Overexpressed fibroblast growth factor receptor 2 in the invasive front of colorectal cancer: a potential therapeutic target in colorectal cancer.

Fibroblast growth factor receptor 2 (FGFR2) is considered a novel therapeutic target for various cancer. We used a silencing strategy to clarify the effect of reduced FGFR2 expression in human colorectal cancer (CRC) cells. The invasive front of cancer cells exhibited stronger FGFR2 expression than the surface area of the cancers.

Nestin is a novel target for suppressing pancreatic cancer cell migration, invasion and metastasis.

Nestin, is a class VI intermediate filament (IF) that is expressed in 30% of pancreatic ductal adenocarcinoma (PDAC) cases, and its expression in PDAC positively correlates with peripancreatic invasion. An expression vector carrying a short hairpin RNA (shRNA) targeting nestin was stably transfected into PANC-1 and PK-45H human pancreatic cancer cells, which express high nestin levels. Alterations in morphology and alignment of actin filaments and α-tubulin were examined by phase-contrast and immunocytochemistry.

Keratinocyte growth factor induces vascular endothelial growth factor-A expression in colorectal cancer cells.

Keratinocyte growth factor (KGF), which is also called fibroblast growth factor (FGF)-7, belongs to the FGF family. KGF is not commonly produced by human cancer cells, but the KGF receptor (KGFR) is expressed in most cancer cells and particularly highly expressed in well-differentiated types of cancer. Recently, it has been reported that vascular endothelial growth factor (VEGF)-A expression is induced by KGF in pancreatic cancer cells.

Expression and roles of lumican in lung adenocarcinoma and squamous cell carcinoma.

Lumican is a member of a small leucine-rich proteoglycan family and is highly expressed in several types of cancer cells and/or stromal tissue. Lumican expression in the cytoplasm in advanced colorectal cancer correlates with poor patient prognosis. The expression of lumican in stromal tissues is associated with a high tumor grade, a low estrogen receptor expression level, and young age in breast cancer and is associated with tumor invasion and advanced stage in pancreatic cancer.

Expression of keratinocyte growth factor and its receptor in human endometrial cancer in cooperation with steroid hormones.

The keratinocyte factor (KGF) and its receptor (KGFR) are implicated in tissue development and repair. We studied the expression and functions of KGF and KGFR in association with estrogen and progesterone in human endometrial tissues and cells. In non-cancerous human endometrial tissues in the secretory phase, a strong immunoreactivity of KGF in glands, stromal cells, and smooth muscle cells of spiral arteries was detected; however, in proliferative-phase tissues, the immunoreactivity of KGF or KGFR was weak or absent.

Keratinocyte growth factor-transfection-stimulated adhesion of colorectal cancer cells to extracellular matrices.

The keratinocyte growth factor (KGF) regulates cell growth and behavior in an autocrine or paracrine manner. In colorectal cancer tissues, KGF is expressed in tumor cells and adjacent stromal fibroblasts. We have constructed a KGF-gene-transfected cell line (HCT15-KGF) from a colorectal cancer cell line, HCT-15, that expresses the KGF receptor, and studied the effects of KGF on cell behavior, particularly growth and adhesion to extracellular matrices (ECMs).

Enhanced expression of keratinocyte growth factor and its receptor correlates with venous invasion in pancreatic cancer.

Keratinocyte growth factor (KGF) and KGF receptor (KGFR) have been implicated in cancer growth as well as tissue development and repair. In this study, we examined whether KGF and KGFR have a role in human pancreatic ductal adenocarcinoma (PDAC). KGFR mRNA was expressed in eight pancreatic cancer cell lines, whereas the KGF mRNA was detected in seven of the cell lines and was absent in MIA PaCa-2 cells.

[Pathological genomics of keloid fibroblastic cells].

Objective: Keloids result from the abnormal repair of the tissues after skin injuries where the pathological overgrowth of large and active fibroblastic cells expands beyond the boundaries of the initiating wound. Imbalanced expression of genes with an as yet unknown regulatory mechanism seems to result in the hypertrophic development of fibroblastic cells and over-productions of collagen. To get information as to genes which function in the actively growing keloid fibroblasts, we have applied a gene expression DNA-microarray technique by analyzing broad range of genes at once in a systematic fashion.

[Investigation of p53 polymorphism for genetic predisposition of keloid and hypertrophic scar].

Objective: To investigate the codon-72 polymorphism of the tumor suppressor gene p53, codon-72 encodes arginine (Arg) or proline (Pro) for a genetic predisposition,to keloid or hypertrophic scar.

Methods: The distribution of codon 72 polymorphism of p53 gene was analyzed from the 54 keloid and 30 hypertrophic scar(HS)of the Japanese patients with restriction fragment length polymorphism analysis and DNA sequence analysis.

Results: The frequency of the Proline-encoding alleles and Arginine-encoding alleles in the hypertrophic scar patients and the piercing-induced ear-lobe keloid patients, was deviated significantly from that in the normal Japanese controls.