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Biomedical subjects

Y Kakeji

Publications and source records attributed to Y Kakeji.

At least 37 records · Page 2Linked to original sources

Intratumoral neovascularization and growth pattern in early gastric carcinoma.

BACKGROUND: The growth pattern of early gastric carcinoma, based on a volumetric analysis, reflects biologic characteristics of the tumor. The authors investigated the microvessel density (MVD), expression of vascular endothelial growth factor (VEGF), and growth patterns in early gastric carcinoma. METHODS: Ninety-four tissue specimens resected from patients with early gastric carcinoma invading the submucosal layer were examined. Microvessel quantification was performed immunohistochemically using a monoclonal antibody against factor VIII-related antigen. VEGF expression was studied using an anti-VEGF polyclonal antibody. Growth patterns were defined as follows: Pen A type: expansively penetrating growth; Pen B type: infiltratively penetrating growth; Super type: superficially spreading growth. RESULTS: The mean MVD was 16.9 (range, 5.2-43.0). MVD was significantly higher in tumors with venous invasion (P<0.01), lymphatic vessel invasion (P<0.05), and lymph node metastases (P<0.05) compared with MVD in tumors without venous or lymphatic vessel invasion or lymph node metastases. The VEGF-positive rate of Pen A type tumors was 66.7% (18 of 27), that Pen B type was 10.0% (1 of 10), that of Super type was 19.4% (6 of 31), and that of the unclassified type was 15.4% (4 of 26). The VEGF-positive rate in patients with Pen A type tumors was significantly higher than that in patients with the other three growth patterns(P<0.01). MVD in patients with Pen A type tumors (25.9+/-9.2) was significantly higher than that in patients with Super type tumors (12.6+/-5.4) (P<0.01). Patients with Pen A type tumors had a poorer prognosis than patients whose tumors had other growth patterns (P<0.05). According to multivariate analysis, VEGF expression and lymphatic vessel invasion were significant prognostic factors. CONCLUSIONS: Pen A type gastric carcinoma tends to secrete VEGF, thus inducing tumor angiogenesis and resulting in venous invasion. Intensive follow-up is necessary for patients with Pen A type tumors, because this tumor type has a greater propensity for hematogenous metastasis.

Aged↗

Clinical implications of serum anti-p53 antibodies for patients with gastric carcinoma.

BACKGROUND: Mutations of p53 can lead to the production of anti-p53 antibodies in sera of cancer patients. Before this study, the value of preoperative serum anti-p53 antibodies in determining the prognoses of patients with gastric carcinoma had yet to be determined. METHODS: The authors used a highly specific enzyme-linked immunosorbent assay (ELISA) kit (Pharma Cell, France) to determine the preoperative presence of serum anti-p53 antibodies in 120 patients with gastric carcinoma. The relation between the positivity of serum anti-p53 antibodies and p53 abnormal staining of gastric carcinoma tissues was examined. Clinicopathologic characteristics and prognoses of these patients were given attention. RESULTS: Anti-p53 antibodies were detected in 19.2%(23 of 120) of these patients with gastric carcinoma. Among those who were positive for anti-p53 antibodies, female patients were predominant, the depth of invasion was greater, and liver metastasis was present, as compared with those who were negative for anti-p53 antibodies. Regarding other factors, there were no differences between those who were positive or negative for anti-p53 antibodies. Gastric carcinoma tissues had a 60.9% (14 of 23) positivity rate of p53 staining with anti-p53 antibodies and a 33.0% (32 of 97) negativity rate, and this difference was statistically significant (P < 0.05). The survival time of patients with anti-p53 antibodies in their sera was shorter than that of subjects with sera negative for anti-p53 antibodies (P < 0.05). The presence of anti-p53 antibodies was not an independent prognostic factor in multivariate analysis. CONCLUSIONS: Serum assay of anti-p53 antibodies is a rapid and readily facilitated test for predicting tumor advancement, depth of invasion, and liver metastasis, and it will show a poorer prognosis for surgically treated patients with gastric carcinoma.

