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The optimal treatment endpoints and duration of continuous therapy for multicentric Castleman disease (MCD) remain controversial. We retrospectively analyzed data from 123 patients with Human Herpesvirus (HHV)-8 negative MCD. We demonstrated that continuous therapy significantly enhanced progression-free survival (PFS) in patients who achieved an optimal response after initial treatment. These findings underscore the critical role of continuous therapy in HHV-8 negative MCD. Further studies with larger cohorts are required to validate these findings. [ABSTRACT FROM AUTHOR]

It was designed to effectively target wild-type BCR-ABL1 and a wide range of BCR-ABL1 mutants, including T315I, making it a promising reinduction therapy for relapsed Ph + B-ALL. E255K, T315I, and a compound of T315I and Q252H mutations were identified in 3 BCR-ABL1 P210-positive patients, respectively, whereas no mutations were found in 2 BCR-ABL1 P190-positive patients. Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph + B-ALL) was one of high risky B-cell ALL subtypes that exhibits resistance to conventional chemotherapy [[1]]. Moreover, the induction therapy for Ph + B-ALL evolved from TKI plus intensive chemotherapy to TKI plus corticosteroids, which also supported that TKI was the backbone for Ph + B-ALL treatments. [Extracted from the article]

Patients with adverse risk according to ELN received allo-HSCT if a suitable donor was available, regardless of MRD status; otherwise, they received venetoclax plus modified intermediate-dose cytarabine-based chemotherapy consolidation unless they developed progressive disease or unacceptable toxicity or stopped due to physician or patient decisions. Keywords: acute myeloid leukaemia; DAV; efficacy; safety; venetoclax EN acute myeloid leukaemia DAV efficacy safety venetoclax 568 572 5 04/20/23 20230501 NES 230501 AUTHOR CONTRIBUTIONS Huafeng Wang and Yiyi Yao designed the study, collected and analysed the data, and wrote the first draft of the manuscript. Thus, 12 of the 13 patients (92.3%, 95% CI 64.0%-99.8%) achieved CR after the completion of all cycles of induction, one patient (P7) failed to achieve remission after induction therapy (Figure 1B,C, Table 1). [Extracted from the article]

The outcomes of myelodysplastic syndrome (MDS) patients with SF3B1 mutation, despite identified as a favorable prognostic biomarker, are variable. To comprehend the heterogeneity in clinical characteristics and outcomes, we reviewed 140 MDS patients with SF3B1 mutation in Zhejiang province of China. Seventy-three (52.1%) patients diagnosed as MDS with ring sideroblasts (MDS-RS) following the 2016 World Health Organization (WHO) classification and 118 (84.3%) patients belonged to lower risk following the revised International Prognostic Scoring System (IPSS-R). Although clonal hematopoiesis-associated mutations containing TET2 , ASXL1 and DNMT3A were the most frequent co-mutant genes in these patients, RUNX1, EZH2, NF1 and KRAS/NRAS mutations had significant effects on overall survival (OS). Based on that we developed a risk scoring model as IPSS-R×0.4+ RUNX1 ×1.1+ EZH2 ×0.6+ RAS ×0.9+ NF1 ×1.6. Patients were categorized into two subgroups: low-risk (L-R, score <= 1.4) group and high risk (H-R, score > 1.4) group. The 3-year OS for the L-R and H-R groups was 91.88% (95% CI, 83.27%-100%) and 38.14% (95% CI, 24.08%-60.40%), respectively (P<0.001). This proposed model distinctly outperformed the widely used IPSS-R. In summary, we constructed and validated a personalized prediction model of MDS patients with SF3B1 mutation that can better predict the survival of these patients. [ABSTRACT FROM AUTHOR]

Myelodysplastic syndrome/myeloproliferative neoplasm, unclassifiable (MDS/MPN-U) is a subtype of MDS/MPN that exhibits a combination of the features of both MDS and MPN. To date, no curative treatment is available for MDS/MPN-U; however, previous studies have suggested a potential survival advantage for ruxolitinib and hypomethylating agents. We reported a case of a JAK2-negative but KRAS-positive MDS/MPN-U patient treated with ruxolitinib plus decitabine. After treatment, the patient's clinical symptoms were moderated, and the size of the spleen and the peripheral blood cell counts were reduced. These effects might be due to the regimen's ability to reduce STAT5 activation and upregulate microRNA-181c to downregulate the variant allele frequency (VAF) of KRAS. [ABSTRACT FROM AUTHOR]

