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  • 1
    Electronic Resource
    Electronic Resource
    Oral UFT (uracil plus futrafur) for neoadjuvant chemotherapy of gastric cancer (1999)
    Springer
    Gastric cancer 2 (1999), S. 64-73 
    Details
    ISSN: 1436-3305
    Keywords: Key words: gastric cancer ; neoadjuvant chemotherapy ; UFT
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Background. Neoadjuvant chemotherapy has become one of the topics of interest in chemotherapy of gastric cancer; the present study assessed the clinical benefits of neoadjuvant chemotherapy with oral uracil and futrafur (UFT) for gastric cancer. Methods. Between 1991 and 1997, 82 patients with gastric cancer (36 with early and 46 with advanced cancers) received UFT at 300–600 mg/day orally for 1–6 weeks before surgery. Objective responses, histological effects, and postsurgical survival rates were assessed. Results. In 69 of the 82 patients, the objective responses of the primary lesions were assessed by endoscopy or upper gastrointestinal series examination, and 2 complete responses (CR)s, 25 partial responses (PRs), and 42 no changes (NCs) were seen (39.1% response). Histological effects were evaluated in 82 patients, and 2 grade 3, 11 grade 2, 11 grade 1b, 27 grade 1a, and 31 grade 0 effects were seen. A longer period of UFT administration was associated with a CR or PR. However, the objective responses did not correlate with the histological effects. All the patients underwent gastrectomy, and during the median follow-up period of 41 months, 3-year survival rates were 97.1% for pTNM stage 1, 75% for stage 2, 86.7% for stage 3, and 41.6% for stage 4. The survival rates of stage 3 and stage 4 patients were higher than those of the historical controls in our department. However, CR or PR did not correlate with the improvement in survival. Side effects before surgery were not serious; they included slight myelotoxicity, liver dysfunction, and anorexia; however, 3 patients (3.7%) had suture insufficiency, 3 patients (3.7%) had methicillin-resistant Staphylococcus aureus (MRSA) enteritis, and 7 patients (8.5%) had liver dysfunction. Conclusions. Preoperative chemotherapy for gastric cancer with oral UFT was safe and resulted in a good local response (macro- and microscopically) which may indicate the possibility of improved survival with neoadjuvant chemotherapy with UFT. Furthermore, preoperative chemotherapy with oral UFT is easy and patients can receive this treatment on an outpatient basis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s101200050023
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  • 2
    Electronic Resource
    Electronic Resource
    Heterotopic autotransplantation of the pancreas segment after pylorus-preserving total pancreatectomy: A case report of successful surgical treatment for chronic pancreatitis (1993)
    Springer
    Surgery today 23 (1993), S. 836-840 
    Details
    ISSN: 1436-2813
    Keywords: chronic calcified pancreatitis ; pylorus-preserving total pancreatectomy ; extracorporeal removal of the pancreatic head ; heterotopic autotransplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 38-year-old man who had suffered for 5 years from persistent abdominal pain caused by alcoholic chronic pancreatitis, presented with diffuse calcification of the entire pancreas with cystic formation of the pancreatic head. After a pylorus-preserving total pancreatectomy, the pancreatic head, including the cyst, was removed extracorporeally by bench surgery, and the remaining segment of the body and tail autotransplanted heterotopically to the iliac vessels with a pancreaticojejunostomy. Total resolution of the pain was achieved postoperatively, and dietary intake has been satisfactory. Both endocrine and exocrine pancreatic functions have been well preserved, and no insulin has been needed. Three months after his operation, the patient has returned to leading a normal life.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00311630
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  • 3
    Electronic Resource
    Electronic Resource
    Heterogeneity of multiorgan metastases of human lung cancer cells genetically engineered to produce cytokines and reversal using chimeric monoclonal antibodies in natural killer cell-depleted severe combined immunodeficient mice (1999)
    Springer
    Cancer chemotherapy and pharmacology 43 (1999), S. S26 
    Details
    ISSN: 1432-0843
    Keywords: Key words Lung cancer ; Multiorgan metastasis ; Macrophage colony-stimulating factor ; Chimeric antibody
