Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment intensification with autologous bone marrow transplantation (ABMT) was administered to 37 cases of Hodgkin's and non-Hodgkin's lymphoma (HL and NHL) who were in complete or partial remission (CR or PR) after chemotherapy (MOPP/ABVD or F-MACHOP respectively) and to 12 cases of HL and NHL who were in relapse. ABMT treatment was BAVC for NHL and BEAM for HL. Marrow cells were harvested from the marrow and cryopreserved. The number of mononuclear marrow cells that was reinfused ranged between 0.19 and 0.80 x 108/Kg b.w. (median 0.39). All the patients were treated with granulocyte colony stimulating factor (G-CSF, Filgrastim) at a dose of 5 mg/Kg b.w. from day +4 until the absolute neutrophil count exceeded 1 x109/L for 3 consecutive days. Engraftment was observed in all cases, and no transplant-related deaths occurred. The patients with NHL and HL received a median of 12 (range 2-19) and 14.5 (range 9-27) doses of G-CSF respectively. Median time to 20 x 109/L platelet count was 14 to 17 days. Median time to an absolute neutrophil count 0.5x109/L was 13 days. A febrile episode during the period of post-transplant aplasia was documented in 35 patients (71%). Fever was associated with Gram+ bacteraemia in 31% of the cases and with Gram- bacteraemia in 11% of cases. Herpes Simplex infection was documented in two cases. No fungal infections were recorded. Median hospitalisation time from reinfusion ranged between 19.5 days (NHL) and 23 days (HL). Thirty-four of 37 cases (92%) who were transplanted in CR or in PR are currently alive and in continuous CR with a median follow-up time of 37 months after ABMT. Three of 12 cases (25%) who were transplanted in relapse are alive and in CR. Our data point out that ABMT followed by G-CSF is a safe and a very effective procedure for high risk malignant lymphomas, when ABMT is planned and is performed not as a rescue procedure but when it is integrated in the treatment strategy from the very beginning.
 ...
PMID:Treatment intensification of malignant lymphomas with autologous bone marrow transplantation and granulocyte colony stimulating factor. 1035 84

A 34-year-old male with a history of chickenpox developed primary abdominal non-Hodgkin's lymphoma (diagnosed in August 1995). Treatment with cyclophosphamide, doxorubicin, vincristine, and prednisolone achieved a partial remission. In July 1996, the disease recurred, and the patient received chemotherapy with carboplatine, etoposide, mitoxantrone, and prednisolone, but no response was noted. Involvement of the central nervous system and meninges was diagnosed on September 12, 1997. Blast cells were detected in the peripheral blood on September 26. Based on these findings, he was diagnosed as having leukemia. On September 27, painless vesicles developed on the left gluteal region. On October 13, the patient was hospitalized because the vesicles had spread over his entire body. Pathologic examination of the roofs of the blisters showed masses of inclusion bodies. Based on this, a diagnosis of varicella-zoster infection was made. Treatment with acyclovir (750 mg/day) for seven days failed to form crusts. New vesicles developed after the drug was discontinued, but crusts formed after acyclovir therapy was resumed. He died of interstitial pneumonia on December 21. Autopsy could not be performed. Histopathologic examination of pulmonary tissue obtained by necropsy did not reveal the presence of inclusion bodies characteristic of herpes simplex or varicella-zoster infection. Varicella-zoster virus (VZV) antigen was negative by an immunochemical staining method using monoclonal antibodies against VZV. Continuous long-term administration of acyclovir has been reported to be effective for non-Hodgkin's lymphoma complicated by recurrent intractable herpes zoster.
 ...
PMID:[Non-Hodgkin's lymphoma complicated by recurrent intractable generalized herpes zoster responsive to long-term acyclovir therapy]. 1035 92

