The Role of c-kit in Pancreatic Cancer
Author Information
Author(s): Yasuda Akira, Sawai Hirozumi, Takahashi Hiroki, Ochi Nobuo, Matsuo Yoichi, Funahashi Hitoshi, Sato Mikinori, Okada Yuji, Takeyama Hiromitsu, Manabe Tadao
Primary Institution: Nagoya City University Graduate School of Medical Sciences
Hypothesis
Does c-kit expression influence the proliferation and invasion of pancreatic cancer cells?
Conclusion
The SCF-KIT pathway enhances proliferation and invasiveness in KIT-positive pancreatic cancer cell lines, and this effect can be inhibited by imatinib mesylate.
Supporting Evidence
- c-kit mRNA and protein were expressed in two pancreatic cancer cell lines, PANC-1 and SW1990.
- SCF significantly enhanced proliferation and invasion in KIT-positive pancreatic cancer cell lines.
- Imatinib mesylate inhibited SCF-enhanced proliferation and invasion in KIT-positive cell lines.
- KIT expression was found in 38.1% of clinical specimens and correlated with venous system invasion.
- Patients co-expressing KIT and SCF had a tendency toward lower survival.
Takeaway
This study found that a protein called c-kit helps pancreatic cancer cells grow and spread, but a drug can stop this from happening.
Methodology
The study used RT-PCR, Western blot analysis, and immunohistochemistry to assess c-kit expression and its effects on pancreatic cancer cell lines.
Potential Biases
Potential bias in the selection of cell lines and clinical specimens.
Limitations
The study was limited to five pancreatic cancer cell lines and 42 clinical specimens, which may not represent all pancreatic cancer cases.
Participant Demographics
42 patients with invasive ductal carcinoma of the pancreas, gender and age not significantly different between groups.
Statistical Information
P-Value
0.046
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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