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Lung cancer is a major cause of cancer deaths, most of which can be attributed to distant multiorgan metastases. To examine the cellular and molecular mechanisms of lung cancer metastasis to distant organs, we have established novel models of human lung cancer (small cell and non-small cell lung cancer) metastasis in natural killer cell-depleted severe combined immunodeficient (SCID) mice. We investigated whether local production of the cytokines responsible for regulation of macrophage function at tumor growth sites affects the pattern of lung cancer metastasis in distant organs. Several lung cancer cell lines were genetically engineered to produce human macrophage colony-stimulating factor (M-CSF) and monocyte chemoattractant protein-1 (MCP-1), and their metastatic potentials were assessed. Interestingly, M-CSF gene transduction had an antimetastatic effect for the liver and lymph nodes, but not the kidneys. In contrast, MCP-1 gene-modified lung cancer cells and their parent cells had identical metastatic potentials. These findings indicate a possible role for cyotokines and suggest that lung cancer has metastatic heterogeneity. Examining ways of controlling human lung cancer metastases, we investigated the antimetastatic effect of chimeric monoclonal antibodies (MAbs) against P-glycoprotein and ganglioside GM2 (MH162 and KM966, respectively). Both MAbs, when given on days 2 and 7, inhibited the development of distant metastases of lung cancer in a dose-dependent fashion. Combined use of anti-P-glycoprotein MAb with M-CSF or MCP-1 gene transduction caused complete inhibition of metastasis of H69/VP cells. The antimetastatic effect of these MAbs in vivo was mainly due to an antibody-dependent cell-mediated cytotoxicity reaction mediated by mouse macrophages. These findings suggest that the mouse-human chimeric MAb in combination with cytokine gene transduction may be useful for the eradication of lung cancer metastases in humans.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002800051094
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  • 4
    Electronic Resource
    Electronic Resource
    Circumvention of multidrug resistance by a quinoline derivative, MS-209, in multidrug-resistant human small-cell lung cancer cells and its synergistic interaction with cyclosporin A or verapamil (1998)
    Springer
    Cancer chemotherapy and pharmacology 42 (1998), S. 483-490 
    Details
    ISSN: 1432-0843
    Keywords: Key words Multidrug resistance ; MS-209 ; Small cell lung cancer ; Cyclosporin A ; Verapamil
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose and methods: To develop a clinically useful approach to circumvent P-glycoprotein (P-gp)-mediated multidrug resistance (MDR) in MDR human small-cell lung cancer (SCLC), we examined the ability of a novel quinoline compound, MS-209, to reverse MDR by inhibition of P-gp function in combination with other MDR-reversing drugs using a cytotoxicity assay. Results: We established MDR human SCLC cells by culture in medium with gradually increasing concentrations of adriamycin (ADM). Compared with the parental human SCLC cells, SBC-3, the MDR variant SBC-3 cells obtained (SBC-3/ADM) were highly resistant to various chemotherapeutic agents due to P-gp expression. MS-209 reversed the resistance to ADM and vincristine (VCR) of SBC-3/ADM and H69/VP cells in a dose-dependent manner. Moreover, MS-209 in combination with cyclosporin A (CsA) or verapamil (VER) synergistically enhanced the antitumor effects of ADM and VCR on SBC-3/ADM cells. MS-209 restored ADM incorporation and this effect was enhanced by CsA and VER, suggesting that these synergistic effects were due to competitive inhibition of P-gp function. Conclusion: MS-209 in combination with CsA or VER might increase the efficacy of these chemotherapeutic agents against MDR human SCLC cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002800050849
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  • 5
    Electronic Resource
    Electronic Resource
    Intrapleural instillation of interferon γ in patients with malignant pleurisy due to lung cancer (1997)
    Springer
    Cancer immunology immunotherapy 45 (1997), S. 93-99 
    Details
    ISSN: 1432-0851