Antibodies, Monoclonal↗

Prognostic value of p53 protein expression for patients with gastric cancer--a multivariate analysis.

Mutations in the p53 gene, one of the most common genetic alterations in human cancer, are implicated in tumorigenesis and tumour progression. Although p53 protein expression appears to be correlated to prognosis in patients with malignancy, its prognostic role in gastric cancer has remained controversial. We examined the clinical significance of p53 overexpression in 427 patients with gastric cancer, using multivariate analysis. Tumour sections of gastric cancer tissues from these 427 Japanese patients were stained immunohistochemically with monoclonal antibody PAb1801. The presence of p53 expression was statistically compared with clinicopathological features and post-operative survival, using univariate and multivariate analyses. p53 expression was detected in 38.6% (165 out of 427) of these gastric cancers and immunoreactivity was not observed in normal mucosa adjacent to the tumour. A higher rate of p53 detection was observed among large tumours and in those with a prominent depth of invasion, lymphatic and vascular invasion and lymph node involvement. Prognosis was significantly worse for patients with p53-positive-staining tumours. The 5-year survival rate was 62.5% for patients with p53-negative tumours and 43.3% for those with positive malignancies. p53 expression was a significant prognostic factor for node-positive gastric cancers in subjects undergoing treatment with curative resection, as assessed by Cox regression analysis. Thus, the expression of p53 was closely related to the potential for tumour advance and a poorer post-operative prognosis for patients with gastric cancer.

Analysis of Variance↗

Recurrences and relation to tumor growth potential and local immune response in node-negative advanced gastric cancer.

Biological characteristics and the prognosis for subjects with node-negative advanced gastric cancer have been given little attention in related literature. We analyzed data on 112 patients with serosally invasive gastric cancer who were lymph node metastasis-negative; all had been surgically treated in the Department of Surgery II, Kyushu University Hospital, between 1970 and 1992. Recurrences and relation to the growth potential of the tumor and local immune response were examined. Thirty patients died with a recurrence of the gastric cancer, and in these patients, the tumor was larger, the whole stomach was more frequently involved and infiltrative growth was more common, compared to findings in patients who were recurrence-free. Peritoneal recurrence was evident in half the number of patients and the 5-year survival rate was 74. 5%. Tumor growth potential was evaluated, based on the level of proliferating cell nuclear antigen (PCNA) of the primary tumor and on dendritic cell infiltration into the tumor, determined as a level of local immune function of the host. Higher growth potential and lower immune levels were more frequent in patients with recurrences. Multivariate analysis revealed that tumor size and PCNA labeling index were significant prognostic factors for node-negative gastric cancers. In a subset of advanced gastric cancers, there was no apparent distinct lymph node metastasis and the prognosis was better. However, cancer cells with a higher growth potential and a lower immune response in the host can biologically amplify and mainly infiltrate the gastric wall, extend to the serosa and disseminate transserosally into the peritoneum.

Aged↗

Role of transforming growth factor-beta 1 in invasion and metastasis in gastric carcinoma.

