We examined the possibility that periodontal ligament (PDL) cells can differentiate into osteoblasts and/or cementoblasts in freshly isolated PDL tissues and in cultured cells derived from PDL. PDL tissues were obtained from the incisor teeth of bovine lower jaws; gingival connective tissues of the same animals were used as controls. Freshly isolated PDL tissues and cultured PDL cells showed an intense alkaline phosphatase (ALPase) activity both histochemically and biochemically. The production of 3',5'-cyclic adenosine monophosphate (cAMP) was greatly increased in response to human parathyroid hormone [PTH(1-34)], in both freshly isolated PDL tissues and cultured PDL cells. In contrast, neither ALPase activity nor PTH-dependent cAMP production was detected in gingival connective tissues and cultured gingival fibroblasts. Furthermore, cultured PDL cells synthesized a protein immunologically cross-reactive with bovine bone gla protein (BGP), a highly reliable marker of osteoblastic cells. When 10(-8) M 1a, 25-dihydroxyvitamin D3 [1a,25(OH)2D3] was added to the PDL cell cultures, the synthesis of the BGP-like protein was increased 2- to 3-fold. The maximal level of the synthesis was obtained 72 h after the addition of 1a,25(OH)2D3. Gingival fibroblasts cultured with or without 1a,25(OH)2D3 did not produce any appreciable amounts of the BGP-like protein. These results indicate that the PDL cells have phenotypes typical of osteoblasts, indicating that they may differentiate into osteoblasts and/or cementoblasts.
These results suggest that the expression patterns of c-met, AMFR, and uPAR may be closely associated with the progression and invasion of gastric carcinoma as well as the prognoses of the patients. Borrmann type 4 gastric carcinoma is characterized by the diverse and simultaneous expression of these three genes.
Background. E‐cadherin (ECD) is known to be an invasion suppressor gene, and urokinase‐type plasminogen activator (uPA) plays a central role in infiltration of solid cancers. Methods. To elucidate the relationship between expression of these factors and metastasis in patients with gastric cancer, the authors examined immunohistochemically a combination analysis of uPA and E‐cadherin expression in 98 primary tumors, and the results were correlated with several parameters related to metastasis. Results. Among 125 tumors, 42 (34%) were evaluated as having E‐cadherin expression (E‐cadherin‐positive), and the other 83 (66%) were defined as having reduced E‐cadherin expression (E‐cadherin‐negative). uPA immunoreactivity was observed in 82 tumors (66%). There were four subtypes of patterns of uPA and E‐cadherin expression: 22 uPA‐negative/E‐cadherin‐positive, 17 uPA‐negative/E‐cadherin‐negative, 21 uPA‐positive/E‐cadherin‐positive, and 65 uPA‐positive/E‐cadherin‐negative. uPA overexpression and reduced E‐cadherin expression were associated with lymph node metastasis, vessel invasion, serosal involvement, and poor prognosis. In addition, uPA‐positive/E‐cadherin‐negative tumors were associated significantly with large tumors, positive serosal invasion, lymph node involvement, and poor prognosis. Patients with uPA‐positive/E‐cadherin‐negative expression had the poorest prognoses, compared with the three other groups of patients. uPA‐positive/E‐cadherin‐negative tumors had a fourfold relative risk of death when compared with uPA‐negative/E‐cadherin‐positive tumors. A Cox proportional hazard model projected lymph node status as the strongest of the prognostic variables, followed by DNA ploidy patterns and uPA/E‐cadherin tissue status. Conclusions. These results indicate that immunohistochemical combination analysis of uPA and E‐cadherin expression may be a powerful aid in evaluating meta‐static potential or the prognosis of patients with gastric cancer. Cancer 1995;76:941–53.
Expression of urokinase-type plasminogen activator (uPA), plasminogen activator inhibitor-1 (PAI-1) and plasminogen activator inhibitor-2 (PAI-2) was evaluated in 125 surgically resected gastric cancers by immunohistochemical analysis. Tissue was stained immunohistochemically with a monoclonal antibody against human uPA and monoclonal antibodies against human PAI-1 and PAI-2. In addition, DNA ploidy patterns were determined by cytofluorometer after staining with propidium iodide. We found that 82 (66%) of the 125 gastric cancers expressed uPA as diffuse cytoplasmic staining, as intensely outlined luminal borders. PAI-1 expression was observed in 62 (50%) of 125 gastric cancer as a fine, diffuse and granular pattern in the cytoplasm. PAI-2 expression was observed in 65 (52%) of the 125 gastric cancers as a diffuse cytoplasmic staining. uPA-positive tumours showed a higher incidence of infiltration, lymph node metastasis and peritoneal dissemination that uPA-negative ones. Patients with uPA-positive tumours proved to have a significantly poorer prognosis than those with negative ones. PAI-1-negative tumours showed a higher incidence of liver metastasis and carried a poorer prognosis than PAI-1-positive ones. There was no significant correlation between uPA or PAI-1 expression and DNA ploidy patterns. Conversely, there was no significant relationship between PAI-2 expression and clinicopathological parameters and prognosis. According to the expression of uPA and PAI-1 status, groups of 19 uPA(-)/PAI-1(-), 44 uPA(+)/PAI-1(-), 23 uPA(-)/PAI-1(+) and 39 uPA(+)/PAI-1(+) were subdivided. Tumours with uPA(+)/PAI-1(-) had a significantly higher incidence of liver metastasis, lymph node metastasis and serosal invasion than the other groups of tumours. Patients with uPA(+)/PAI-1(-) tumours had a significantly poorer prognosis than those with uPA(-)/PAI-1(+) tumours. These results indicate that uPA expression is a useful biological prognostic indicator, and that uPA expression is a useful biological prognostic indicator, and that uPA and PAI-1 may play an important part in the tumour progression and metastasis in gastric cancer.
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