Hemophagocytic lymphohistiocytosis (HLH) is a prototype of the hemophagocytic syndrome and occurs most often in children. Progress in cytokine research has now made it possible to show that HLH occurs as a consequence of uncontrolled, dysregulated cellular immune reactivity caused by a number of different underlying diseases. Three major risk groups of HLH can be identified: (1) familial HLH (FHL), (2) Epstein-Barr virus-associated HLH (EBV-HLH), and (3) life-threatening infection-associated or underlying disease-unknown HLH in infancy. Diagnostic criteria now exist that allow the differential diagnosis of these groups, which is important because distinct therapeutic measures are advised for each group. FHL patients require immediate application of immunochemotherapy with a core combination of corticosteroids and etoposide together with monitoring of central nervous system disease by early and repeated magnetic resonance imaging of the brain, followed by timely stem cell transplantation (SCT). EBV-HLH should also be treated with a combination of corticosteroids and etoposide. Aggressive or relapsed cases should be treated with cyclosporin A and, if necessary, with more intensive chemotherapy, such as that used for non-Hodgkin's lymphoma. SCT may also be needed in these refractory cases. In cases of herpes simplex virus, adenovirus 7, and other pathogen-undetermined HLH in early infancy, it is of great importance to administer appropriate antiviral or antibacterial agents. The most important point to make regarding HLH treatment is that the underlying cause of HLH must be promptly established to enable the rapid application of the appropriate therapy. Currently, 30% to 40% of HLH cases have a poor outcome. It is necessary for hematologists to cooperate with specialists in other fields so that early diagnosis, which is critical for improvements in outcome, can be made.
 ...
PMID:Advances in the management of hemophagocytic lymphohistiocytosis. 1097 2

Soluble CD27 (sCD27) reportedly is a sensitive and specific marker for leptomeningeal involvement (LI) of CD27-expressing lymphoproliferations such as B-cell non-Hodgkin's lymphoma (B-NHL) or chronic B-lymphocytic leukemia (B-CLL). Because morphological analysis of cerebrospinal fluid (CSF) in patients suspected of LI is false negative in one-third of patients, a diagnostic marker for LI by B-NHL or B-CLL would be very valuable. sCD27 was determined in the first CSF sample from each of 102 unselected patients submitted for (immuno)morphologic detection of malignant cells. The patients were considered to have LI if either (immuno)morphologic analyses showed tumor cells or if neuroradiological evaluation showed typical abnormalities consistent with LI. Patients were suspected of having LI if CSF samples revealed atypical lymphocytes and/or if clinical symptoms and signs suggestive of LI were present, but clinical follow-up was shorter than 3 months because of deterioration of the patient. LI was considered absent if (immuno)morphologic analyses of CSF samples were negative without evidence for LI during 3 months of clinical follow-up. In patients with chronic lymphoproliferative disorders [mainly B-non-Hodgkin's lymphoma (NHL)], sCD27 concentrations were significantly higher in the CSF samples of 16 patients with confirmed or suspected LI than in those of 46 patients without LI. However, sCD27 was also increased in a variety of other predominantly inflammatory neurological disorders including herpes simplex and zoster infections. The positive predictive value of sCD27 determination for LI was only 54%, but the negative predictive value was 92%. Normal sCD27 concentrations in CSF samples of patients with chronic lymphoproliferation makes LI unlikely, but the determination of CSF sCD27 is not sufficiently specific to serve as a reliable tumor marker.
 ...
PMID:Increased levels of soluble CD27 in the cerebrospinal fluid are not diagnostic for leptomeningeal involvement by lymphoid malignancies. 1197 19

LIGHT (homologous to lymphotoxins, shows inducible expression, and competes with herpes simplex virus glycoprotein D for herpesvirus entry mediator, a receptor expressed by T lymphocytes) is a member of the tumor necrosis factor superfamily that can interact with lymphotoxin-beta receptor (LTbetaR), herpes virus entry mediator, and decoy receptor (DcR3). In our previous study, we showed that LIGHT is able to induce cell death via the non-death domain containing receptor LTbetaR to activate both caspase-dependent and caspase-independent pathway. In this study, a LIGHT mutein, LIGHT-R228E, was shown to exhibit similar binding specificity as wild type LIGHT to LTbetaR, but lose the ability to interact with herpes virus entry mediator. By using both LIGHT-R228E and agonistic anti-LTbetaR monoclonal antibody, we found that signaling triggered by LTbetaR alone is sufficient to activate both caspase-dependent and caspase-independent pathways. Cross-linking of LTbetaR is able to recruit TRAF3 and TRAF5 to activate ASK1, whereas its activity is inhibited by free radical scavenger carboxyfullerenes. The activation of ASK1 is independent of caspase-3 activation, and kinase-inactive ASK1-KE mutant can inhibit LTbetaR-mediated cell death. This suggests that ASK1 is one of the factors involved in the caspase-independent pathway of LTbetaR-induced cell death.
 ...
PMID:The role of apoptosis signal-regulating kinase 1 in lymphotoxin-beta receptor-mediated cell death. 1256 58