PURPOSE: Transforming growth factor-beta1 (TGF-beta1) is a major modulator of cellular proliferation and extracellular matrix formation. We determined the role of TGF-beta1 in invasion and metastasis in gastric cancer. MATERIALS AND METHODS: We detected TGF-beta1 expression in primary and lymph node metastatic lesions of gastric cancer, using an antibody and in situ hybridization. The plasma TGF-beta1 levels in the peripheral vein and in the tumor drainage vein were assayed. RESULTS: In the cytoplasm of cancer cells, TGF- beta1 was immunostained in 35.9% (78 of 217) of primary gastric carcinomas, and this expression was confirmed by in situ hybridization. Of 59 gastric carcinomas with a TGF-beta1-negative primary tumor, metastatic lymph nodes were positive for TGF-beta1 staining in 32 cases (54.2%). Positive staining of TGF-beta1 in gastric cancer tissues was closely related to serosal invasion, infiltrative growth, and lymph node metastasis. Multivariate analysis showed that the expression of TGF-beta1 was an independent risk factor for serosal invasion and infiltrative growth of the tumor. The plasma level of TGF-beta1 did not differ between TGF-beta1-negative and -positive groups. There were also no differences in plasma TGF-beta1 levels among each tumor stage, between the peripheral and the tumor drainage veins, and between preoperative and postoperative testings. CONCLUSION: Transforming growth factor-beta1 is closely related to the invasion and metastasis of gastric cancer, and production of TGF-beta1 in the tumor does not contribute to the total amount of TGF-beta1 in the blood circulation. We interpret our observations to mean that in a tumor microenvironment, TGF-beta1 alters the biologic behavior of the tumor.

Aged↗

Long-term survival of patients with stage IV gastric carcinoma.

BACKGROUND: Survival of patients with Stage IV (based on general rules established by the Japanese Research Society for Gastric Cancer) gastric carcinoma often is unfavorable. Among patients with a poor prognosis, a few do survive > 5 years. The authors examined pathologic and biologic features of tumors of long term survivors. METHODS: The authors analyzed data from 442 patients with Stage IV gastric carcinoma, including 20 surviving for > 5 years after gastrectomy (Group A) and 422 who died of gastric carcinoma within 5 years (Group B). Mutant p53 was immunohistochemically stained using the monoclonal antibody PAb1801. Proliferative activity was estimated by argyrophilic nuclear organizer region (AgNOR) staining and proliferating cell nuclear antigen (PCNA) staining. RESULTS: Group A had smaller and more localized tumors than Group B (P < 0.05 and P < 0.01, respectively). Lymphatic or venous invasion and peritoneal dissemination were less frequent in Group A than in Group B (P < 0.01). Abnormalities of p53 expression were found in 3 of the 14 tumors in Group A (21%), a value significantly lower than the 58 of 118 tumors in Group B (49%; P < 0.05). AgNOR count and percentage of PCNA labeling were not significantly different between Groups A and B. A multivariate analysis showed that lymph node dissection, liver metastasis, gastric resection, venous invasion, and tumor size were independent prognostic factors. CONCLUSIONS: Even in patients with Stage IV gastric carcinoma, radical gastrectomy and extensive lymph node dissection can lead to long term survival. The authors believe that combination analysis of pathologic features and p53 overexpression predict length of survival for patients with Stage IV gastric carcinoma.

Adult↗

Interrelation between tumor-associated cell surface glycoprotein and host immune response in gastric carcinoma patients.

BACKGROUND: Expression of changes in cell surface glycoprotein may correlate with the malignant potential and development of gastric carcinoma. Immunologic defense mechanisms of the host against the tumor can be effective in preventing the development of gastric carcinoma. The authors studied the effects of immunologic defense of the host against the tumor, using infiltration of S-100 protein positive dendritic cells (DC) as a marker. In cases with or without changes in the surface glycoprotein of tumor cells, determinations were made by binding of Helix pomatia agglutinin (HPA). METHODS: Paraffin blocks of 123 gastric carcinoma specimens were prepared for immunohistochemical staining with the antibody against HPA and S-100 protein. Clinicopathologic factors and patient prognosis were examined for each indicator. RESULTS: Patients with HPA positive tumors had a more aggressive character in several important prognostic aspects and poorer 5-year survival rates compared with patients with HPA negative tumors. The degree of infiltration of DC had no particular correlation with pathologic factors, and there was no significant difference between the prognosis of patients with slight and marked DC infiltration. In the HPA negative patients there was no significant difference in the 5-year survival rates between patients with slight and marked DC infiltration; however, in the HPA positive patients the 5-year survival rates of patients with marked infiltration of DC were higher. Further investigation showed that patients with marked DC infiltration had better 5-year survival rates than patients with slight DC infiltration, especially in patients with HPA positive and histologically advanced disease. CONCLUSIONS: Patients with a higher immunologic defense against cancer cells, as indicated by marked infiltration of DC, had a better prognosis in cases of gastric carcinomas of highly malignant potential, as indicated by a positive HPA.

