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

IVIg is a preparation of normal polyspecific IgG obtained from pooled plasma of a large number of healthy donors. IVIg treatment of patients with chronic lymphocytic leukemia induced a reduction in the total number of lymphocytes in the peripheral blood. Regression of Kaposi's sarcoma was also noted in an HIV patient treated with IVIg. The aim of this study was to determine whether F(ab')2 prepared from IVIg binds to cellular structures of different tumor tissues. Biotinylated F(ab')2 was prepared from 3 different preparations of IVIg and from affinity purified IgG from a patient with multiple myeloma. Direct immunohistochemistry using a streptavidin peroxidase staining method was performed on biopsy samples of 18 different tumor tissues. Positive staining of the cytoplasm, cell membrane and nuclear membrane of several types of malignant tumors by F(ab')2 from IVIg was immunohistochemically demonstrated. Nuclear staining of tumor cells by IVIg was rare. IVIg bound to different tumors of epithelial origin, especially colon carcinoma, breast carcinoma and squamous cell carcinoma of the lung. Malignant tumors of mesenchymal origin such as leiomyosarcoma have also demonstrated positive staining by IVIg. IVIg contains antibodies to the cytoplasm, nuclear membrane and cell membrane of different malignant tumors especially of epithelial origin. This binding might provide a basis for the assumption that IVIg treatment of cancer patients may induce antibody dependent cell mediated cytotoxicity response against tumors, and implies that it can be potentially beneficial as adjuvant treatment of malignant diseases.
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PMID:Antibodies to the cytoplasm, cell membrane and nuclear membrane of malignant neoplasms in pooled normal human polyspecific immunoglobulin G. 1056 13

We investigated the incidence of post-transplant solid tumors in a cohort of 109 patients who had undergone auto-peripheral blood stem cell transplantation (PBSCT) for acute myelogenous leukemia (n = 18), acute lymphoblastic leukemia (n = 7), non-Hodgkin's lymphoma (n = 52), Hodgkin's disease (n = 5), multiple myeloma (n = 16), chronic myelogenous leukemia (n = 1), myelodysplastic syndrome (n = 3) and solid tumors (n = 7). The patients were followed up for a median of 32 months after PBSCT. Five second solid malignancies developed in 4 patients within 14 to 43 months after PBSCT: large cell carcinoma of the lung, adenocarcinoma of the rectum, cholangiocellular carcinoma of the liver, squamous cell carcinoma of the mouth, and adenocarcinoma of the gallbladder. The affected patients were 3 of 52 with non-Hodgkin's lymphoma and one of 16 with multiple myeloma. One of the patients was in the 5th decade of life (n = 31) and 3 were in the 6th decade (n = 31). The cumulative actuarial risk for developing post-transplant solid tumors was 8% at 8 years. Elderly patients (> or = 60 year old) who have undergone PBSCT need to be observed carefully for second neoplasms because of their increased risk of post-transplant solid tumors.
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PMID:[Secondary solid tumors in autologous-peripheral blood stem cell transplantation recipients]. 1102 Sep 88

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

The Swedish Family-Cancer Database was used to analyse site-specific risk of second primary malignancies following 53 159 haematolymphoproliferative disorders (HLPD) diagnosed between 1958 and 1996. Standardized incidence ratio (SIR) of a second malignancy was calculated as the ratio of observed to expected numbers of second malignancies by applying site-, sex-, age-, period-, residence- and occupation-specific rates in the corresponding population in the Database to the appropriate person-years at risk. Among 18 960 patients with non-Hodgkin's lymphoma (NHL), there was over a 3-fold significant increase in cancer of the tongue, small intestine, nose, kidney and nervous system, squamous cell carcinoma (SCC) of the skin, NHL, Hodgkin's disease (HD) and lymphoid and myeloid leukaemia. Among 5353 patients with HD, there was over a 4-fold significant increase in cancer of the salivary glands, nasopharynx and thyroid, NHL and myeloid leukaemia, and over a 1.6-fold increase in cancer of the stomach, colon, lung, breast, skin (melanoma and SCC), nervous system and soft tissues and lymphoid leukaemia. Among 28 846 patients with myeloma and leukaemia, there was a significant increase in cancer of the skin, nervous system and non-thyroid endocrine glands and all HLPD except for myeloma. Our findings showed some clustering between first and second primaries among Epstein-Barr virus-, ultraviolet radiation- and immunosuppression-related cancers.
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PMID:Second primary neoplasms among 53 159 haematolymphoproliferative malignancy patients in Sweden, 1958-1996: a search for common mechanisms. 1159 72

