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Most infected patients are unaware of their past exposure to HBV, which may have resolved B ( b past HBV infection, diagnosed by HB surface antigen (HBsAg)-negative and HB core antibody (HBcAb)-positive serology] or that they have chronic HBV infection [(CHB) HBsAg - positive)]. It is estimated that more than two billion people worldwide have been exposed to hepatitis B virus (HBV), with more than 260 million people actively infected with HBV, making HBV one of the leading causes of chronic liver disease, cirrhosis and hepatocellular carcinoma [[1]]. In addition, Dominguez et al., reported a patient with CLL with past HBV infection, who had HBVr almost 5 years after completion of FCR. An alternative pathway is monitoring HBsAg and HBV DNA every 3 months, during anticancer therapy and for up to 12 months after last anticancer therapy, with immediate preemptive antiviral therapy (during anticancer therapy and for up to 12 months after last anticancer therapy), if HBV reactivation is detected [[11]]. [Extracted from the article]

It is unknown whether rituximab increases the risk of second primary malignancies (SPMs) in patients with diffuse large cell B-cell lymphoma (DLBCL). We assessed SPMs in DLBCL patients diagnosed between 1996 and 2014 in comparison with the general Israeli population and dependent on rituximab treatment. Jewish patients had no increased risk for SPMs. Arab-DLBCL females had a higher SPMs rate compared to the general Arab-females population [SIR (95%CI) 1.86 (1.08–2.98)]. Incidence and time to SPMs, in both Jewish and Arab patients, were unaffected by rituximab. Risk for breast and thyroid cancers, in Arab and Jewish females respectively, were higher in the pre-rituximab era [SIR(95%CI) 5.25 (1.41–13.43) and SIR(95%CI) 3.85 (1.41–8.38), respectively]. Age ≥60 years was the only predictor for increased risk of SPM (HR = 2.5, p <.01). The increased risk of SPMs in specific subgroups of patients that were treated in the pre-rituximab era may reflect stringent medical surveillance employed in these populations. [ABSTRACT FROM AUTHOR]

The article presents a study on the use of the mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) inhibitor in analyzing chronic lymphocytic leukemia (CLL) cells. It notes that studied CLL cells were taken from patients' blood samples. A chart is presented on the Mi-2 apoptosis in CLL cells.

Patients with diffuse large B-cell lymphoma (DLBCL) presenting with intestinal involvement are prone to develop perforation. Identification of those who are at high risk for this complication would enable a rational-based decision regarding preemptive surgery. Although computed tomography (CT) is widely used at diagnosis, data regarding its ability to predict intestinal perforation are scanty. We performed a retrospective single-center study, including all consecutive DLBCL patients presented with intestinal involvement, assessing predictors for perforation with an emphasis on CT-related parameters. Forty-nine patients were included, 43 (88%) underwent CT scan at diagnosis. Ten patients (20%) developed intestinal perforation. A univariate regression analysis found increased risk among patients with a concentric, transmural lesion, and a longer involved intestinal segment. In conclusion, CT scan results can define patients with DLBCL and intestinal involvement who are at risk for perforation, suggesting that a preemptive surgical resection should be considered in these cases. [ABSTRACT FROM AUTHOR]

Follicular lymphoma (FL) is the most common subtype of indolent non-Hodgkin lymphoma. Patients with stage I disease are usually treated with radiotherapy (RT). In previous studies, mostly from the pre positron emission tomography-computed tomography (PET-CT) era, the 5 year progression-free survival (PFS) and overall survival (OS) rates of stage I disease were 60-80% and 80-93%, respectively. This study retrospectively evaluated the outcome of stage I FL which was treated with involved field RT in the PET-CT era between 2002 and 2015. Ninety-one patients were enrolled. Five year PFS and OS rates were 73% and 97%, respectively. Relapse occurred in 19 (21%) patients, 74% occurring outside the radiation field. In conclusion, PET-CT staging of clinical stage I FL may contribute to the improved prognosis in patients treated with RT compared to historical cohorts, possibly due to better identification of “genuine” stage I disease. [ABSTRACT FROM AUTHOR]

The risk of developing non-Hodgkin lymphoma increases with age, yet elderly patients are under-represented in clinical trials. Here, we evaluate a combination regimen including ifosfamide, carboplatin and etoposide with or without rituximab (ICE ± R) in 32 fit elderly patients (median age 75.6 years) with relapsed or refractory diffuse large B-cell lymphoma. ICE ± R was generally administered in reduced doses and was well tolerated. The overall response rate (ORR) was 53.1% with a complete response (CR) rate of 40.6%. The median progression free survival (PFS) and overall survival (OS) were 3.9 and 17.0 months, respectively. Patients who responded to ICE ± R achieved median PFS of 47.2 months and OS of 78.9 months. Patients ineligible for autologous transplantation who responded to ICE ± R were treated with additional cycles, and achieved a median PFS of 18.9 months and OS of 21.7 months. Previous response to first-line therapy was the strongest predictor of response, PFS and OS to second-line treatment. [ABSTRACT FROM AUTHOR]

A multi-center retrospective analysis of a cohort of patients in Israel treated with any bendamustine containing regimen between 2010-2014 was performed in order to determine the incidence and predictors for infection. The Kaplan Meier Model, employing log rank analysis, was used to assess time-to-infection. The Cox Proportional Hazards model was used to analyze multivariate effects of risk and 234 patients were included in the analysis. One hundred and nine (46.6%) developed at least one infection and 33.76% had severe infections. Seventy-six (41.5%) developed bacterial infection, nine (3.8%) fungal infection and 26 (11.5%) had viral infections. Factors significantly associated with time to infection on multivariable analysis were: bendamustine-combinations [hazard ratio (HR) = 0.589 (95% CI = 0.374-0.926), p = 0.022], Hb level [HR = 0.791 (95% CI = 0.716-0.875), p < 0.0001] and ischemic heart disease [HR = 1.828 (95% CI = 1.165-2.868), p = 0.009]. Infections were associated with a higher mortality and hospitalization rate. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented regarding a study on the correlation between Th17 cell counts and Tregs peripheral blood lymphocytes in patients with early stage chronic lymphocytic leukemia (CLL).

In this article the authors discuss lenalidomide and T-cell homeostasis and the article "Lenalidomide Consolidation and Maintenance Therapy After Autologous Stem Cell Transplant for Multiple Myeloma Induces Persistent Changes in T-cell Homeostasis" by E. Clave, C. Douay, T. Coman et al. within the issue. They are cautiously supportive of several points raised in Clave et al.'s article and suggest that the article leads to more questions about the use of lenalidomide for treating cancers.

The author comments on a research study which examined the link of regulatory T-cells (Tregs) to the prognosis of chronic lymphocytic leukemia (CLL). A discussion on the relation between peripheral blood Tregs and the severity of CLL at diagnosis, during disease progression and at the time of development of autoimmune cytopenia in Indian patients is presented. The author agrees with the inverse correlation between the percentage and absolute Treg cell numbers and lymphocyte doubling time (LDT).

In this article the author discusses the expansion mechanism of regulatory T-cells (Tregs) in B chronic lymphocytic leukemia (CLL). It states that Tregs have an ability to inhibit anti-tumor immune responses. It cites the study by Jak and colleagues which rejected the notion that chronic antigenic stimulation induces Treg expansion in CLL due to reduced apoptosis. It concludes that Treg expansion results from T and B cell activation that lead to CLL cell immune avoidance.