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)

Human monoclonal antibodies (HuMAb) specific for a 14-kDa perchloric acid-soluble protein (defined as UK114) were produced by somatic fusion of the human-mouse myeloma K6H6/B5 with Epstein-Barr virus-transformed peripheral B lymphocytes from a cancer patient previously treated with UK101 preparations, containing the UK114 protein. Three IgM-secreting clones were selected on the criteria of specificity for the purified UK114 protein immobilized onto plastic and adapted to grow in a serum-free medium. The reactivity of these antibodies showed a broad distribution pattern restricted to fresh tumor tissues and tumor cell lines, mainly of the adenocarcinoma type. None of the normal cells, nonmalignant cell lines, and normal tissues surrounding the neoplastic lesions were reactive. The immunochemical analysis of the target antigens showed that the HuMAb recognize a molecule of 220 kDa selectively expressed by the surface of tumor cells, as well as a cytoplasmic 14-kDa protein. The 220-kDa antigen was different from other tumor-associated antigens with similar molecular mass and, so far, unique. In the presence of human complement, two of three HuMAb are cytotoxic for tumor cells expressing the 220-kDa surface antigen. The tumor specificity and the lytic ability attributed to these HuMAb are promising features for the exploration of future clinical applications.
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PMID:Identification of a 220-kDa membrane tumor-associated antigen by human anti-UK114 monoclonal antibodies selected from the immunoglobulin repertoire of a cancer patient. 1006 72

Germline mutations of LKB1/Peutz-Jeghers syndrome gene predispose carriers to hamartomatous polyposis of the gastrointestinal tract as well as to cancer of different organ systems. Although Peutz-Jeghers syndrome patients frequently present with neoplasms of the colon, stomach, small intestine, pancreas, breast, ovaries, and cervix, somatic mutations appear to be rare in the sporadic tumor types thus far studied (colorectal, gastric, testicular, and breast cancers). To evaluate whether somatic mutations of LKB1 contribute to the tumorigenesis of yet unstudied tumor types, we screened 14 cell lines and 129 tumor specimens from different cancers for a genetic defect in LKB1. Six melanoma and eight myeloma cell lines were scrutinized for LKB1 somatic mutations by genomic sequencing. No changes were found in the coding LKB1 sequence and exon/intron boundaries. Next, we analyzed 12 pancreatic, 8 gastric, 12 ovarian granulosa cell, 26 cervical, 28 lung, 24 soft tissue, and 19 renal tumors by single-strand conformational polymorphism analysis. Three changes in LKB1 coding nucleotide sequence were identified. One base pair deletion at A957 and G958 substitution by T occurred in a cervical adenocarcinoma sample, resulting in a frameshift and premature stop codon at position 335. Substitution of A581 by T occurred in a lung adenocarcinoma sample, resulting in the change of aspartic acid at position 194 to valine. A loss of another allele was detected in this sample. One silent change, C1257T, was found in a pancreatic carcinoma sample. The changes were not present in the matched normal tissue DNA samples. Our results suggest that mutational inactivation of LKB1 is a rare event in most sporadic tumor types.
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PMID:LKB1 somatic mutations in sporadic tumors. 1007 45

Fine-needle aspiration (FNA) has been increasingly utilized as a diagnostic tool in evaluating salivary gland masses, primarily to differentiate nonneoplastic from neoplastic lesions. Patients infected with human immunodeficiency virus (HIV) frequently present with salivary gland lesions. In this study, we reviewed the cytology of salivary gland lesions in HIV-infected patients and assessed the value of FNA in the diagnosis of salivary gland lesions in HIV-infected patients. One hundred and three FNAs of salivary gland lesions from 78 HIV-infected patients (63 males and 15 females) were included in our study. The patients' ages ranged from 7-65 yr, with a mean age of 40.9 yr. FNAs were classified into three categories: benign lymphoepithelial lesions (BLL) (77 cases or 74.8%), inflammatory processes (14 cases or 13.6%), including 3 reactive lymphoid hyperplasia, and neoplastic lesions (6 cases or 5.8%). The latter included three malignant lymphomas, a multiple myeloma, a metastatic adenocarcinoma from a lung primary, and a direct extension of basal-cell carcinoma. Six (5.8%) aspirates were nondiagnostic. No false-positive or false-negative cases were noted during follow-up of these patients. In conclusion, FNA is a simple and cost-effective procedure for the diagnosis of HIV-related salivary gland lesions. The majority of these lesions are cystic BLL and can be managed conservatively. Malignant lesions are rarely encountered and are readily recognized by FNA. Diagn. Cytopathol. 1999;21:260-264.
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PMID:Utility of fine-needle aspiration in the diagnosis of salivary gland lesions in patients infected with human immunodeficiency virus. 1049 19