A 69-year-old Chinese man presented in 2001 with a blistering eruption over the upper and lower limbs associated with oral ulceration for 1 month. He had stage IIIA follicular small cell cleaved non-Hodgkin's lymphoma diagnosed 5 years previously, and had received several lines of palliative chemotherapy, including two courses of chlorambucil, six cycles of cyclophosphamide, adriamycin, vincristine, and prednisolone (CHOP), and two four-cycle courses of rituximab, with disease stabilization at the time of presentation. Examination revealed erythematous, annular plaques with raised, urticarial borders studded with tense bullae and vesicles over the thighs. Some lesions were arciform and annular, with vesicles arranged in a ring at the border (Fig. 1). There was involvement of the feet with desquamation at the tips of the toes (Fig. 2). Severe erosions with hemorrhagic crusts on the lips, tongue, and buccal mucosa were seen. Herpes simplex virus serology was negative. A biopsy specimen from a vesicle on the left thigh showed suprabasal acantholysis (Fig. 3), some apoptotic keratinocytes (Fig. 4), satellite cell necrosis in the epidermis, and a superficial perivascular infiltrate of lymphocytes and eosinophils. Direct immunofluorescence showed intercellular immunoglobulin G (IgG) and C3 within the epidermis and along the basement membrane zone. Indirect immunofluorescence on monkey esophagus was positive for anti-intercellular antibody at a titre of 1/160 and positive on rat bladder at a titre of 1/80. A presumptive diagnosis of paraneoplastic pemphigus was made. This was later confirmed by the presence of antibodies against envoplakin (210 kDa), periplakin (190 kDa), and desmoglein 1 on immunoprecipitation studies. He was started on prednisolone 60 mg/day (1 mg/kg/day), with complete resolution of skin lesions within 1 week, but persistence of oral ulcers. Cyclophosphamide was added at a low dose of 1 mg/kg/day as he had baseline leukopenia. Cyclosporine was later added to a maximum of 4 mg/kg/day with only mild improvement of the oral lesions. He declined rituximab therapy. He died 2 months later from fulminant pneumonia.
 ...
PMID:Paraneoplastic pemphigus resembling linear IgA bullous dermatosis. 1696 19

LIGHT (homologous to lymphotoxins, exhibits inducible expression, competes with herpes simplex virus glycoprotein D for HVEM, a receptor expressed by T lymphocytes) is an apoptosis-inducing member of the tumor necrosis factor family of ligands. Messenger RNAs encoding LIGHT and its receptors, lymphotoxin-beta receptor (LTbetaR), decoy receptor-3 (DcR3) and herpes virus entry mediator (HVEM), are present in first trimester and term placentas. Proteins have been localized to specific cells in term but not earlier gestation placentas. Here, we have studied LIGHT and its receptors in early (6-7 weeks) and early-to-middle (8-13 weeks) gestation using immunohistology. Notable cell-specific, gestation-related features were identified. LIGHT and two of its receptors, a membrane-bound receptor that mediates apoptosis (LTbetaR) and a soluble receptor that interferes with LIGHT signaling (DcR3), were present in syncytiotrophoblast and cytotrophoblast cells in all samples but were detected in placental stromal cells only at week 8 and thereafter. HVEM, a membrane-bound receptor that protects against apoptosis, was expressed only on syncytiotrophoblast. These observations suggest that the LIGHT system may regulate early to middle stages of placental development via cell-specific, temporally programmed expression of the ligand and its receptors, and may also assist in preserving placental immune privilege.
 ...
PMID:Differential cellular expression of LIGHT and its receptors in early gestation human placentas. 1701 Apr 47

A 54-year-old woman, a known case of non-Hodgkin's lymphoma (NHL) in complete remission, presented with floaters and diminution of vision in her left eye. The eye had vitritis with non-haemorrhagic retinitis mimicking intraocular lymphoma and acute retinal necrosis. A vitreous sample was positive for cytomegalovirus (CMV) and herpes simplex virus 1 (HSV-1) DNA by PCR. The possibility of intraocular lymphoma was not confirmed by the immunohistochemistry of the vitreous sample. The patient had a relapse of NHL along with rapid deterioration of vision in her left eye to no perception of light, due to optic nerve involvement. The right eye developed a new patch of focal haemorrhagic retinitis threatening the fovea. Based on the laboratory results and the clinical findings, she was successfully managed as a case of bilateral CMV retinitis and the vision in her right eye was salvaged.
...
PMID:Atypical cytomegalovirus retinitis in non-Hodgkin's lymphoma. 2624 Jan 5


<< Previous 1 2 3