A 75-year-old man, known with Morbus Kahler, was referred with a history of uveitis and hypopyon at the left eye. The uveitis did not respond to any steroid treatment. It was complicated with high intraocular pressure. Anterior chamber punction showed atypical cells of epithelial origin. Several weeks prior to this presentation an atypical pterygium of the same eye was biopsied. Histopathologic examination at that time showed mild atypical actinic changes. The biopsy specimen was reviewed in our laboratory and revealed an invasive squamous cell carcinoma originating from the bulbar conjunctiva. The eye was eventually enucleated. Histologic examination of the enucleated eye showed invasion of the cornea, sclera, trabeculum, anterior chamber angle and choroid by a muco-epidermoid squamous cell carcinoma.
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PMID:Invasive squamous cell carcinoma of the conjunctiva. 1176 60

DNA amplifications at 11q13 are frequently observed in esophageal squamous cell carcinoma (ESC) and correlate with a malignant phenotype. Although this amplicon spans a region of several megabases and harbors numerous genes, CCND1 and EMS1 are thought to be the relevant candidates in ESC. We investigated whether the putative transforming gene MYEOV, mapping 360 kb centromeric to CCND1 and activated concomitantly with CCND1 in a subset of t(11;14)(q13;q32) positive multiple myeloma cell lines, represents a target of 11q13 amplification in ESC. To evaluate the role of MYEOV in ESC, we tested 31 ESC cell lines and 48 primary tumors for copy number levels of MYEOVand demonstrated that MYEOV was always coamplified with CCND1. However, MYEOV expression levels correlated only inconsistently with DNA amplification data. Treatment with the demethylating agent 5-aza-2'-deoxycytidine restored MYEOV expression in a subset of cell lines exhibiting DNA amplification without high MYEOV expression, suggesting that MYEOV is transcriptionally silenced by a DNA methylation mechanism in most of the latter cell lines. Our results indicate that MYEOV is a coamplified gene with CCND1 at 11q13, but its activation is sometimes inhibited by an epigenetic mechanism.
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PMID:MYEOV, a gene at 11q13, is coamplified with CCND1, but epigenetically inactivated in a subset of esophageal squamous cell carcinomas. 1220 83

Lung cancer is the leading cause of cancer-related death in developed countries. Non-small cell lung cancer (NSCLC) represents 80% of the total lung cancer cases and is comprised of adenocarcinoma, adenosquamous carcinoma, squamous cell carcinoma and large cell carcinoma (LCC) subtypes. The ability of LCC to metastasize earlier than the other forms of lung cancer suggests anti-angiogenic drugs as effective agents to combat this cancer. Thalidomide is an anti-angiogenic drug that has shown promise in multiple hematological diseases, and myeloma and other cancers. However, the molecular mechanism by which thalidomide exerts its effects is poorly understood. Therefore, we evaluated the effectiveness of thalidomide on NSCLC cell growth, and found that LCC cells were growth inhibited by 40-60%. This effect seemed specific to LCC cancer cells, since other forms of NSCLC were only mildly affected by thalidomide. At the molecular level, thalidomide increased peroxisome proliferator-activated receptor gamma (PPARgamma) protein dose-dependently, and peroxisome proliferator response element activity. Further, thalidomide treatment of LCC cells decreased nuclear factor kappa B activity in a dose-dependent fashion, increased apoptosis and decreased the expression of angiogenic proteins. In our mouse xenograft model of lung cancer, we found that intratumoral thalidomide caused a 64% decrease in tumor growth; moreover, tumors from the thalidomide-treated mice expressed higher PPARgamma, than tumors from control mice. This study shows the antitumor activity of thalidomide against LCC tumors and suggests a model in which thalidomide exerts its antitumor effects on LCC cells through the induction of PPARgamma and subsequent downstream signaling. To our knowledge, this is the first study to show a link between thalidomide and PPARgamma.
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PMID:The effect of thalidomide on non-small cell lung cancer (NSCLC) cell lines: possible involvement in the PPARgamma pathway. 1520 58

