Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Murine, antihuman melanoma cell monoclonal antibody (mAb) 16.C8 was generated by fusing the murine myeloma cell line P3X63/Ag8.653 with splenocytes from a nude mouse bearing a human melanoma xenograft, after reconstitution with splenocytes from syngeneic immunocompetent BALB/c mice. The antibody reacted strongly with fresh human melanoma cells and exhibited preferential reactivity with established human melanoma and neuroectodermal tumor cell lines. Electrophoresis and Western blotting experiments indicated that 16.C8 is directed against a sialoglycoprotein antigen with a molecular weight of 110-120 kDa. mAb 16.C8 mediated lysis of melanoma cells in vitro in antibody-dependent cellular cytotoxicity assays using human mononuclear effector cells isolated from normal volunteers or malignant melanoma patients. In addition, the administration of mAb 16.C8 to nude mice bearing established human melanoma lung and liver metastases resulted in significant inhibition of tumor growth as shown by gross and histologic examination. In contrast, animals treated with Hanks' balanced salt solution or nonspecific immunoglobulin exhibited a large tumor burden. These results suggest that mAb 16.C8 may be of value in treatment of metastatic melanoma in humans.
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PMID:Cell binding and tumor inhibiting functions of a new antihuman melanoma murine monoclonal antibody. 176 67

A hybridoma, C-50, obtained by fusion of mouse myeloma cells with spleen cells from a mouse immunized with cells from the colorectal carcinoma cell line COLO 205, produced antibodies that detected ganglioside antigen in human adenocarcinomas in many organs. The major ganglioside antigen fraction isolated from liver metastases of a pancreatic adenocarcinoma, behaving as a homogenous band on thin-layer chromatography, consisted of three different gangliosides. One of them, A (25%), had the same carbohydrate structure as the ganglioside antigen defined by monoclonal antibody 19-9, NeuAc alpha 2-3Gal beta 1-3(Fuc alpha 1-4)GlcNAc beta 1-3Gal beta 1-4Glc-Cer(Fuc-3'-isoLM1) Magnani, J.L., Nilsson, B., Brockhaus, M., Zopf, D., Steplewski, Z., Koprowski, H. and Ginsburg, V. (1982) J. Biol. Chem. 257, 14365-14369). The major ganglioside, B (60%), was the isomeric hexasaccharide ganglioside (NeuAc alpha 2-3Gal beta 1-4(Fuc alpha 1-3)GlcNAc beta 1-3-Gal beta 1-4Glc-Cer(Fuc-3'-LM1) and the third ganglioside, C, was 6'-LM1, NeuAc alpha 2-6Gal beta 1-4GlcNAc beta 1-3Gal beta 1-4Glc-Cer (15%). Ganglioside B, isolated from human kidney, did not react with the C-50 MAb. Based on this result and on studies of COLO 205 cell induced tumours where the ganglioside antigen fraction only consisted of A, it is suggested that the C-50 MAb defines an antigen determinant present in A.
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PMID:Chemical structure of carcinoma ganglioside antigens defined by monoclonal antibody C-50 and some allied gangliosides of human pancreatic adenocarcinoma. 397 12

By fusion of C3H mouse spleen cells, immunized with a PCA extract from liver metastases of a colon tumor, and Sp2/O-Ag14 myeloma cells, we produced several clones secreting monoclonal antibodies (MAb) with reactivity against carcinoembryonic antigen (CEA). For the screening of the different MAb, an ELISA technique with PCA extract and highly purified CEA coupled with alkaline phosphatase was employed. The specificities of the MAb prescreened with the ELISA technique were analyzed further by immunoprecipitation and separation on SDS-PAGE, followed by enzyme digestion and thin-layer chromatography for fingerprint analysis. The MAb recognized (a) an antigenic determinant present only on CEA, (b) common determinants present on CEA and at least six other molecules separated by SDS-PAGE and (c) antigenic determinants not present on CEA. The fingerprint analysis showed the relationship of the molecules on the basis of protein chemistry.
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PMID:Monoclonal antibodies against CEA. Comparison of the immunoprecipitates by fingerprint analysis. 618 85

