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At least 379 records · Page 21Linked to original sources
PubMed1994

Postoperative immunochemotherapy including streptococcal lysate OK-432 is effective for patients with gastric cancer and serosal invasion.

The effects of postoperative immunochemotherapy including the streptococcal preparation OK-432 on the rate of peritoneal recurrence and survival time after curative resection were studied in 36 patients with gastric cancer. Patients randomized to group B received 18 months of a therapy that is widely used in Japan for patients with gastric cancer: mitomycin C (MMC) and UFT, a combination of tegafur and uracil in a molar ratio of 1:4. Patients randomized to group A received the same drugs given to group B plus an intraperitoneal injection of OK-432 on postoperative day 0 and intradermal injections of OK-432 for 18 months at 2-week intervals. There were no differences between the two groups in any known prognostic factor or dose of any drug received, except for OK-432. There was no difference in the toxicity rates between the groups. The concomitant administration OK-432 and anticancer drugs significantly decreased the rates of peritoneal recurrence and lengthened survival time (P < 0.05).

Adjuvants, Immunologic↗
PubMed1999

Membranous tracheobronchial injury repaired with gastric serosal patch.

This unusual case involves pharyngolaryngoesophagectomy complicated by injury to the membranous trachea and right bronchus. Repair was possible after partial sternal split and elevation of the tracheostoma through the anterior mediastinum, pulling the stomach to the neck, and using the stomach as a patch to repair the injury to the membranous portion of the airway.

Bronchi↗
PubMed1997

Prognostic study of gastric cancer without serosal invasion: reevaluation of the definition of early gastric cancer.

BACKGROUND: Early gastric cancer, a term defined by Japanese researchers in the 1960s, is equivalent to pT1 tumor stage regardless of nodal status. Recently, there were suggestions to exclude node-positive pT1 gastric cancer from this entity and to consider node-negative pT2 gastric cancer as early gastric cancer. STUDY DESIGN: A survival analysis was conducted of 294 patients who underwent resection for gastric cancers confined within the gastric wall (pT1, n = 164; pT2, n = 130) between 1986 and 1992. RESULTS: The cumulative 5-year survival rate was 93.5% for pT1 patients and 67.9% for pT2 patients, with an overall survival of 82.5%. There was a significant difference in the 5-year survival rate between node-positive and node-negative pT1 patients (72.8% versus 95.6%; p = 0.0095). The 5-year survival rate of node-negative pT2 patients (80.4%) was significantly worse than that of node-negative pT1 patients (p = 0.011) but was not significantly better than that of node-positive pT1 patients (p = 0.4). If excellent prognosis is a prerequisite for the definition of early gastric cancer, then node-positive pT1 cancer and node-negative pT2 cancer should not be considered early gastric cancer. CONCLUSIONS: In the 1990s, now that new imaging techniques such as endoscopic ultrasonography has been introduced, the preoperative staging of gastric cancer can be made more accurately than in the 1960s, when the term "early gastric cancer" was defined. Because the prognosis of early gastric cancers, if subcategorized by nodal status, is not homogeneously excellent, a reevaluation of the definition of early gastric cancer may be necessary.

Adolescent↗
PubMed1998

Expression of p53 and p21 are independent prognostic factors in patients with serosal invasion by gastric carcinoma.

To evaluate whether the expression of p53 and that of p21 are independent prognostic factors in patients with advanced gastric cancer, we investigated clinicopathological factors and the expression of p53 and p21 in 158 patients with gastric cancer that had invaded the serosa and who had undergone curative gastrectomy. In multivariate survival analysis of 156 surviving patients, we evaluated the size of the tumor, lymph node metastasis, venous invasion, lymph node dissection, expression of p53, and expression of p21 as independent prognostic factors. Moreover, we divided patients into four groups according to the expression of p53 and p21 in their tumors [group A, p53-/p21-, N = 40 (one died within 30 days of surgery); group B, p53-/p21+, N = 23; group C, p53+/p21-, N = 58; and group D, p53+/p21+, N = 37 (one died within 30 days of surgery)]. The 5- and 10-year survival rates of 39 patients in group A were 71.7% and 64.3%, those of 23 patients in group B were 81.4% and 81.4%, those of 58 patients in group C were 35.6% and 30.2%, and those of 36 patients in group D were 67.9% and 60.7%. The prognosis of patients in group C was poorer than that of patients in the other three groups. This result indicates that the evaluation of the expression of both p53 and p21 expression might provide prognostic information that is more accurate than that provided by evaluation of the expression of p53 alone.

