Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1261473 (sarcoma)
25,952 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a monoclonal antibody specific to the Lewis X antigen (anti-Lex), the authors studied 103 cases of Hodgkin's disease (HD) in comparison with 57 cases of non-Hodgkin's lymphoma (NHL); three cases of granulocytic sarcoma (GS); two cases of malignant histiocytosis (MH); one case of monoblastic leukemia (ML); one case of interdigitating reticulum cell sarcoma (IRCS); six cases of histiocytosis X (HX); one case of reticulohistiocytoma (RH); 44 various reactive conditions of the lymph node (LN). Reed-Sternberg and related (R-S) cells stained selectively in 80 of 92 cases of HD (87.0%), excluding 11 cases of lymphocyte predominance type. The stain was better in B-5-fixed specimens than in formalin-fixed specimens, showing a dense deposit of reaction products at a paranuclear site and on the cell surface. The staining results were compared with those of Leu-M1 and found to be superior both qualitatively and quantitatively (detection rate of R-S cells: 87.0% versus 68.5% of Leu-M1). Granulocytes, rare epithelioid histiocytes, and some endothelial and/or erythrocytes also stained with anti-Lex. The stain had positive results in three cases of GS showing a diffuse cytoplasmic staining pattern. Of NHL, two of 29 peripheral T-cell lymphomas stained to show rare paranuclear deposits without cell surface staining. The stain had negative results in MH, ML, IRCS, HX, and RH. Of 45 reactive LN, minute subcapsular collections of Lewis X+, altered-appearing Langerhans'-like cells, were observed in all ten LN from human immunodeficiency virus (HIV)-associated persistent generalized lymphadenopathy (PGL). The stain had negative results in all other various reactive conditions of LN. In conclusion, Lewis X staining is useful as a marker for R-S cells in paraffin sections with staining results superior to those of Leu-M1. Lewis X staining also detects subcapsular clustering of altered-appearing Langerhans'-like cells in PGL, which has not been described previously and warrants additional study.
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PMID:The Lewis X antigen. A new paraffin section marker for Reed-Sternberg cells. 170 18

A new class of compounds, 9-[(2RS)-3-fluoro-2-phosphonylmethoxypropyl] [(RS)-FPMP] derivatives of purines, is described that has selective activity against a broad spectrum of retroviruses [including human immunodeficiency virus type 1 (HIV-1) and type 2 (HIV-2)] but not other RNA or DNA viruses. This activity spectrum is completely different from that of the parental compounds, 9-[(2S)-3-hydroxy-2-phosphonylmethoxypropyl] [(S)-HPMP] derivatives of purines, which are active against a broad range of DNA viruses. The racemic (RS)-FPMP derivatives of adenine and 2,6-diaminopurine, termed (RS)-FPMPA and (RS)-FPMPDAP, respectively, are markedly more selective as in vitro antiretroviral agents than their 9-(2-phosphonylmethoxyethyl) (PME) counterparts, PMEA and PMEDAP. Also, (RS)-FPMPA and (RS)-FPMPDAP have a substantially higher therapeutic index in mice in inhibiting Moloney murine sarcoma virus-induced tumor formation and associated death and are markedly less inhibitory to human bone marrow cells than PMEA and PMEDAP. The diphosphate derivative of (RS)-FPMPA [(RS)-FPMPApp] is a potent and selective inhibitor of HIV-1 reverse transcriptase but not of HSV-1 DNA polymerase or DNA polymerase alpha. (RS)-FPMPApp, akin to PMEA diphosphate (PMEApp), acts as a DNA chain terminator. The DNA chain-terminating properties of PMEApp and (RS)-FPMPApp seem to be a prerequisite for acyclic nucleoside phosphonates to exhibit antiretrovirus (i.e., anti-HIV) activity.
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PMID:9-[(2RS)-3-fluoro-2-phosphonylmethoxypropyl] derivatives of purines: a class of highly selective antiretroviral agents in vitro and in vivo. 171 Dec 14

9-(2-Phosphonylmethoxyethyl)adenine (PMEA) and 9-(2-phosphonylmethoxyethyl)-2,6-diaminopurine (PMEDAP) are selectively inhibitory to human immunodeficiency virus and other retroviruses. We have now investigated the effects of different PMEA and PMEDAP treatment schedules in newborn mice infected with Moloney murine sarcoma virus (MSV). Administration of a single dose of PMEA or PMEDAP on the day of MSV inoculation conferred a greater protective effect against MSV-induced tumor formation than when this dose was divided over two, four or seven injections per week. Also, the therapeutic index of PMEA and PMEDAP was increased if administered as a single dose. Furthermore, PMEA and PMEDAP afforded a marked antiviral protection if administered within one day before MSV infection. Thus, single doses of PMEA or PMEDAP, when administered shortly before or after MSV infection, appear to be effective in preventing the manifestations of the retroviral disease.
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PMID:Single-dose administration of 9-(2-phosphonylmethoxyethyl)adenine (PMEA) and 9-(2-phosphonylmethoxyethyl)-2,6-diaminopurine (PMEDAP) in the prophylaxis of retrovirus infection in vivo. 177 76

