Measurement of B --> K*gamma branching fractions and charge asymmetries.

The branching fractions of the exclusive decays B0-->K(*0)gamma and B+-->K(*+)gamma are measured from a sample of (22.74+/-0.36)x10(6) BB decays collected with the BABAR detector at the PEP-II asymmetric e(+)e(-) collider.

Whole-body positron emission tomography using 18F-fluorodeoxyglucose for initial staging of patients with Hodgkin's disease.

An accurate initial staging of patients with Hodgkin's disease (HD) is important for the evaluation of clinical stage and risk factors, which are crucial for the choice of an appropriate treatment. 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) is useful for detecting active tumor tissue in patients with lymphoproliferative diseases and may contribute to conventional staging methods in patients with HD. Twenty-two patients who presented with newly diagnosed HD underwent conventional staging methods including computed tomography (CT) as well as FDG PET.

Proficient mismatch repair protein expression in Hodgkin and Reed Sternberg cells.

Hodgkin and Reed-Sternberg (H/RS) cells are characterized by chromosomal instability. Nevertheless, neither specific nor consistent chromosomal alterations could be characterized in H/RS cells. Microsatellite instability (MSI) is another form of genomic instability but its role in the pathogenesis of classical Hodgkin's disease (cHD) has not been investigated so far.

Search for the decay B0-->gammagamma.

We present a limit on the branching fraction for the decay B0-->gammagamma using data collected at the Upsilon(4S) resonance with the BABAR detector at the PEP-II asymmetric energy e+e- collider. Based on the observation of one event in the signal region, out of a sample of 21.3x10(6) e+e--->Upsilon(4S)-->BB decays, we establish an upper limit on the branching fraction of B(B0-->gammagamma)<1.

Measurement of the B--> J/psiK*(892) decay amplitudes.

We present a measurement of the decay amplitudes in B-->J/psiK*(892) channels using 20.7 fb(-1) of data collected at the Upsilon(4S) resonance with the BABAR detector at PEP-II. We measure a P-wave fraction R(perpendicular) = (16.

Deregulation of immunoglobulin gene transcription in the Hodgkin-Reed Sternberg cell line L1236.

Hodgkin-Reed Sternberg (H-RS) cells harbour clonal immunoglobulin gene (Ig) rearrangements in almost all cases of classical Hodgkin's disease but lack Ig gene expression. In the H-RS cell line L1236, a somatic mutation of the Ig heavy-chain gene promoter octamer motif has been described as a putative reason for absence of Ig gene expression. We addressed transcriptional activity of this mutated promoter by performing reporter gene studies and gel retardation assays.

Thoracic positron emission tomography using 18F-fluorodeoxyglucose for the evaluation of residual mediastinal Hodgkin disease.

Residual mediastinal masses are frequently observed in patients with Hodgkin disease (HD) after completed therapy, and the discrimination between active tumor tissue and fibrotic residues remains a clinical challenge. We studied the diagnostic value of metabolic imaging by 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) in detecting active mediastinal disease and predicting relapse. Twenty-eight HD patients with a residual mediastinal mass of at least 2 cm after initial therapy or after salvage chemotherapy were prospectively assigned to 29 examinations with FDG PET and were evaluated as 29 "subjects.

Measurement of the B(0) and B(+) meson lifetimes with fully reconstructed hadronic final states.

The B(0) and B(+) meson lifetimes have been measured in e(+)e(-) annihilation data collected in 1999 and 2000 with the BABAR detector at center-of-mass energies near the Upsilon(4S) resonance. Events are selected in which one B meson is fully reconstructed in a hadronic final state while the second B meson is reconstructed inclusively. A combined fit to the B(0) and the B(+) decay time difference distributions yields tau(B(0)) = 1.

Measurement of J/psi production in continuum e(+)e(-) annihilations near square root of s = 10.6 GeV.

The production of J/psi mesons in continuum e(+)e(-) annihilations has been studied with the BABAR detector at energies near the Upsilon(4S) resonance. The mesons are distinguished from J/psi production in B decays through their center-of-mass momentum and energy. We measure the cross section e(+)e(-)-->J/psi X to be 2.

Measurement of branching fractions and search for CP-violating charge asymmetries in charmless two-body B decays into pions and kaons.

We present measurements, based on a sample of approximately 23x10(6) BB pairs, of the branching fractions and a search for CP-violating charge asymmetries in charmless hadronic decays of B mesons into two-body final states of kaons and pions. We find the branching fractions B(B0-->pi(+)pi(-)) = (4.1+/-1.

Measurement of the decays B--> phiK and B--> phiK*.

We have observed the decays B--> phiK and phiK(*) in a sample of over 45 million B mesons collected with the BABAR detector at the PEP-II collider. The measured branching fractions are B(B+--> phiK+) = (7.7(+1.

Observation of CP violation in the B(0) meson system.

We present an updated measurement of time-dependent CP-violating asymmetries in neutral B decays with the BABAR detector at the PEP-II asymmetric B Factory at SLAC. This result uses an additional sample of Upsilon(4S) decays collected in 2001, bringing the data available to 32 x 10(6) BB macro pairs. We select events in which one neutral B meson is fully reconstructed in a final state containing charmonium and the flavor of the other neutral B meson is determined from its decay products.

Quantitative PCR in EBV-infected renal transplant patients.

In this study we investigated the levels of Epstein Barr virus (EBV) DNA by quantitative polymerase chain reaction (Q-PCR) in serum, whole blood and peripheral blood mononuclear cells (PBMC) from anti-EA IgG seropositive or anti-EA IgG seronegative EBV infected renal transplant recipients. We compared serological data with the viral load to monitor the risk of developing post-transplant lymphoproliferative disorders (PTLD). All patients were asymptomatic and none of them developed PTLD at the time of the study.