Adult↗

Laparoscopic repair of a perforated duodenal ulcer in two patients.

The laparoscopic repair of a perforated duodenal ulcer was effectively done in two patients both of whom were poor risks for surgery. One was a 39-year-old woman with a history of bronchial asthma since she was 20 years of age, while the other was a 76-year-old man with hepatocellular carcinoma, lung cancer, and diabetes mellitus. The postoperative course of these patients was uneventful. Based on these findings, the laparoscopic repair of a perforated duodenal ulcer should thus be considered as a first choice of treatment for a perforated duodenal ulcer, even in poor-risk patients.

Adult↗

Gastric carcinoma with pyloric stenosis.

BACKGROUND: The surgical outcome of gastric carcinomas with pyloric stenosis and their prognostic factors are sparsely documented. METHODS: A clinicopathologic study of gastric carcinoma with pyloric stenosis (PS group, n = 122) was done and findings were compared with the cases involving the antrum (A group, n = 695). Independent prognostic factors for survival of the patients with PS were determined by Cox's proportional hazard model. RESULTS: There were no differences in age and gender between the two groups. The PS group was characterized by an infiltrating growth pattern and undifferentiated adenocarcinoma. The incidence of serosal invasion, direct invasion into neighboring organs, peritoneal dissemination, lymph node metastasis, and liver metastasis of the PS group was higher than those of the A group (p < 0.01). The resection rate and 5-year survival of the PS group were 78% and 22%, respectively; these values were significantly lower than 98% and 58% of the A group (p < 0.01). Multivariate analyses showed that operative curability, resection of the stomach, liver metastasis, serosal invasion, and histologic type were the independent prognostic factors of the PS group. CONCLUSIONS: In cases of gastric carcinoma with pyloric stenosis, efforts should be made to do a curative operation, but for other patients with poor prognostic factors, intensive surgery and adjuvant therapy should be considered.

Aged↗

Tumor angiogenesis and micrometastasis in bone marrow of patients with early gastric cancer.

In a subset of patients with early gastric cancer, there were recurrences of the disease after a curative resection had been done. Direct evidence of tumor seeding in distant organs at the time of surgery for gastric cancer is not available. An immunocytochemical assay for epithelial cytokeratin protein may fill this gap because it is a feature of epithelial cells that would not normally be present in bone marrow. From 1994-1997, the bone marrow of 45 patients with early gastric cancer was examined for tumor cells, using immunocytochemical techniques and an antibody reacting with cytokeratin, a component of the intracytoplasmic network of intermediate filaments. Intratumoral microvessels were stained with anti-CD31 monoclonal antibody. Clinicopathological characteristics were determined for subjects with cytokeratin-positive cells in the bone marrow. Of these 45 patients, 9 (20.0%) had cytokeratin-positive cells in the bone marrow at the time of primary surgery. These positive findings were not related to tumor advance-related factors of lymph node metastasis and distinct lymphatic and vascular invasion. Microvessel density in the primary tumor exceeded 2-fold in cytokeratin-positive cells, compared with findings in negative cells (P < 0.05). Tumor cells in bone marrow are indicative of the general disseminative metastasis in patients with early gastric cancer, and the metastatic potential was closely related to angiogenesis in the primary tumor.

Aged↗

Lymph node metastasis and relation to tumor growth potential and local immune response in advanced gastric cancer.

