Background: Myocardial diseases such as myocarditis and cardiomyopathies are clinically important and can cause complications such as heart failure and arrhythmias, which increase the risk of death. The combination of myocarditis with cardiomyopathy is difficult to diagnose because their manifestations often overlap, and multiple myocardial diseases are usually not included in the diagnostic search. Hypertrophic cardiomyopathy (HCM) is the most common cardiomyopathy; however, few studies have examined the combination of myocarditis and HCM, thereby highlighting the importance of this problem. This article aimed to analyze the influence of myocarditis on clinical features and outcomes in patients with HCM. Methods: A literature search was performed using PubMed and the Scientific Electronic Library eLIBRARY.ru databases. Relevant studies, published until November 2023, were analyzed in detail. Studies were selected in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) standards. Results: Twelve studies (three original articles and nine clinical cases) were isolated from a total cohort of 1504 publications and were included in the study. The prevalence of myocarditis in HCM ranged from 23.5% to 46.7%. The presence of concomitant myocarditis in patients with HCM was associated with heart failure progression, worsening of ventricular arrhythmias, and an increased risk of sudden cardiac death. Conclusions: The incidence of myocarditis in HCM is high. Early detection and treatment of myocarditis in patients with HCM can slow the progression of heart failure rhythm disturbances and improve the disease prognosis. The PROSPERO Registration: The systematic review was registered in the International Prospective Register of Systematic Reviews PROSPERO (CRD42024499672, https://www.crd.york.ac.uk/PROSPERO/view/CRD42024499672).

Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of aggressive non-Hodgkin lymphoma and is characterized by pronounced molecular heterogeneity that is not always fully captured by standard histopathological assessment. Circulating tumor DNA (ctDNA) is increasingly regarded as a promising liquid-biopsy biomarker that enables non-invasive molecular tumor profiling, assessment of tumor burden, dynamic monitoring of treatment response, and detection of measurable/minimal residual disease (MRD). Modern analytical platforms, ranging from PCR-based assays to next-generation sequencing approaches, including CAPP-Seq and PhasED-Seq, have substantially expanded the possibilities of molecular monitoring in DLBCL. This review summarizes current data on the biological characteristics of ctDNA, contemporary methods for its analysis, concordance between ctDNA and tumor-tissue mutational profiles, and the clinical significance of baseline ctDNA levels, early molecular response, post-treatment MRD status, and molecular surveillance during remission. Special attention is given to ctDNA monitoring in patients receiving novel immunotherapies, including CAR-T cell therapy, bispecific antibodies, and antibody–drug conjugates. Emerging multi-omic approaches integrating genomic, epigenomic, and fragmentomic data are discussed as promising future directions. Key limitations of clinical implementation include insufficient standardization of preanalytical and analytical workflows, the confounding effect of clonal hematopoiesis of indeterminate potential, variability across technological platforms, and the lack of completed prospective randomized interventional studies demonstrating improved outcomes when therapy is modified according to ctDNA status. Overall, ctDNA is currently a highly informative prognostic biomarker in DLBCL; however, its full implementation as a predictive tool for treatment selection requires further harmonization, prospective validation, and confirmation in interventional clinical trials.

Background: Diffuse large B-cell lymphoma (DLBCL) with TP53 abnormalities, corresponding to the LymphGen A53 molecular subtype, represents a biologically high-risk group associated with primary resistance to standard R-CHOP therapy. Epigenetic sensitization using hypomethylating agents may enhance chemosensitivity in this setting. We prospectively evaluated the clinical activity and safety of a molecularly adapted DAC-R-CHOP regimen in newly diagnosed A53-DLBCL. Methods: In this single-center prospective pilot cohort study, 70 consecutive patients with newly diagnosed DLBCL underwent targeted next-generation sequencing using a 60-gene panel with integrated copy number variation analysis. Six patients (8.5%) were classified as the A53 subtype. All patients received one cycle of standard R-CHOP. From cycle 2 onward, A53 patients received decitabine (10 mg/m² IV, days 1–5) prior to R-CHOP (DAC-R-CHOP), for a total of six cycles. The primary endpoint was complete metabolic response (CMR) according to Lugano 2014 criteria. Exact 95% confidence intervals (CI) were calculated. Results: The median age of the A53 cohort was 65 years. CMR was achieved in all six patients (100%; 95% CI, 54%–100%). At a median follow-up of 6 months, all patients remained alive in confirmed CMR. Grade III–IV hematologic toxicity occurred in all cases. Febrile neutropenia developed in 100% of patients, requiring mandatory G-CSF support and anti-infective therapy; no treatment-related mortality or permanent dose reductions were observed. Two patients (33%) experienced gastrointestinal bleeding related to local tumor lysis, which was managed conservatively without protocol discontinuation. Conclusions: In this prospective molecularly stratified pilot cohort, integration of decitabine into front-line immunochemotherapy showed promising clinical activity in A53-DLBCL, albeit at the cost of substantial hematologic toxicity requiring intensive supportive care. Given the small sample size, short follow-up, and absence of a comparator arm, these findings should be considered hypothesis-generating and warrant validation in larger multicenter phase II studies with integrated translational biomarker analyses.