Somatic cell hybridization between nonmetastatic tumor cells and normal cells of the lymphoreticular system results in hybrid cells manifesting metastatic properties of defined target organ specificity. Thus, fusion of the nonmetastatic BALB/c originated NSI plasmacytoma with C57BL B lymphocytes resulted in hybridomas, each of which were metastatic. Of 10 hybridomas, 7 generated metastases in the spleen and liver, whereas 3 generated liver metastases. The generation of liver metastases by hybridomas which homed to both spleen and liver, but not by those which homed to the liver only, was controlled by the spleen. The acquisition of metastatic properties via somatic cell fusion seems to represent a general principle, in which the normal partner determines the target organ specificity for the metastatic growth. Thus, fusion of SP2/O myeloma cells with syngeneic B lymphocytes also resulted in a hybrid cell metastasizing to the spleen and liver, yet a somatic hybrid between NSI and a macrophage or dendritic-like cell metastasized to the lung. Cell surface molecules encoded by the genome of the normal partner was demonstrated to control the target organ specificity: antibodies against MHC-encoded antigens of the normal B cell partner prevented the generation of metastases by hybridomas metastasizing to the spleen and liver, but not by those metastasizing to the liver only. This is in accordance with the function of MHC molecules on lymphocytes in controlling their homing to lymphoid organs. Hybridomas of T cell lymphomas also manifested metastatic properties. Analysis of the cell surface Thy-1 antigens of a hybridoma (DCH10), produced via somatic fusion between BW5145 lymphoma and a putative macrophage cell indicated that cells of liver metastases (DCH10-Li) generated by the hybrid cells might have undergone further somatic cell fusion in vivo with host (T?) cells. These cells have acquired new metastatic properties, generating metastases in spleen, liver and kidneys. In fact, even the inoculation of the parental BW lymphoma cells resulted in a case of liver metastasis (BW-Li). Such BW-Li cells, upon reinoculation, also generated metastases in the spleen, liver and kidneys. Analysis of the Thyl phenotype indicated that BW-Li cells may also have undergone somatic cell fusion in vivo with host (T?) cells, resulting in the acquisition of metastatic properties. The pattern of cell-cell interactions (adhesion, infiltration) with liver cell monolayers of BW-Li cells and of DCH10-Li (T-cell lymphomas) was identical, and differed from cells of liver metastases of the myeloma-B cell hybridomas which might be based on responses to liver growth signals.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nonmetastatic tumor cells acquire metastatic properties following somatic hybridization with normal cells. 637 Apr 19

Gastrointestinal stromal tumors (GISTs) are rare tumors, which represent approximately 1% of the neoplasms of the gastrointestinal tract. These tumors rarely give extra-abdominal metastases. However, their clinical outcome is potentially adverse. In some rare cases, co-existance of GISTs with other malignancies has been reported. Here we present a case of a 74-year old male with GIST, which was managed by surgical resection. Fourteen months later, the patient presented with liver metastases and imatinib mesylated was administered. During treatment, the patient reported skeletal pain and plane X-rays revealed osteolytic bone lesions. Further investigation revealed the presence of multiple myeloma. To the best of our knowledge, this is the first report of the co-existence of multiple myeloma (MM) with GIST.
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PMID:Development of multiple myeloma in a patient with gastrointestinal stromal tumor treated with imatinib mesylate: a case report. 1746 9

Antiresorptive drugs have been widely used to treat patients with hypercalcemia caused by malignancy, bone metastasis, multiple myeloma, and osteoporosis. However, it is well known that antiresorptive drugs can cause osteonecrosis of the jaw (ONJ). Herein, we report a rare case of nasal septal abscess caused by medication related osteonecrosis of the jaw (MRONJ) in a breast cancer patient. A 69-year-old woman was referred to our clinic for evaluation of nasal obstruction. Physical examination revealed a cherry-like swelling of the nasal mucosa emanating from the septum that obstructed both nasal cavities and a fistulous tract showing pus discharge after extraction of the bilateral maxillary central incisors (MCI) and the right maxillary lateral incisor (MLI). Computed tomography and panoramic radiography revealed extensive osteonecrosis of the maxilla and swelling of the nasal mucosa. The clinical diagnosis was nasal septal abscess caused by osteonecrosis of the maxilla. Surgical procedure was undertaken for this case. An indwelling drain was placed in the oral cavity, and sequestrectomy was performed with incision and drainage of the anterior portion of left nasal septum. The patient was doing well at the 7-month follow-up. The patient had a medical history of breast cancer with bone, lung, liver metastases, and had received intravenous bisphosphonate, which is one of the antiresorptive medicines, over the past 4 years. We suspect that this history played an important role in MRONJ induced nasal septal abscess.
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PMID:A case of nasal septal abscess caused by medication related osteonecrosis in breast cancer patient. 2677 49