To evaluate the relation between the degree of lymph node metastasis and the growth potential of tumour cells and the local immune function in gastric cancer, we analyzed data on 444 patients with advanced serosally invasive gastric cancer who underwent curative gastrectomy. Tumour growth potential was evaluated based on the value proliferating cell nuclear antigen (PCNA) in the primary tumour, and dendritic cell infiltration into the tumour was determined as an indicator of local immune function. The values of PCNA labeling in the primary tumour increased and the infiltration of dendritic cells into the tumour decreased in relation to the extent of lymph node metastasis. High growth potential and low immune function were seen in cases with n3 lymph node metastasis. There was a reverse relation between the PCNA labeling index and dendritic cell infiltration. A variety of forms of recurrence was noted in patients with lymph node metastasis while the prognosis was less favorable, in relation to the degree of lymph node metastasis. Thus, the potential for nodal spread appears to be associated with the growth potential of tumour cells and with the local immune status of the tumour.

Cell Count↗

Reversal of in vivo drug resistance by the transforming growth factor-beta inhibitor decorin.

Transforming growth factor-beta (TGF-beta) has been implicated in the in vivo resistance of the EMT-6/CTX and EMT-6/ CDDP murine mammary tumors. Both of these tumors have a higher number of intratumoral vessels than the EMT-6/ parent tumor. Animals bearing the resistant tumors have higher plasma levels of TGF-beta than animals bearing the parent tumors; however, upon treatment with cytotoxic therapies there is a greater rise in plasma TGF-beta levels in animals bearing the parent tumor than in animals bearing the resistant tumors. In situ hybridization for TGF-beta mRNA and immunohistochemical staining for TGF-beta protein showed that the resistant tumor levels of this growth factor are higher than those of the parent tumor prior to treatment; however, after cytotoxic therapy the increase in TGF-beta is greater in the parent tumor than in the resistant tumors. Treatment of tumor-bearing animals with the naturally occurring TGF-beta inhibitor decorin did not alter the sensitivity of the parent tumor to cyclophosphamide or to CDDP as determined by tumor cell survival assay. However, administration of decorin increased the sensitivity of the EMT-6/CTX tumor to cyclophosphamide and of the EMT-6/CDDP tumor to CDDP so that the drug resistance of these tumors was nearly ablated. A similar pattern was observed in the drug response of the bone marrow granulocyte-macrophage colony-stimulating factor of animals bearing each of the 3 tumors.

Animals↗

Dynamics of tumor oxygenation, CD31 staining and transforming growth factor-beta levels after treatment with radiation or cyclophosphamide in the rat 13762 mammary carcinoma.

PURPOSE: Tumors are dynamic tissues that undergo marked molecular, biochemical, and physiologic changes in response to cytotoxic anticancer therapies. Understanding the changes in tumor oxygenation and transforming growth factor-beta expression may allow improved treatment regimens to be developed. METHODS AND MATERIALS: The effects of a single dose of radiation therapy (20 Gy) or a single dose of chemotherapy (cyclophosphamide, 250 mg/kg) on several molecular and physiologic parameters of the rat 13762 mammary carcinoma growing subcutaneously in female Fischer 344 rats were explored. RESULTS: Treatment of the tumor-bearing animals with 20 Gy of radiation killed about two logs (99%) of the 13762 tumor cells, and treatment with cyclophosphamide (250 mg/kg) killed about 1.5 logs (95%) of the 13762 tumor cells. Hypoxia, as determined by a pO2 electrode, initially decreased in the tumors of treated animals until 6 h. posttreatment and then increased, so that 24 h. after administration of the radiation therapy or the chemotherapy the number of intratumoral vessels as determined by CD31 staining increased until about 24 h after cytotoxic therapy. Transforming growth factor-beta1, measured by radioimmunoassay, peaked in the serum between 6 h and 18 h and again between 72 h and 96 h after radiation therapy and peaked in the tumor at 24 h and again at 72 h after radiation therapy. The first serum peak after cyclophosphamide was 3 h after drug injection, with second peaks at 36 h and 48 h after drug administration. In the tumor, transforming growth factor-beta1 peaked between 6 h and 8 h after drug administration and again 36 h and 72 h after drug. Apoptosis was maximal 6 h after 20 Gy and 24 h after cyclophosphamide. Vascular endothelial growth factor was also increased in tumors after cytotoxic therapy. CONCLUSIONS: These changes in the tumor physiologic status are sufficient to protect the tumor from a second cytotoxic insult administered days afterwards and to result in a restructuring of the tissue.