    Keywords: Key words Interferon γ ; Malignant pleurisy ; Lung cancer ; Interleukin-1 receptor antagonist ; Pro-inflammatory cytokines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The effect of intrapleural instillation of recombinant human interferon γ (IFNγ) at increasing doses of (1–12) × 106 U was examined in six patients with cytologically positive pleural effusion due to lung cancer. Intrapleural instillation was repeated up to three times. Clinically, no reaccumulation of pleural effusion was observed in one patient and disappearance of lung cancer cells from the pleural effusion was seen in two other patients. No severe side-effects were observed. Considerable levels of IFNγ remained in the pleural effusion as well as in patients’ serum up to 7 days after instillation of 2 × 106 U and higher doses. The total cell number showed a transient decrease on day 1 of therapy. Levels of pro-inflammatory cytokines, such as tumor necrosis factor α, interleukin(IL)-1β and IL-6, in the pleural effusion remained almost stable after IFNγ instillation. On the other hand, intrapleural IL-1 receptor antagonist levels were remarkably elevated by the instillation of IFNγ. IL-2- and IL-12-inducible killer activity of pleural mononuclear cells tended to increase slightly. Despite the inability of IFNγ to control pleural effusion in this treatment schedule, IFNγ instilled by an intrapleural route had a potential local antitumor activity. Moreover, since IFNγ persists in pleural effusions for a long time after a single instillation, such a therapy in combination with other fibrogenic biological response modifiers can be promising.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002620050407
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  • 6
    Electronic Resource
    Electronic Resource
    Expression of vascular endothelial growth factor by human renal cancer cells enhances angiogenesis of primary tumors and production of ascites but not metastasis to the lungs in nude mice (1999)
    Springer
    Clinical & experimental metastasis 17 (1999), S. 831-840 
    Details
    ISSN: 1573-7276
    Keywords: angiogenesis ; renal cell carcinoma ; tumor growth ; VEGF
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We determined the role that vascular endothelial growth factor (VEGF), also known as vascular permeability factor (VPF), plays in the progression of human renal cell cancer in nude mice. Low metastatic and low VEGF/VPF-expressing human renal cancer cells SN12C were transfected with the VEGF165 cDNA or plasmid alone as control. VEGF165-transfected SN12C cells produced large amounts of biologically active VEGF in culture that did not affect cell doubling time or confluence. Subsequent to implantation into the renal subcapsule of nude mice, the VEGF165-transfected SN12C cells produced fast-growing (PCNA labeling), large tumors that expressed high levels of VEGF/VPF and were well vascularized (CD3-positive vessels). The tumors produced hyperpermeability of peritoneal blood vessels (Evans blue dye-leak assay), bloody ascites, and short survival time. Parental or control transfected SN12C cells produced less vascularized, slower growing tumors with no ascites. Regardless of in vivo expression level of VEGF, the incidence of spontaneous lung metastasis was low, suggesting that in itself, the expression of VEGF/VPF by renal cancer cells is not sufficient to produce metastasis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006792007063
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  • 7
    Electronic Resource
    Electronic Resource
    Immunological circumvention of multiple organ metastases of multidrug resistant human small cell lung cancer cells by mouse-human chimeric anti-ganglioside GM2 antibody KM966 (2000)
    Springer
    Clinical & experimental metastasis 18 (2000), S. 353-360 
    Details
    ISSN: 1573-7276
    Keywords: antibody-dependent cellular cytotoxicity ; complement-dependent cytotoxicity ; cytokine ; metastasis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The formation of metastases in multiple organs and acquired multi-drug resistance (MDR) are the major obstacles for treatment of human small-cell lung cancer (SCLC). To explore the possibility of immunological overcoming of multiple-organ metastases produced by refractory SCLC, we established the MDR variant (SBC-3/DOX), expressing P-glycoprotein, of parental SBC-3 cells by culturing with gradually increasing concentration of adriamycin. Both SBC-3 and SBC-3/DOX cells expressed a high amount of ganglioside GM2, an ideal target of SCLC cells. A mouse-human chimeric anti-GM2 monoclonal antibody (KM966) induced antibody-dependent cellular cytotoxicity (ADCC) mediated by human mononuclear cells (lymphocytes and monocytes) and complement-dependent cytotoxicity (CDC) mediated by human AB serum against SBC-3/DOX cells to a similar extent compared with parental SBC-3 cells. Pretreatment of human effector cells with various cytokines