Resveratrol, trans-3,5,4'-trihydroxystilbene, was first isolated in 1940 as a constituent of the roots of white hellebore (Veratrum grandiflorum O. Loes), but has since been found in various plants, including grapes, berries and peanuts. Besides cardioprotective effects, resveratrol exhibits anticancer properties, as suggested by its ability to suppress proliferation of a wide variety of tumor cells, including lymphoid and myeloid cancers; multiple myeloma; cancers of the breast, prostate, stomach, colon, pancreas, and thyroid; melanoma; head and neck squamous cell carcinoma; ovarian carcinoma; and cervical carcinoma. The growth-inhibitory effects of resveratrol are mediated through cell-cycle arrest; upregulation of p21Cip1/WAF1, p53 and Bax; down-regulation of survivin, cyclin D1, cyclin E, Bcl-2, Bcl-xL and clAPs; and activation of caspases. Resveratrol has been shown to suppress the activation of several transcription factors, including NF-kappaB, AP-1 and Egr-1; to inhibit protein kinases including IkappaBalpha kinase, JNK, MAPK, Akt, PKC, PKD and casein kinase II; and to down-regulate products of genes such as COX-2, 5-LOX, VEGF, IL-1, IL-6, IL-8, AR and PSA. These activities account for the suppression of angiogenesis by this stilbene. Resveratrol also has been shown to potentiate the apoptotic effects of cytokines (e.g., TRAIL), chemotherapeutic agents and gamma-radiation. Phamacokinetic studies revealed that the target organs of resveratrol are liver and kidney, where it is concentrated after absorption and is mainly converted to a sulfated form and a glucuronide conjugate. In vivo, resveratrol blocks the multistep process of carcinogenesis at various stages: it blocks carcinogen activation by inhibiting aryl hydrocarbon-induced CYP1A1 expression and activity, and suppresses tumor initiation, promotion and progression. Besides chemopreventive effects, resveratrol appears to exhibit therapeutic effects against cancer. Limited data in humans have revealed that resveratrol is pharmacologically quite safe. Currently, structural analogues of resveratrol with improved bioavailability are being pursued as potential therapeutic agents for cancer.
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PMID:Role of resveratrol in prevention and therapy of cancer: preclinical and clinical studies. 1551 85

There are a number of reports on collision occurrence of non-hematologic cancers and Non-Hodgkin's lymphoma (NHL) and multiple myeloma. In this report we present a case of patient with immunoproliferative disease, extramedullary plasmocytoma and NHL-lymphoplasmocytoid lymphoma (LPL) and squamous cell carcinoma of the lung. After diagnosis of extramedullary plasmocytoma cytostatic therapy was commenced and the patient was well. Five years after patient was clinically worse and diagnostic evaluation this time revealed lymphoplasmocytoid cells in bone marrow. Five months later malignant morphologically undifferentiated cells were found in bone marrow which were by immunocytochemistry established as CD38 positive. After the patient's death, disseminated NHL-LPL and squamous cell carcinoma of lung was confirmed. In the report, we compared clinical course and diagnostic findings of our patient with literature data. We have also discussed the possible relationship of multiple B-cell lymphoid tumors and squamous cell carcinoma concluding that multidiscplinary diagnostic tools are essential not only for carcinoma diagnosis and follow-up, but also for further understanding of carcinogenesis.
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PMID:Patient with immunoproliferative disease and lung carcinoma: a case report. 1563 71

We report a case of solitary extramedullary plasmacytoma (SEP) of the oropharynx. A 53-year-old man presented who had had bloody phlegm and a sore throat for a few days. A mass was endoscopically detected in his right posterior oropharyngeal wall, and biopsy revealed a neoplasm consisting of a uniform population of plasma cells. Computed tomography (CT) showed a broad-based papillary soft tissue density mass projecting into the oropharynx from the right posterior wall of the pharynx, and post-contrast CT showed marked enhancement of the tumor. The tumor showed slightly higher signal intensity compared with surrounding muscle on MR Tl-weighted images (T1WI) and high signal intensity on MR T2-weighted images (T2WI). The mass showed homogeneous enhancement on post-contrast T1WI. Further clinical examination showed an absence of multiple myeloma (MM). The patient was diagnosed as having SEP. Following radiation therapy, a reduction in tumor size was observed. Although SEP is a rare tumor, it should be included in the differential diagnosis of tumors of the oropharynx because of its imaging similarities to other, more common malignant tumors, such as squamous cell carcinoma and lymphoma.
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PMID:CT and MRI findings of a solitary extramedullary plasmacytoma of the oropharynx: case report. 1655 68


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