Animals↗

Host distribution and response to antitumor alkylating agents of EMT-6 tumor cells from subcutaneous tumor implants.

PURPOSE: Minimal residual tumor or minimal residual metastatic disease is a major clinical problem for detection and treatment. The purpose of the study was to develop a model system to detect the occurrence and response to therapy of minimal residual tumor in distant organs. METHODS: Animals bearing subcutaneously growing established (day 8) murine EMT-6 mammary carcinoma tumors were treated with single doses of the antitumor alkylating agents, cyclophosphamide, melphalan, cis-diamminedichloroplatinum(II) (CDDP) or thiotepa. Tumors, livers, lungs, brain, spleen, blood and bone marrow were collected from the animals 24 h later and single-cell suspensions of these tissues were plated and cultured under conditions suitable for tumor cell colony growth. RESULTS: Tumor cell colonies grew from each of the tissues with varying frequency ranging from about 6 x 10(3) tumor cell colonies per 10(6) cells plated from the liver, to about 2 tumor cell colonies per 10(6) cells plated from the brain. There was a wide range of sensitivity, spanning 2- to 3-log of the tumor cells, to the antitumor alkylating agents depending upon the tissue in which the tumor cells were located. Tumor cells in the circulating blood were most sensitive to the antitumor alkylating agents with no colony growth after treatment of the animals with any of the four drugs tested. The primary tumor growing subcutaneously in the upper hindleg of the animals was also relatively sensitive to each of the four antitumor alkylating agents tested. EMT-6 tumor cells in the spleen were very sensitive to cyclophosphamide, moderately sensitive to melphalan, less sensitive to CDDP and least sensitive to thiotepa. EMT-6 tumor cells in the bone marrow were moderately sensitive to cyclophosphamide, melphalan and thiotepa but less sensitive to CDDP. EMT-6 tumor cells in the lungs were relatively sensitive to thiotepa, moderately sensitive to cyclophosphamide and CDDP and least sensitive to melphalan. EMT-6 tumor cells in the liver or brain were least responsive to treatment of the host with any of the four antitumor alkylating agents tested. CONCLUSIONS: Treatment of the tumor-bearing animals with the antiangiogenic combination, TNP-470/minocycline, markedly increased EMT-6 tumor cell killing by cyclophosphamide in the liver, lungs and bone marrow. These results indicate that location within the host is an important determinant in the response of tumor cells to therapy.

Animals↗

Preclinical studies of the combination of angiogenic inhibitors with cytotoxic agents.

TNP-740, minocycline, suramin and genistein have demonstrated antiangiogenic activity in various experimental systems. The effect of these agents alone and in two agent combinations on the number of intratumoral vessels and response to cytotoxic anticancer therapies was assessed in animals bearing the Lewis lung carcinoma. Treatment with each of the antiangiogenic agents alone and in two agent combinations decreased the number of intratumoral vessels visualized by CD31 or Factor VIII staining to 30% to 50% of the number in the untreated control tumors. In general, the antiangiogenic agents are more effective adjuvants to cytotoxic therapies when used as two agent combinations than as single agents. The most effective antiangiogenic combinations were: TNP-470/minocycline > TNP-470/genistein > TNP-470/suramin. The increases in the response of the primary tumor to cyclophosphamide, adriamycin, CDDP, BCNU, x-rays or 5-fluorouracil and the lung metastases occur to about the same level with the addition of antiangiogenic agents to the therapies. With the treatment combination TNP-470/minocycline/cyclophosphamide 40% of the animals were cured. The results of these studies indicate that antiangiogenic agents can be very useful additions to treatment regimens for solid tumors.