Background: A recent outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2), which began in Wuhan, China, with a high level of human-to-human transmission has been reported. There are limited data available on Coronavirus Disease 2019 (COVID-19) patients with hematological malignancies with more than 60 days of follow-up. This study describes the clinical characteristics, including multiple recurrences of COVID-19, in a patient with chronic lymphocytic leukemia (CLL) during 69 days of follow-up. Case Presentation: A 72-year-old female was admitted to hospital isolation after being infected with COVID-19 as part of a family cluster on January 30, 2020. Apart from SARS-Cov-2 virus infection, laboratory results revealed lymphocytosis of uncertain etiology and abnormal distribution of T lymphocytes. On blood smears, small blue lymphocytes with scant cytoplasm were observed, and the presence of high levels of circulating clonal B cells was also demonstrated by flow cytometry. The patient was diagnosed with COVID-19 and CLL. Among her family members, she had the highest viral loads and the fastest progression on lung injury and developed severe pneumonia. Serological results showed she had both 2019-nCoV-specific IgM and IgG antibodies; however, only IgG antibodies were detected in her husband's plasma. Results: A combination regimen of antiviral therapy and high-dose intravenous immunoglobulin (IVIG) in the early stage seemed to be effective for treating CLL and SARS-Cov-2 infection. Because of the low humoral immune response, the CLL patient could not effectively clear the SARS-Cov-2 infection and suffered from recurrence twice during the 69-day follow-up. Conclusion: In CLL, a neoplastic antigen-specific B-cell clone proliferates, and the progeny cells accumulate and outgrow other B cells, leading to immune deficiency. Considering the low humoral immune response and ineffective clearance of SARS-Cov-2 in CLL patients, the follow-up and home quarantine period should be extended. We need further studies to clarify suspending or continuing CLL therapy during COVID infection. For those patients who are prone to progression to severe disease, administering humoral immunity therapies can help to prevent disease progression and quickly meet the cure criteria. [ABSTRACT FROM AUTHOR]

To determine the incidence, risk factors, and relative survival of acute myeloid leukemia (AML) secondary to myelodysplastic syndrome (MDS) in the Surveillance, Epidemiology, and End Results (SEER) database. Retrospective analysis of all patients with new MDS onset in the SEER-18 database from 2001 to 2013. We identified 36 558 patients with primary MDS. The rate of secondary AML (sAML) was 3.7% among patients 40 years or younger and 2.5% among those older than 40 (P = .039). The median transformation interval was significantly shorter for the younger group (4.04 vs 13.1 mo; P < .001). For both age groups, median overall and cancer-specific survival were significantly longer for patients who did not develop sAML. Although the younger patients survived longer than the older patients, sAML development had a more negative effect on the survival of younger patients. Female sex, age, and World Health Organization (WHO) type MDS with single lineage dysplasia (MDS-SLD) were associated with a decreased risk of sAML for older but not younger patients. Among older patients with MDS, a married status, Black race, female sex, shorter time to sAML, and WHO type MDS-SLD or MDS with ringed sideroblasts were favorable prognostic factors for survival. In the SEER database, the rate of sAML among patients with MDS is lower than that in previous reports, but these patients still have worse survival. Risk assessment should include clinical and demographic factors. [ABSTRACT FROM AUTHOR]

Acute myeloid leukemia (AML) originates from the abnormal clonal proliferation of myeloblasts. Immunoglobulin is secreted by B cells. AML with monoclonal antibody often indicates a poor prognosis. Here we report a case of BCOR mutation and TLS-ERG expression in AML with monoclonal immunoglobulinemia. After chemotherapy, the patient achieved bone marrow complete remission. BCOR mutation and TLS-ERG fusion gene in patient's bone marrow were not detected, at the same time, peripheral blood monoclonal immunoglobulin also disappeared. BCOR mutation or TLS-ERG fusion gene expression is associated with poor prognosis, AML with monoclonal immunoglobulin may have the same prognostic significance. [ABSTRACT FROM AUTHOR]

Objective: Acute lymphoblastic leukemia (ALL) is a malignant disease characterized by the accumulation of lymphoblasts, and a poor prognosis for adults with ALL is closely associated with disease recurrence. Thus far, treatment approaches have been limited, particularly in patients who are unable to tolerate chemotherapy. In this study, we report an effective treatment for such patients. Materials and methods: A 52-year-old man diagnosed with Ph-negative B-precursor ALL went into remission after inductive treatment. Unfortunately, when he subsequently relapsed, severe complications drove him to refuse intensive chemotherapy. Instead, he received a cycle of dendritic cells-cytokine-induced killer cells (DC-CIK) before chemotherapy. Result: The patient tolerated rituximab in combination with a vincristine, daunorubicin, l-asparaginase, and prednisone regimen without complications, and was in remission after DC-CIK infusion. After consolidation chemotherapy, including rituximab followed by eight cycles of DC-CIK, the patient has been free of leukemia for 2 years since the relapse. Conclusion: This case of relapsed ALL was successfully treated with DC-CIK combined with a rituximab regime. [ABSTRACT FROM AUTHOR]