In populations with non-HIV immunodeficiency, non-Hodgkin lymphoma and soft tissue sarcoma, especially Kaposi's sarcoma, are the most prominent tumours, but Hodgkin's disease, gastric carcinoma, squamous cell skin cancer, malignant melanoma, hepatoma, myeloid leukaemia and/or colorectal carcinoma have been linked in various studies. Population based cancer registries and cohort studies of HIV infected persons have generally failed to detect HIV related increases in total cancer incidence or in specific tumours other than non-Hodgkin lymphoma and Kaposi's sarcoma; however, associations with anal carcinoma, hepatoma and Hodgkin's disease have been suggested by some studies. Although not indicating increased risk, HIV induced immunosuppression has been linked to an acceleration of cervical and anal neoplasia and to increased aggressiveness of Hodgkin's disease with a relative excess of the mixed cellularity type. Advances in treatment for HIV infection will delay progression to AIDS and may allow an altered natural history to emerge, including the occurrence of excesses of additional cancer types.
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PMID:HIV infection and cancers other than non-Hodgkin lymphoma and Kaposi's sarcoma. 182 20

In older persons, the humoral immune response, as reflected morphologically by proliferation and expansion of germinal centers, is relatively subdued in comparison with the florid reactive follicular hyperplasia (RFH) which may be observed in younger age groups. The presence of RFH in lymph node biopsies in patients 60 yr or older, which we have regarded with concern since 1972, appears to represent an imbalance of the immune system, in some patients, on the background of which predominantly non-Hodgkin's malignant lymphoma (NHL) may be present or will develop. Fifty-eight patients 60 yr old or more who presented with enlarged lymph nodes exhibiting inappropriate RFH for age were identified during the interval from 1969 to 1989. An apparent etiology was initially identified for the reactive follicular hyperplasia in only 12 cases: five with documented rheumatoid arthritis; one each with a history of trauma, positive monospot test, and combination of thrombophlebitis and fungal skin infection, and two each with elevated Epstein-Barr virus (EBV) titers and human immunodeficiency virus type 1 (HIV-1) seropositivity. While most were alive or died of nonlymphomatous causes and one was lost to follow-up, 18 (31%) patients either had concurrent lymphoma or subsequently developed diffuse NHL. There were ten diffuse interfollicular (I-Foll) lymphomas (six concurrent), two diffuse mixed cell lymphomas (DMCL), one diffuse large cell lymphoma (DLCL), one diffuse immunoblastic sarcoma (DIBS), two diffuse small noncleaved cell lymphomas (DSNCL), one unclassified NHL, and only one Hodgkin's disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical implications of nodal reactive follicular hyperplasia in the elderly patient with enlarged lymph nodes. 202 Jun 58

9-(2-Phosphonylmethoxyethyl)adenine (PMEA) is a potent and selective inhibitor of the in vitro replication of a number of retroviruses, including HIV-1 and HIV-2, simian immunodeficiency virus (SIV), simian AIDS-related virus (SRV), feline immunodeficiency virus (FIV) and Moloney murine sarcoma virus (MSV). PMEA causes a dose-dependent suppression of the induction of anti-SIVmacgp120 antibodies in SIV mac-infected rhesus monkeys. Complete suppression of anti-SIVmacgp120 antibodies was achieved in SIV-infected animals treated with PMEA at 2 x 10 or 2 x 5 mg/kg per day for 29 days. No toxic side-effects were noted during this treatment period. Antibodies against SIVmac gp120 appeared 1-2 weeks after PMEA treatment was stopped, but the antibody titre reached in these animals was significantly lower than in the SIVmac-infected animals who had not been treated with PMEA. Our data strongly suggest that PMEA should be pursued for its potential in the treatment of AIDS and other retrovirus infections.
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PMID:9-(2-Phosphonylmethoxyethyl)adenine (PMEA) effectively inhibits retrovirus replication in vitro and simian immunodeficiency virus infection in rhesus monkeys. 205 58