Adult↗
PubMed2001

Activation of paracrine TGF-beta1 signaling upon stimulation and degranulation of rat serosal mast cells: a novel function for chymase.

As a source of transforming growth factor beta1 (TGF-beta1), mast cells have been implicated as potential effector cells in many pathological processes. However, the mechanisms by which mast cells express, secrete, and activate TGF-beta1 have remained vague. We show here by means of RT-PCR, immunoblotting, and immunocytochemistry that isolated rat peritoneal mast cells synthesize and store large latent TGF-beta1 in their chymase 1-containing secretory granules. Mast cell stimulation and degranulation results in rapid secretion of the latent TGF-beta1, which is converted by chymase 1 into an active form recognized by the type II TGF-beta serine/threonine kinase receptor (TbetaRII). Thus, mast cells secrete active TGF-beta1 by a unique secretory mechanism in which latent TGF-beta1 and the activating enzyme chymase 1 are coreleased. The activation of latent TGF-beta1 specifically by chymase was verified using recombinant human latent TGF-beta1 and recombinant human chymase. In isolated TbetaRI- and TbetaRII-expressing peritoneal macrophages, the activated TGF-beta1 induces the expression of the plasminogen activator inhibitor 1 (PAI-1), whereas in the mast cells, the levels of TbetaRI, TbetaRII, and PAI-1 expression were below detection. Selective stimulation of mast cells in vivo in the rat peritoneal cavity leads to rapid overexpression of TGF-beta1 in peritoneal mast cells and of TbetaRs in peritoneal macrophages. These data strongly suggest that mast cells can act as potent paracrine effector cells both by secreting active TGF-beta1 and by enhancing its response in target cells.

Animals↗
PubMed2005

Transforming growth factor-beta promotes pro-fibrotic behavior by serosal fibroblasts via PKC and ERK1/2 mitogen activated protein kinase cell signaling.

OBJECTIVE: To assess the role of fibroblasts, transforming growth factor (TGF)-beta, and cell signal pathways in promoting fibrosis in Crohn's disease (CD). SUMMARY BACKGROUND DATA: Intestinal strictures are a major source of morbidity in CD. Fibroblasts found at sites of stricture promote fibrogenesis. The mechanisms underlying this pro-fibrotic behavior remain elusive. METHODS: Fibroblasts were isolated from strictured and macroscopically normal serosa in patients with CD and from normal serosa in patients with colorectal cancer. Whole cell connective tissue growth factor (CTGF) and fibronectin expression were determined by Western blot analysis. Fibroblast type I collagen expression was evaluated by real-time PCR, while fibroblast contractile activity was measured using fibroblast populated collagen lattices. Cells were stimulated with TGF-beta1 and inhibitors of the protein kinase C (PKC) and ERK 1/2 mitogen activated protein (MAP) kinase cell signaling pathways. RESULTS: Stricture fibroblasts displayed enhanced constitutive expression of fibronectin. TGF-beta promoted fibroblast CTGF, fibronectin, and type I collagen expression and enhanced fibroblast contractile activity. Inhibition of PKC reduced basal collagen expression and contractile activity in Crohn's fibroblasts and attenuated the effect of TGF-beta on fibroblast CTGF, fibronectin, and collagen I expression as well as fibroblast contractility. ERK 1/2 inhibition had a similar effect on TGF-beta-induced CTGF and fibronectin expression. CONCLUSIONS: TGF-beta is a critical pro-fibrotic growth factor in CD, and its effects are mediated via PKC and ERK 1/2 MAP kinase cell signaling. These pathways may represent novel therapeutic targets for patients with CD characterized by recurrent intestinal stricture formation.

Adult↗