It has been proposed that common aphidicolin-inducible fragile sites, in general, predispose to specific chromosomal breakage associated with deletion, amplification, and/or translocation in certain forms of cancer. Although this appears to be the case for the fragile site FRA3B and may be the case for FRA7G, it is not yet clear whether this association is a general property of this class of fragile site. The major aim of the present study was to determine whether the FRA16D chromosomal fragile site locus has a role to play in predisposing DNA sequences within and adjacent to the fragile site to DNA instability (such as deletion or translocation), which could lead to or be associated with neoplasia. We report the localization of FRA16D within a contig of cloned DNA and demonstrate that this fragile site coincides with a region of homozygous deletion in a gastric adenocarcinoma cell line and is bracketed by translocation breakpoints in multiple myeloma, as reported previously (Chesi, M., et al., Blood, 91: 4457-4463, 1998). Therefore, given similar findings at the FRA3B and FRA7G fragile sites, it is likely that common aphidicolin-inducible fragile sites exhibit the general property of localized DNA instability in cancer cells.
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PMID:Chromosomal fragile site FRA16D and DNA instability in cancer. 1074 40

Case details were reviewed from 2021 patients treated surgically for nasal polyposis between 1991 and 1999, seen by six surgeons serving a catchment population of 805,000. The aim of this study was to determine the incidence of discrepancies between clinical and histological diagnosis. Twenty-two patients (1.1 per cent) were identified as having a lesion that differed histologically from the clinical diagnosis made at the time of surgery and which altered their further management. Amongst them were 11 cases of inverted papilloma, two of Wegener's granulomatosis; and two of sarcoid. The rest of the cases comprised three of squamous cell carcinoma, one of adenocarcinoma, one of myeloma, one of angiofibroma and one of microcystic papillary adenoma. In this series, the occurrence of malignancy, inverted papilloma, or other clinically significant pathology among the group of patients with otherwise clinically unsuspected histology justifies sending nasal polyps for routine pathologic examination. A cost-benefit analysis showed that, on the basis of 250 cases per year, the cost of laboratory and pathological services would be 12,000 Pounds, in comparison with the estimated average medicolegal cost of 51,000 Pounds per year incurred as a result of a delay in diagnosis together with the pain and suffering which would result given the case mix in this series.
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PMID:All nasal polyps need histological examination: an audit-based appraisal of clinical practice. 1154 14

It is extremely important to look for tropical and other exotic diseases in travellers who return with illness or become ill after travelling. Especially tropical diseases and exotic infectious diseases have to be excluded because of their possible fatal outcome. On the other hand, many travellers return with 'common' not-exotic illnesses not related to their journey. When in such cases attention is only given to exotic causes of their illness, diagnosis can be delayed which may be harmful. This was the case in 5 patients: a woman aged 44 years who suffered for months from bloody diarrhoea since her return from Brasil, due to a rectal adenocarcinoma, a 61-year-old man with diarrhoea upon returning from Egypt, who had hairy-cell leukaemia, a 17-year-old boy who developed a ketoacidotic diabetic crisis whilst on a journey in Uganda, but in whose case the first thoughts went to malaria, a 50-year-old man who suffered from throat pain since a journey through East Africa, during which he contracted a flu-like disease, and in whom Kahler's disease was diagnosed, and 69-year-old man suffering from recurrent fever and cough, in whom a radiological lesion was observed in the thorax which proved to be part of Wegener's disease.
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PMID:[Illness after travel not always due to exotic disease]. 1123 88

There is increased interest in the treatment of cancer with thalidomide because of its antiangiogenic, immunomodulating and sedative effects. In animal models, the antitumour activity of thalidomide is dependent on the species, route of administration and coadministration of other drugs. For example, thalidomide has shown antitumour effects as a single agent in rabbits, but not in mice. In addition, the antitumour effects of the conventional cytotoxic drug cyclophosphamide and the tumour necrosis factor inducer 5,6-dimethylxanthenone-4-acetic acid (DMXAA) were found to be potentiated by thalidomide in mice bearing colon 38 adenocarcinoma tumours. Further studies have revealed that thalidomide upregulates intratumoral production of tumour necrosis factor-alpha 10-fold over that induced by DMXAA alone. Coadministration of thalidomide also significantly reduced the plasma clearance of DMXAA and cyclophosphamide. All these effects of thalidomide may contribute to the enhanced antitumour activity. Recent clinical trials of thalidomide have indicated that it has minimal anticancer activity for most patients with solid tumours when used as a single agent, although it was well tolerated. However, improved responses have been reported in patients with multiple myeloma. Palliative effects of thalidomide on cancer-related symptoms have also been observed, especially for geriatric patients with prostate cancer. Thalidomide also eliminates the dose-limiting gastrointestinal toxic effects of irinotecan. There is preliminary evidence indicating that the clearance of thalidomide may be reduced in the elderly. The exact role of thalidomide in the treatment of cancer and cancer cachexia in the elderly remains to be elucidated. However, it may have some value as part of a multimodality anticancer therapy, rather than as a single agent.
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PMID:Thalidomide in cancer treatment: a potential role in the elderly? 1195 Mar 76