Animals↗

Scientific basis for the combination of tegafur with uracil.

Fujii et al reported that Uracil potentiated the antitumor activity of fluorouracil (5-FU) and 1-(2-tetrahydrofuryl)-5-fluorouracil (tegafur). This effect was due to inhibition of the degradation of 5-FU, yet the phosphorylation of 5-FU was unaffected. The molar ratio of tegafur and uracil was 1:4, a combination that has since been widely prescribed in Japan for the treatment of cancer patients. We present here our experimental and clinical results when investigating the antineoplastic effects of this combination of drugs--known as UFT--and provide evidence that UFT is an effective treatment for patients with cancer.

Chemotherapy, Adjuvant↗

Interaction of interleukin-11 with cytotoxic therapies in vitro against CEM cells and in vivo against EMT-6 murine mammary carcinoma.

Interleukin-11(rhIL-11) is a cytokine that has been shown to enhance the recovery of bone marrow and intestinal crypt cells after cytotoxic insult with radiation or anticancer drugs. The current study examined the effects of rhIL-11 on the response of CEM human lymphoblastic leukemia cells and on the EMT-6 murine mammary carcinoma in vivo to cytotoxic anticancer therapies. Exposure of CEM cells to rhIL-11 for 24 hr did not alter the cytotoxicity of melphalan or radiation, increased the cytotoxicity of CDDP (100 muM) and 4-hydroperoxycyclophosphamide (50 betaM) and decreased the cytotoxicity of 5-fluorouracil and ara-C toward the cells. Treatment of mice bearing the EMT-6 tumor with rhIL-11 twice daily for 4 days prior to and the day of cytotoxic therapy resulted in no significant change in the tumor cell killing or bone marrow CFU-GM killing by melphalan, cyclophosphamide, thiotepa, CDDP, radiation, 5-fluorouracil or ara-C. Administration of rhIL-11 twice per day on days 7-18 to EMT-6 tumor bearing animals receiving high dose chemotherapy (melphalan, thiotepa or cyclophosphamide) as a single dose on day 7 followed by mobilized peripheral blood cells on day 8 and rhG-CSF on days 8-20, tended to prolong the tumor growth delay produced by the drugs. This rhIL-11 treatment also resulted in a more rapid recovery of white blood cells and granulocytes in the animals. Furthermore, animals treated with rhIL-11 had improved survival rates compared with animals receiving all other normal tissue support without rhIL-11.

Animals↗

Age-related characteristics of gastric carcinoma in young and elderly patients.

BACKGROUND: The clinicopathologic features of young and elderly patients with gastric carcinoma have been analyzed. METHODS: We analyzed the data from 174 patients with gastric carcinoma age 40 years and younger and from 356 patients with gastric carcinoma age 70 years and older who were surgically treated at the Department of Surgery II, Kyushu University, Japan. RESULTS: The rate of multiple gastric carcinomas was 2.9% (5/174) for the young patients and 13.2% (47/356) for the elderly. In subjects older than 70 years, male patients predominated, tumors were smaller, differentiated lesions more common, vascular involvement more frequent, tumors were less infiltrative, and the rate of liver metastasis was higher. For patients younger than age 40 years, undifferentiated type with infiltrative growth was frequent and the rate of liver metastasis was higher. There were no differences in the positive rate of p53 overexpression and the proliferating activity of the cancer cells determined by PCNA LI, between the young and elderly patients. The survival rate after curative resection was lower for the elderly compared with that for the young patients; hematogenous recurrence was higher in the former. CONCLUSIONS: The clinicopathological features of gastric carcinoma differed between the young and elderly patients, and these differences should be considered when age-oriented treatment is being designed.

Adult↗