induced further enhancement of the KM966-dependent ADCC against SBC-3/DOX cells. Intravenous injection of SBC-3 or SBC-3/DOX cells into natural killer (NK) cell-depleted severe combined immunodeficient (SCID) mice developed metastases in multiple organs (liver, kidneys and lymph nodes). Interestingly, SBC-3/DOX cells produced metastases more rapidly than SBC-3 cells, suggesting more aggressive phenotype of SBC-3/DOX cells than their parental cells in vivo. Systemic treatment with KM966, given on days 2 and 7, drastically inhibited the formation of multiple-organ metastases produced by both SBC-3 and SBC-3/DOX cells, indicating that KM966 can eradicate metastasis by SCLC cells irrespective of MDR phenotype. These findings suggest that the mouse-human chimeric KM966 targets the GM2 antigen, and might be useful for the immunological circumvention of multiple-organ metastases of refractory SCLC.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1010941513570
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  • 8
    Electronic Resource
    Electronic Resource
    Ki-ras point mutation in codon 12 and expression ofp53 in mucin-producing tumor of the pancreas (1997)
    Springer
    Journal of hepato-biliary-pancreatic surgery 4 (1997), S. 83-90 
    Details
    ISSN: 1436-0691
    Keywords: mucin-producing tumor of the pancreas ; intraductal papillary tumor of the pancreas ; Ki-ras, p53
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mucin-producing tumors (MPTs) of the pancreas show a variety of clinical characteristics, including massive production of mucin in the pancreatic duct, dilatation of the main pancreatic duct, and a better prognosis than common invasive ductal carcinoma (IDC). These characteristics suggest that MPTs and IDCs have different cytomolecular backgrounds. The present study was designed to assess the differences in cytomolecular background between MPTs and IDCs, especially the differences in Ki-ras point mutation (PM) and wild and mutant typep53 expression. Cytomolecular backgrounds were compared in a 13 MPTs [8 carcinomas (MPCas) and 5 benign tumors (MPBTs)] and 36 IDCs. Cytomolecular studies included the evaluation of Ki-ras PM and the expression of Ki-ras p21, wild-typep53 (w-p53), and mutant-typep53 (m-p53). Ki-ras PM was assessed by the allele-specific oligonucleotide dot blot hybridization method, and the expression of p21 andp53 was assessed by an immunohistochemical staining method with monoclonal antibodies. Ki-ras PM was seen in 97% of IDCs and in 77% of MPTs (100% of MPCas and 40% of MPBTs), and MPBTs showed a significantly lower incidence of Ki-ras PM (versus IDC,P 〈 0.01). Guanine-Guanine-Thymine (GGT) to Guanine-Adenine-Thymine (GAT) mutation was seen in 55% of IDCs and 62% MPTs (87% of MPCas and 20% of MPBTs), and MPCas showed a significantly higher incidence of percent GAT mutation (versus IDC,P 〈 0.05). Ki-ras p21 was expressed in 43% of IDCs and in 31 % of MPTs (50% of MPCas and 20% of MPBTs). w-p53 and m-p53 were expressed in 51 % and 78% of IDCs and in 54% and 62% of MPTs (38% and 63% of MPCas and 20% and 60% of MPBTs), respectively. In MPBTs, hyperplasias showed higher rates of p21, w-p53, and m-p53 expression than cystadenomas. The study suggested that GAT mutation may be involved in the tumorigenesis of MPTs. It is suggested that MPBTs, especially hyperplasias, may be classified as low-grade malignancies like MPCas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01211347
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  • 9
    Electronic Resource
    Electronic Resource
    Case report of xanthogranulomatous cholecystitis accompanied by Mirizzi syndrome (1995)
    Springer
    Journal of hepato-biliary-pancreatic surgery 2 (1995), S. 95-98 
    Details
    ISSN: 1436-0691
    Keywords: xanthogranulomatous cholecystitis ; Mirizzi syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Xanthogranulomatous cholecystitis (XGC) is a rare type of inflammatory disease of the gallbladder; this entity has also been termed fibroxanthogranulomatous inflammation, and ceroid or ceroid-like histiocytic granuloma of the gallbladder. Clinically, XGC sometimes is confused with a malignant neoplasm. Recently, we encountered a patient with XGC and Mirizzi syndrome, which was difficult to differentiate from gallbladder cancer accompanied by obstructive jaundice. It is important to realize that, pathologically, XGC is a benign disease, but that, in some cases, patients manifest an unusual clinical course.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02348296
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