Vinorelbine (NVB) is a newly synthesized vinca alkaloid that has been used to treat advanced malignant diseases including lung adenocarcinoma and lymphoma. The effect of NVB on myeloma, however, is unknown. We therefore examined the effect of NVB on the growth of human myeloma cell lines (RPMI8226, U266 and KPMM2) using the trypan blue dye exclusion test and Alamar blue assay. NVB inhibited the growth of myeloma cells of all three cell lines dose-dependently and this effect was intensified when NVB was combined with dexamethasone at 1.0 x 10(-6)mol/l. Flow cytometric analysis using annexin V (AN) and 7-amino-actinomycin D (7AAD) showed that NVB-induced apoptosis of these myeloma cells in all the cell lines. NVB appears to be a potent inducer of apoptosis in myeloma cells, and might have some benefit in the treatment of myeloma patients.
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PMID:Effect of vinorelbine on the growth of human myeloma cell lines in vitro. 1219 68

Prostate adenocarcinoma is associated with the formation of osteoblastic metastases in bone. It has been hypothesized that osteoclastic bone resorption is a critical component before the development of these osteoblastic lesions in bone. This observation has led researchers to test agents that inhibit osteoclastic activity to prevent or halt the formation of metastatic prostate cancer lesions in bone. Bisphosphonates inhibit osteoclast activity, and previous studies showed that they have the ability to reduce the osteolytic bone resorption associated with multiple myeloma and breast cancer. The objective of this study was to evaluate the efficacy of zoledronate in limiting the formation and/or progression of osteoblastic lesions produced by the injection of known prostate cancer cells (LAPC-9 and PC-3 cells) into the tibia of SCID mice. The mice were treated with either 30- micro g or 150- micro g doses of zoledronate before tumor implantation (pretreatment group), or at weekly intervals after tumor implantation (weekly treatment group), or weekly starting one month after tumor implantation (delayed-treatment group). The zoledronate was very effective in limiting the formation of osteolytic lesions in PC-3 implanted tibias by inhibiting osteoclast activity. Radiographic and histological analysis at weekly intervals revealed that osteolytic lesions developed in the control tibias by 2 weeks, and there was complete destruction of the cortical bone in much of the proximal tibias by 4 weeks. In the treatment groups, there was minimal cortical destruction noted in the weekly treatment groups at both doses, whereas mild cortical erosion was evident in the pretreatment groups, with more cortical destruction noted in the 30- micro g group compared with the 150- micro g group. Tartrate-resistant acid phosphatase (TRAP) staining showed that zoledronate decreased osteoclastic numbers and that there was a dose-dependent response. In tibias implanted with the LAPC-9 cells, the zoledronate was not effective in halting the formation of the osteoblastic lesions. Radiographic and histological analysis revealed that osteoblastic lesions either had formed or were developing in 18 of 18 of the control tibias and 36 of 36 of the treated tibias at 8 weeks regardless of dose or treatment schedule. Furthermore, TRAP staining demonstrated that osteoblastic lesions had formed in the LAPC-9 tibias under conditions in which osteoclast numbers were significantly reduced. These results suggest that osteoclast activity may not be critical for the development of osteoblastic lesions associated with prostate tumor cells. Hence, bisphosphonates may not be ideal agents to prevent the formation of osteoblastic lesions associated with prostate cancer metastases to bone.
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PMID:Use of zoledronate to treat osteoblastic versus osteolytic lesions in a severe-combined-immunodeficient mouse model. 1235 69

We present the case of a 77-year-old man with recurrence of prostate adenocarcinoma and widespread skeletal lesions. The skeletal lesions were found to be caused by multiple myeloma rather than metastatic spread of prostate adenocarcinoma. Various aspects of the radiographic imaging, evaluation of elevated prostate-specific antigen, and treatment of prostate adenocarcinoma are discussed.
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PMID:Recurrence of prostate adenocarcinoma presenting with multiple myeloma simulating skeletal metastases of prostate adenocarcinoma. 1247 84


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