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Biomedical subjects

H Hatanaka

Publications and source records attributed to H Hatanaka.

355 records · Page 20Linked to original sources
PubMedDate not supplied

Physiological antagonism between prostaglandin E2 and neuropeptide Y on thermoregulation in the dog.

These experiments were undertaken to determine whether neuropeptide Y (NPY) could suppress a prostaglandin hyperthermia in conscious dogs. Prostaglandin E2 (PGE2) (5 micrograms), injected into the lateral cerebral ventricle (ILV), evoked a hyperthermia of approximately 1 degrees C. Addition of ILV NPY (5 micrograms) significantly attenuated the PGE2-induced hyperthermia, whereas pancreatic polypeptide (PP), another member of the PP family peptide, did not. These results provide evidence for a role of NPY on thermoregulation in the dog.

Animals↗
PubMedDate not supplied

A human lung cancer xenograft producing granulocyte-colony stimulating factor and parathyroid hormone-related protein.

A human lung cancer xenograft, LC-GP, producing granulocyte-colony stimulating factor and parathyroid hormone-related protein was established by transplantation into severe combined immunodeficient (SCID) mice. The lung cancer patient and SCID mice bearing LC-GP showed leukocytosis and hypercalcemia. G-CSF and PTHrP gene expression were demonstrated in the primary lung cancer, metastatic lesions and LC-GP xenograft. Immunohistochemical analysis confirmed the presence of G-CSF protein in LC-GP xenograft cells. LC-GP possessed activated c-Ki-ras oncogene (point mutation at codon 12). This LC-GP lacked apparent G-CSF receptor expression. The expression of G-CSF and PTHrP may be coregulated by the activated c-Ki-ras oncogene, and autocrine stimulation of G-CSF is unlikely.

Animals↗
PubMedDate not supplied

Inhibition of liver metastasis of colon cancer by in vivo administration of anti-vascular endothelial growth factor antibody.

Cancer metastasis via blood vessels is a complicated process involving a number of stages. Vascularization in the cancer stroma is essential for the metastatic process. Vascular endothelial growth factor (VEGF) is an angiogenic factor, and has important roles in tumor progression or metastasis. In this study, we developed a polycolonal antibody to VEGF and examined whether the anti-VEGF antibody could inhibit the metastasis of human xenografts expressing VEGF in nude mice. The xenograft Col-23-JCK expressing VEGF formed metastatic lesions in the liver and/or pancreas when inoculated via the portal vein (splenic vein) into nude mice. The anti-VEGF polyclonal antibody inhibited metastasis to the liver and/or pancreas (4.75+/- 3.62, anti-VEGF-treated vs. 9.73 +/- 8.24, w/o anti-VEGF treatment; Student's t-test, p=0.035). Vascularity in the metastatic lesions was also decreased by anti-VEGF treatment. These results suggest that anti-VEGF antibody administration may be therapeutically useful for prevention of colon cancer metastasis.

Animals↗
PubMedDate not supplied

In vivo chemosensitivity of human malignant cystosarcoma phyllodes xenografts.

Malignant cystosarcoma phyllodes (MCSP) is a rare breast tumor. Chemotherapeutic regimens for treatment of MCSP have not been established. We previously established an MCSP xenograft line MC-3-JCK. In this study, we established a new MCSP xenograft line, MC-10-JCK, by serial transplantation in nude mice. We studied the chemosensitivity of these two MCSP tumor xenografts to anticancer drugs in vivo. We also examined the expression of multidrug resistance-related proteins such as p-glycoprotein (Pgp) and multidrug resistance-associated protein (MRP) by immunohistochemical analysis. These two xenografts were sensitive to doxorubicin, vincristine and cyclophosphamide in vivo. Immunohistochemically, clinical specimens and xenografts were negative for Pgp and MRP expression. These results are consistent with the chemosensitivity of human MCSP to lipophilic anticancer compounds.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMedDate not supplied

A case of pulmonary adenocarcinoma with overexpression of multidrug resistance-associated protein and p53 aberration.

A 66-year-old female patient underwent left upper lobectomy and dissection of the mediastinal lymph nodes. The pathological diagnosis was well-differentiated papillary adenocarcinoma of the lung with metastasis to the mediastinal lymph nodes, p-T2N2MO, stage IIIA. After the operation, she was treated by chemotherapy including lipophilic anticancer compounds (carboplatin and VP-16). The patient unexpectedly showed long survival for 6 years and 2 months without obvious recurrence or metastasis of the cancer. The anticancer compounds were not effective on the recurrent lesions and then she died due to respiratory failure 8 months after recurrence. The autopsy revealed pleural dissemination and intrapulmonary metastasis. Immunohistochemical analysis showed increased multidrug resistance-associated protein (MRP)-positive tumor cells in the recurrent and metastatic lesions, while few MRP-positive cells were apparent in the primary lesion. The MRP-positive cells were accompanied by p53 nuclear accumulation in the carcinoma. This was a case of pulmonary adenocarcinoma with acquired multidrug resistance caused by MRP overexpression and aberrant p53 after chemotherapy.

Adenocarcinoma, Papillary↗
PubMedDate not supplied

Modulation of multidrug resistance in a cancer cell line by anti-multidrug resistance-associated protein (MRP) ribozyme.

Multidrug resistance-associated protein (MRP) is the major candidate molecule responsible for non-P-glycoprotein (PGp)-mediated multidrug resistance. We used a hammerhead anti-MRP ribozyme (alpha MRP-Rz) to inactivate MRP function in a multidrug resistant cancer cell line, KB8-5. The beta-actin promoter-driven alpha MRP-Rz sequence (pH beta/alpha MRP-Rz) was introduced into KB8-5 cells (KB8-5/alpha MRP-Rz) and we evaluated growth of the cell line. The gene expression of multidrug resistance-related molecules was estimated. Drug sensitivity was estimated by MTT assay in vitro. MRP mRNA expression was decreased in KB8-5/alpha MRP-Rz cells. The MTT assay showed increased IC50 values or resistance to doxorubicin (DOX), etoposide (VP-16) and cisplatin (CDDP) in KB8-5/alpha MRP-Rz cells. No significant differences were observed in expression of multidrug resistance gene (MDR1), thymidylate synthase, glutathione S-transferase pi or topoisomerase II alpha. The hammerhead ribozyme-mediated simple suppression of MRP mRNA expression was not sufficient to reverse multidrug resistance in the cancer cell line KB8-5.

ATP Binding Cassette Transporter, Subfamily B↗