous cell carcinoma progression and invasion.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Esophageal squamous cell carcinoma (ESCC) frequently metastasizes, even in early stages.
- Investigating genetic changes in circulating tumor cells is crucial for understanding metastasis.
Purpose of the Study:
- To identify genetic alterations in circulating esophageal tumor cells from lymph node metastasis.
- To explore the role of specific gene alterations in ESCC progression and invasion.
Main Methods:
- Array-based comparative genomic hybridization (CGH) on xenografts derived from thoracic duct lymph.
- Quantitative Southern blot analysis on primary tumors and lymph nodes.
- Matrigel invasion assays to assess the functional role of p16.
Main Results:
- Identified candidate amplified loci (e.g., CCND1) and homozygously deleted loci (e.g., p16) in circulating tumor cells.
- Found high frequencies of p16 homozygous deletion (75%) and CCND1 amplification (62.5%) in xenografts.
- p16 homozygous deletion was observed in primary tumors (30.8%) and lymph nodes (50%).
- Restoring p16 function inhibited ESCC cell invasion, suggesting its role in metastasis.
Conclusions:
- p16 homozygous deletion and CCND1 amplification are associated with ESCC progression.
- p16 inactivation may contribute to ESCC cell invasion and metastasis.
- This study provides novel insights into the genetic landscape of circulating tumor cells in ESCC.
