Cachexia is a risk factor for negative clinical and functional outcomes in patients receiving chimeric antigen receptor T-cell therapy for B-cell non-Hodgkin lymphoma.

Cachexia is a muscle-wasting syndrome that is known to impact the clinical course of several cancer populations but has not been specifically investigated in patients receiving chimeric antigen receptor T (CAR-T) cell therapy. In this study, we investigated the relationship between cachexia markers and several cancer and functional outcomes in a pilot population of aggressive B-cell non-Hodgkin lymphoma patients receiving CAR-T. We found that the prognostic nutritional index was linked to progression-free survival, overall survival, and disability-free survival, while several additional weight and serum-based markers of cachexia were also associated with negative outcomes.

Draft Genome Sequence of 49, a Potential Probiotic That Produces Multiple Bacteriocins.

49, isolated from dog feces, is active against , vancomycin-resistant enterococci, and Its draft genome sequence reported herein contains a gene cluster encoding multiple bacteriocins and indicates the absence of genes for virulence factors. These characteristics signify the strain's potential for use as a probiotic.

The Vibrio cholerae type VI secretion system employs diverse effector modules for intraspecific competition.

Vibrio cholerae is a Gram-negative bacterial pathogen that consists of over 200 serogroups with differing pathogenic potential. Only strains that express the virulence factors cholera toxin (CT) and toxin-coregulated pilus (TCP) are capable of pandemic spread of cholera diarrhoea. Regardless, all V.

Dual expression profile of type VI secretion system immunity genes protects pandemic Vibrio cholerae.

The Vibrio cholerae type VI secretion system (T6SS) assembles as a molecular syringe that injects toxic protein effectors into both eukaryotic and prokaryotic cells. We previously reported that the V. cholerae O37 serogroup strain V52 maintains a constitutively active T6SS to kill other Gram-negative bacteria while being immune to attack by kin bacteria.

Type VI secretion system regulation as a consequence of evolutionary pressure.

The type VI secretion system (T6SS) is a mechanism evolved by Gram-negative bacteria to negotiate interactions with eukaryotic and prokaryotic competitors. T6SSs are encoded by a diverse array of bacteria and include plant, animal, human and fish pathogens, as well as environmental isolates. As such, the regulatory mechanisms governing T6SS gene expression vary widely from species to species, and even from strain to strain within a given species.

Genomic and functional analysis of the type VI secretion system in Acinetobacter.

The genus Acinetobacter is comprised of a diverse group of species, several of which have raised interest due to potential applications in bioremediation and agricultural purposes. In this work, we show that many species within the genus Acinetobacter possess the genetic requirements to assemble a functional type VI secretion system (T6SS). This secretion system is widespread among Gram negative bacteria, and can be used for toxicity against other bacteria and eukaryotic cells.

Constitutive type VI secretion system expression gives Vibrio cholerae intra- and interspecific competitive advantages.

The type VI secretion system (T6SS) mediates protein translocation across the cell membrane of Gram-negative bacteria, including Vibrio cholerae - the causative agent of cholera. All V. cholerae strains examined to date harbor gene clusters encoding a T6SS.

VasH is a transcriptional regulator of the type VI secretion system functional in endemic and pandemic Vibrio cholerae.

The gram-negative bacterium Vibrio cholerae is the etiological agent of cholera, a disease characterized by the release of high volumes of watery diarrhea. Many medically important proteobacteria, including V. cholerae, carry one or multiple copies of the gene cluster that encodes the bacterial type VI secretion system (T6SS) to confer virulence or interspecies competitiveness.

Vibrio cholerae requires the type VI secretion system virulence factor VasX to kill Dictyostelium discoideum.

The type VI secretion system (T6SS) is recognized as an important virulence mechanism in several Gram-negative pathogens. In Vibrio cholerae, the causative agent of the diarrheal disease cholera, a minimum of three gene clusters--one main cluster and two auxiliary clusters--are required to form a functional T6SS apparatus capable of conferring virulence toward eukaryotic and prokaryotic hosts. Despite an increasing understanding of the components that make up the T6SS apparatus, little is known about the regulation of these genes and the gene products delivered by this nanomachine.