Aim. To evaluate the structure and effectiveness of therapy for newly diagnosed diffuse large B-cell lymphoma (DLBCL) in adults in real clinical practice according to the Moscow Oncology Registry data. Materials and methods. Data from 1060 patients with newly diagnosed DLBCL from the Moscow Oncology Registry who received treatment from 2022 to 2025 in a Moscow healthcare setting were retrospectively analyzed. The median age was 69 years. The majority of patients were in the older age group (60.4 %), with advanced disease stages (70 %), non-GCB subtypes (60 %), and high risk according to the international prognostic index (67 %). Of all patients included, 62.1 % received immunochemotherapy according to the R-CHOP program (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone), 12.6 % received R-DA-EPOCH (rituximab, etoposide, prednisolone, vincristine, cyclophosphamide, doxorubicin), 2.6 % received intensive regimens, 14.7 % received R-miniCHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone in reduced doses), 7.8 % received RB (rituximab, bendamustine) or R-CVP (rituximab, cyclophosphamide, vincristine, prednisolone). Results. In the overall patient cohort (n = 1060), the objective response rate was 79.7 % (n = 845). Complete metabolic response was achieved by 66.4 % (n = 704) of patients. The complete response rate varied depending on the treatment regimen: in the R-CHOP group it was 68.4 % (n = 451), when using R-DA-EPOCH – 69.4 % (n = 93), intensive regimens – 89.3 % (n = 25). Among patients receiving R-miniCHOP, complete response was achieved in 62.2 % (n = 97) of cases, while in the RB / R-CVP group this rate was the lowest and amounted to 45.8 % (n = 38). With a median follow-up of 24 months, the 2-year overall survival in the total group was 70 % (95 % confidence interval 67–73), and the 2-year progression-free survival was 44 % (95 % confidence interval 40–48). Conclusion. Results of first-line DLBCL therapy efficacy analysis indicate unsatisfactory treatment outcomes, particularly in the high-risk group for early progression. We suggest that biologically targeted antitumor therapy based on the identified tumor genotype represents the most promising clinical approach for patients with newly diagnosed DLBCL.

Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of aggressive non-Hodgkin lymphomas and is characterized by pronounced molecular heterogeneity that is not always fully captured by standard histopathological assessment. At present, analysis of circulating tumor DNA (ctDNA) is regarded as a promising liquid biopsy tool that enables non-invasive molecular tumor profiling, assessment of tumor burden, and dynamic monitoring of minimal residual disease (MRD). Modern analytical platforms, ranging from PCR-based technologies to next-generation sequencing, including CAPP-Seq and PhasED-Seq, have substantially expanded the possibilities of molecular monitoring in DLBCL. This review summarizes data on the biological characteristics of ctDNA and contemporary methods for its analysis, as well as evidence regarding the concordance between ctDNA mutational profiles and tumor tissue. Particular attention is paid to the clinical significance of baseline ctDNA levels, early assessment of molecular eradication of the tumor clone, MRD status after completion of therapy, and molecular monitoring during remission. The principal limitations of clinical integration are also discussed, including insufficient standardization of the analytical workflow, the influence of clonal hematopoiesis, and the absence of completed interventional studies demon-strating improved clinical outcomes when therapy is modified according to molecular status. Thus, ctDNA currently represents a highly informative prognostic biomarker in DLBCL; however, its full implementation in routine clinical practice requires further standardization, validation, and confirmation of its role in treatment selection within personalized strategies.

Background: Diffuse large B-cell lymphoma (DLBCL) with TP53 abnormalities, corresponding to the LymphGen A53 molecular subtype, represents a biologically high-risk group associated with primary resistance to standard R-CHOP therapy. Epigenetic sensitization using hypomethylating agents may enhance chemosensitivity in this setting. We prospectively evaluated the clinical activity and safety of a molecularly adapted DAC-R-CHOP regimen in newly diagnosed A53-DLBCL. Methods: In this single-center prospective pilot cohort study, 70 consecutive patients with newly diagnosed DLBCL underwent targeted next-generation sequencing using a 60-gene panel with integrated copy number variation analysis. Six patients (8.5%) were classified as the A53 subtype. All patients received one cycle of standard R-CHOP. From cycle 2 onward, A53 patients received decitabine (10 mg/m² IV, days 1–5) prior to R-CHOP (DAC-R-CHOP), for a total of six cycles. The primary endpoint was complete metabolic response (CMR) according to Lugano 2014 criteria. Exact 95% confidence intervals (CI) were calculated. Results: The median age of the A53 cohort was 65 years. CMR was achieved in all six patients (100%; 95% CI, 54–100%). At a median follow-up of 6 months, all patients remained alive in confirmed CMR. Grade III–IV hematologic toxicity occurred in all cases. Febrile neutropenia developed in 100% of patients, requiring mandatory G-CSF support and anti-infective therapy; no treatment-related mortality or permanent dose reductions were observed. Two patients (33%) experienced gastrointestinal bleeding related to local tumor lysis, which was managed conservatively without protocol discontinuation. Conclusions: In this prospective molecularly stratified pilot cohort, integration of decitabine into front-line immunochemotherapy showed promising clinical activity in A53-DLBCL, albeit at the cost of substantial hematologic toxicity requiring intensive supportive care. Given the small sample size, short follow-up, and absence of a comparator arm, these findings should be considered hypothesis-generating and warrant validation in larger multicenter phase II studies with integrated translational biomarker analyses.