Resistance to CD95-mediated apoptosis in breast cancer is not due to somatic mutation of the CD95 gene.

Resistance to CD95 (Apo-1/Fas)-mediated apoptosis is a typical feature of breast cancer cells. Recent studies identified deleterious mutations of the CD95 gene not only in a variety of B cell lymphomas but also in a number of solid tumor entities. Therefore, we amplified and sequenced selected regions of the CD95 gene from 48 breast cancer cases and 10 cell lines but no mutation was found.

Measurement of CP-violating asymmetries in B0 decays to CP eigenstates.

We present measurements of time-dependent CP-violating asymmetries in neutral B decays to several CP eigenstates. The measurement uses a data sample of 23x10(6) Upsilon(4S)-->BbarB decays collected by the BABAR detector at the PEP-II asymmetric B Factory at SLAC. In this sample, we find events in which one neutral B meson is fully reconstructed in a CP eigenstate containing charmonium and the flavor of the other neutral B meson is determined from its decay products.

Cell fusion is not involved in the generation of giant cells in the Hodgkin-Reed Sternberg cell line L1236.

The mechanism of multinucleated cell formation in Hodgkin's disease has not yet been elucidated. We asked whether the giant multinucleated cells of the H-RS cell line L1236 develop via fusion of the predominant smaller cells. As a positive control for the fusion assay, human B cells from the B-cell lymphoma cell line BJA-B were split into two fractions, stained with the fluorochromes CMTMR and CMFDA, respectively, and fused using the polyethylene glycol 1500 cell hybridization protocol.

Oct-2 and Bob-1 deficiency in Hodgkin and Reed Sternberg cells.

Hodgkin and Reed Sternberg (H-RS) cells represent the malignant cells in classical Hodgkin's disease. Although derived from germinal center B cells, they do not express surface immunoglobulin. This has been explained by the presence of crippling mutations within the immunoglobulin genes in numerous cases of Hodgkin's disease.

Somatic mutation of the CD95 gene in human B cells as a side-effect of the germinal center reaction.

Somatic hypermutation specifically modifies rearranged immunoglobulin (Ig) genes in germinal center (GC) B cells. However, the bcl-6 gene can also acquire somatic mutations during the GC reaction, indicating that certain non-Ig genes can be targeted by the somatic hypermutation machinery. The CD95 gene, implicated in negative selection of B lymphocytes in GCs, is specifically expressed by GC B cells and was recently identified as a tumor suppressor gene being frequently mutated in (post) GC B cell lymphomas.

Somatic mutations of the CD95 gene in Hodgkin and Reed-Sternberg cells.

Hodgkin and Reed-Sternberg (H/RS) cells in classical Hodgkin's disease (cHD) are thought to be derived from preapoptotic germinal center B cells. However, little is known about the transforming events rescuing the precursor of the H/RS cells from apoptosis. Given the importance of CD95 (Apo-1/Fas)-mediated apoptosis for negative selection within the germinal center, single micromanipulated H/RS cells from 10 cases of cHD were analyzed for somatic mutations within the CD95 gene.

Lack of BCL10 mutations in Hodgkin's disease-derived cell lines.

The pathogenetic events leading to the malignant transformation of Hodgkin-Reed-Sternberg cells are unknown. As Hodgkin-Reed-Sternberg cells are resistant to CD95-mediated apoptosis and chromosomal aberrations involving the 1p22 region harbouring the proapoptotic BCL10 gene represent a recurrent event in Hodgkin's disease-derived cell lines, analysis of the BCL10 gene and its transcripts was performed. As transcription of wild-type BCL10 was detected in all Hodgkin's disease-derived cell lines analysed, alterations of the coding sequence of the BCL10 gene are unlikely to contribute to the malignant transformation of the Hodgkin-Reed-Sternberg cell.

Guillain-Barré syndrome in a patient with non-Hodgkin's lymphoma.

We describe a case of Guillain-Barré syndrome (GBS) in a patient with non-Hodgkin's lymphoma (NHL). A 21-year-old woman with a newly diagnosed stage IV high-grade lymphoma (precursor T-cell NHL according to the R.E.

Cultivated H-RS cells are resistant to CD95L-mediated apoptosis despite expression of wild-type CD95.

Objective: In most cases of classic Hodgkin's disease (HD), Hodgkin and Reed-Sternberg (H-RS) cells clonally derive from germinal-center B cells. Within their rearranged immunoglobulin genes, somatic mutations rendering potentially functional immunoglobulin gene rearrangements nonfunctional were detected, indicating that H-RS cells do not express a B-cell receptor. Under physiologic conditions, these cells would undergo apoptosis within the germinal center.

Two cases of toxoplasmic encephalitis in patients with acute T-cell leukaemia and lymphoma.

Two cases of opportunistic cerebral infections in HIV-negative cancer patients due to chemotherapy induced immunosuppression are reported. A 61-year-old patient with low grade lymphoma (immunocytoma as referred to the Kiel classification) developed stereotactical biopsy proven toxoplasmic encephalitis 6 months after initiation of fludarabine treatment. The lymphoma had been diagnosed 8 years earlier and had been treated with several different regimens.

Progressive multifocal leukoencephalopathy after autologous bone marrow transplantation and alpha-interferon immunotherapy.

A patient with a stage IV mantle cell lymphoma (according to the REAL classification) was treated with high-dose chemotherapy and autologous bone marrow transplantation. One year later while on alpha-interferon immunotherapy she suffered from progressive loss of short-term memory and reported difficulties in recognizing objects. Magnetic resonance imaging (MRI) showed a vast ring-enhancing lesion of the left postcentral parietal area.