Antibiotic resistance mechanisms of Vibrio cholerae.

As the causative agent of cholera, the bacterium Vibrio cholerae represents an enormous public health burden, especially in developing countries around the world. Cholera is a self-limiting illness; however, antibiotics are commonly administered as part of the treatment regimen. Here we review the initial identification and subsequent evolution of antibiotic-resistant strains of V.

The Vibrio cholerae type VI secretion system displays antimicrobial properties.

The acute diarrheal disease cholera is caused by the marine bacterium Vibrio cholerae. A type VI secretion system (T6SS), which is structurally similar to the bacteriophage cell-puncturing device, has been recently identified in V. cholerae and is used by this organism to confer virulence toward phagocytic eukaryotes, such as J774 murine macrophages and Dictyostelium discoideum.

The Vibrio Cholerae Type VI Secretion System: Evaluating its Role in the Human Disease Cholera.

Vibrio cholerae, the marine bacterium responsible for the diarrheal disease cholera, utilizes a multitude of virulence factors to cause disease. The importance of two of these factors, the toxin co-regulated pilus (TCP) and cholera toxin (CT), has been well documented for pandemic O1 and epidemic O139 serogroups. In contrast, endemic non-O1 and non-O139 serogroups can cause localized outbreaks of cholera-like illness, often in the absence of TCP and CT.

The novel expanded porphyrin, motexafin gadolinium, combined with [90Y]ibritumomab tiuxetan for relapsed/refractory non-Hodgkin's lymphoma: preclinical findings and results of a phase I trial.

Purpose: Therapeutic strategies to enhance the efficacy of radioimmunotherapy have not been explored. Motexafin gadolinium is a novel anticancer agent that targets redox-dependent pathways and enhances sensitivity of tumor cells to ionizing radiation.

Experimental Design: We did preclinical studies examining motexafin gadolinium combined with rituximab and/or radiation in lymphoma cells.

The type VI secretion system: translocation of effectors and effector-domains.

A number of prominent Gram-negative bacteria use the type VI secretion system (T6SS) to transport proteins across the bacterial envelope. Rapid progress is being made in elucidating the structural components of the T6SS apparatus, and a few effectors have been reported to pass through it. However, this is not the complete story: a family of T6SS proteins, the VgrGs, share structural features with the cell-puncturing device of the T4 bacteriophage, and may be used in a similar fashion by bacteria to puncture host cell membranes and insert the T6SS apparatus into the host cytosol.

CD23+ mantle cell lymphoma: a clinical pathologic entity associated with superior outcome compared with CD23- disease.

Mantle cell lymphoma (MCL) commonly lacks expression of CD23. However, a significant minority of MCLs express CD23, as assessed by flow cytometric immunophenotyping (FCIP). The aims of our study were to investigate the expression of CD23 by FCIP in patients with MCL and to correlate CD23 expression with pathologic and clinical parameters, including outcome.

G-CSF is not necessary to maintain over 99% dose-intensity with ABVD in the treatment of Hodgkin lymphoma: low toxicity and excellent outcomes in a 10-year analysis.

Dose-intensity of chemotherapy is important in the treatment of Hodgkin lymphoma (HL) and granulocyte-colony stimulating factor (G-CSF) is commonly used to maintain it. We reviewed all newly diagnosed HL patients who were treated at our institution between 1996 and 2005. Fifty-nine patients received adriamycin, bleomycin, vinblastine, and dacarbazine (ABVD) chemotherapy with no dose reductions, treatment delays, and without G-CSF, regardless of absolute neutrophil count (ANC).

Gemcitabine added to doxorubicin, bleomycin, and vinblastine for the treatment of de novo Hodgkin disease: unacceptable acute pulmonary toxicity.

Background: Gemcitabine is an effective treatment for recurrent Hodgkin disease (HD), with relatively minimal associated toxicity. The authors conducted a trial substituting this drug for dacarbazine in the standard regimen to form ABVG (doxorubicin, bleomycin, vinblastine, gemcitabine) for patients with newly diagnosed, high-risk HD.

Methods: Twelve patients (median age, 34 years) with advanced-stage de novo HD were enrolled.