2',3'-Dideoxyinosine (DDI) and 2',3'-dideoxy-2,6-diaminopurine riboside (ddDAPR) are potent and selective inhibitors of human immunodeficiency virus (HIV) replication in MT-4 cells. They are also inhibitory to the transformation of C3H/3T3 cells by Moloney murine sarcoma virus (MSV). In vivo, they are only marginally effective in delaying MSV-induced tumor formation, and mortality associated therewith in newborn NMRI mice. When combined with ribavirin, DDI and ddDAPR become much more effective in inhibiting MSV and HIV replication in vitro and MSV-induced tumor formation in vivo. These observations point to the potential role of ribavirin in potentiating the anti-HIV activity of DDI in AIDS patients.
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PMID:Potentiating effect of ribavirin on the in vitro and in vivo antiretrovirus activities of 2',3'-dideoxyinosine and 2',3'-dideoxy-2,6-diaminopurine riboside. 212 3

The acyclic purine nucleoside analogue 9-(2-phosphonomethoxyethyl)adenine [PMEA; formerly referred to as 9-(2-phosphonylmethoxyethyl)adenine] is a potent and selective inhibitor of human immunodeficiency virus replication in vitro and of Moloney murine sarcoma virus-induced tumor formation in mice. In the latter system PMEA has stronger antiretroviral potency and selectivity than 3'-azido-3'-thymidine (AZT). We have now investigated the effect of the drug in cats infected with the feline immunodeficiency virus (FIV). In vitro, PMEA was found to efficiently block FIV replication in feline thymocytes (50% effective dose, 0.6 microM). When administered to cats at doses of 20, 5, or 2 mg/kg per day, PMEA caused a dose-dependent suppression of FIV replication and virus-specific antibody production. Seropositive field cats with signs of opportunistic infection (gingivitis, stomatitis, and diarrhea) showed clinical improvement during PMEA therapy (5 mg/kg per day) and recurrence of the disease after treatment was discontinued. Thus, FIV infection in cats is an excellent model to test the efficacy of selective anti-human immunodeficiency virus agents in vivo.
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PMID:Suppression of feline immunodeficiency virus infection in vivo by 9-(2-phosphonomethoxyethyl)adenine. 215 2

Kaposi sarcoma is a common, though not inevitable consequence of AIDS. There is a body of opinion that believes that this sarcoma is derived from lymphatic endothelium, or at least from a failure of vascular endothelium to distinguish between whether it is attempting to be a blood vessel or a lymphatic. While immunodeficiency and its consequences have proved to be the most significant area of research, the general biology of endothelium, and especially angiogenesis, has perhaps been neglected. I predict that the most important new concept in the biology of endothelium is the recognition of mechanico-receptors as a determinant of its behavior. The concept is illustrated by articles from Oxford (Ryan 1989), from Boston, Massachusetts (Ingber & Folkman 1989), and from Moscow (Shirinsky et al 1989). Most authors studying endothelium have concentrated on blood vascular endothelium and ignored the rich lymphatic bed. Since the lymphatic is par excellence a mechanical receptor, this is perhaps surprising. The lymphatic functions by its responsiveness to mechanical forces, it is a fine control for hydrostatic pressure within the interstitium, and morphologically, its flat and attenuated endothelium linked to strong anchoring fibers is biologically exactly the kind of behavior required of a cell that is responsive to mechanical factors. Perhaps the best known mechanical receptor is the stretch receptor in the muscle fiber. The linkage of this receptor to the enzyme protein kinase C has been described. Ryan has also pointed out that protein kinase C may be an important mechanico-receptor in the fibroblast and possibly also universally in all cells, including lymphatic endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Grip and stick and the lymphatics. 221 67

Kaposi's sarcoma (KS), a major complication of AIDS, is found more frequently in the Western hemisphere among homosexual and bisexual male AIDS patients than among other patients with AIDS. Theory and arguments for the possibility of infectious cofactors playing a role in the cause and transmission of the sarcoma are reviewed. While cytomegalovirus, Epstein-Barr, and human herpesvirus have been explored as potential cofactors in AIDS-related KS, the focus here is on the suggestion that Kaposi's sarcoma in a person with AIDS may be caused by an unidentified infectious agent spread through sexual contact. The 1st of 4 arguments supporting this theory is that patients acquiring HIV via sexual contact instead of through parenteral or vertical means experience a much greater risk of KS. 2nd, women acquiring HIV heterosexually from bisexual men experienced a 4 times greater risk of KS than those having other sexual partners. The identification of benign and localized KS in 6 homosexual or bisexual men from New York City without HIV antibodies suggests that the KS causal agent is the same regardless of the presence or absence of HIV infection. There is some evidence that circumstances permitting the heterosexual spread of AIDS in Africa also facilitate the transmission of the KS causal agent. Laboratory and epidemiologic investigations are needed to identify the sexually transmitted cofactor or cause of KS. KS in its classic and endemic African forms is described, followed by discussion of KS and immunodeficiency. 2 sections are then devoted to exploration of AIDS-associated KS in the US and the AIDS-related KS epidemic in Africa, respectively.
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PMID:Recent developments in sexually transmitted diseases: is Kaposi's sarcoma a sexually transmitted disease? 226 87


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