Rita Ahmad

Human herpesvirus 6 (HHV-6) reactivation is a rare but serious complication of chimeric antigen receptor T-cell (CAR-T) therapy that can overlap with immune effector cell-associated neurotoxicity syndrome (ICANS) or cytokine release syndrome (CRS), making diagnosis and management challenging. We describe a 68-year-old man with relapsed/refractory IgA kappa multiple myeloma who received multiple prior therapies, including CyBorD, mVRD-lite, Dara-CyBorD, VD-ACE, and KPd, before undergoing lymphodepleting chemotherapy and CAR-T infusion. Early after infusion he developed grade 2 CRS and ICANS that improved with tocilizumab and corticosteroids, followed by recurrent encephalopathy with progressive neurologic decline. Initial infectious evaluation was negative, but repeat cerebrospinal fluid (CSF) and plasma polymerase chain reaction testing revealed HHV-6 reactivation. Antiviral therapy with foscarnet, later switched to ganciclovir, was initiated with corticosteroids and intravenous immunoglobulin. Although repeat CSF testing showed transient viral clearance, neurologic function continued to decline, and brain MRI demonstrated findings consistent with ICANS, including scattered white matter signal abnormalities and dural enhancement. Despite aggressive management, the patient developed multiorgan failure and died. This case illustrates the diagnostic complexity of HHV-6 reactivation during CAR-T therapy, where overlapping clinical and radiologic features with ICANS can obscure recognition; profound immunosuppression from prior treatment and CAR-T-induced immune dysregulation likely predisposed to viral reactivation. HHV-6 reactivation is a critical, underrecognized cause of neurotoxicity after CAR-T therapy, and clinicians should maintain a high index of suspicion in patients with delayed or atypical neurotoxicity, since early virologic testing and prompt antiviral therapy may improve outcomes in this vulnerable population.

Background: Outcomes in chronic myeloid leukemia (CML) remain heterogeneous despite effective BCR::ABL1 tyrosine kinase inhibitors (TKIs). Somatic mutations in epigenetic regulators, particularly additional sex combs-like 1 (ASXL1), have been implicated in adverse prognosis, but their clinical impact in CML has not been systematically defined. Methods: A systematic review was conducted using CINAHL, EMBASE, MEDLINE Ultimate, and PubMed from inception through August 2025. A total of 1339 records were identified; the eligible studies included adult and pediatric patients with chronic and advanced-phase (accelerated or blast) CML. After duplicate removal and screening, 11 studies met the inclusion criteria; these included adult patients only and were included in a qualitative synthesis and meta-analysis. ASXL1 mutation status was assessed using validated molecular methods. The outcomes included the molecular response, cytogenetic response, survival, and treatment resistance. Random-effects models were used to calculate the pooled odds ratios (ORs) with 95% confidence intervals (CIs). Statistical heterogeneity was assessed using the I² statistic. Results: Across the included studies, ASXL1 mutations were detected in approximately 15% of patients. At 12 months, patients with ASXL1 mutations had significantly lower odds of achieving a major molecular response (MMR) compared with ASXL1-wildtype patients (OR 0.29; 95% CI 0.16–0.51; p < 0.0001; I² = 30%). No statistically significant difference was observed in the complete cytogenetic response (CCyR) (OR 0.30; 95% CI 0.02–5.31; p = 0.41; I² = 68%). Compared with patients harboring other non-ASXL1 somatic mutations, an ASXL1 mutation was not associated with a significant difference in MMR (OR 0.49; 95% CI 0.23–1.05; p = 0.067; I² = 0%). Conclusions: ASXL1 mutations may be associated with an inferior molecular response to TKI therapy in CML, supporting their role as an adverse prognostic biomarker. These findings highlight the potential value of incorporating myeloid mutation profiling into future CML risk-stratification strategies.

Sphenoid sinusitis is a rare form of sinusitis characterized by inflammation of the sphenoid sinuses, located deep within the skull. Despite its rarity, sp

Background: Outcomes in chronic myeloid leukemia (CML) remain heterogeneous despite effective BCR::ABL1 tyrosine kinase inhibitors (TKIs). Somatic mutations in epigenetic regulators, particularly additional sex combs like 1 (ASXL1), have been implicated in adverse prognosis, but their clinical impact in CML has not been systematically defined. Methods: A systematic review was conducted using CINAHL, EMBASE, MEDLINE Ultimate, and PubMed from inception through August 2025. A total of 1,339 records were identified; after duplicate removal and screening, 11 studies met inclusion criteria and were included in qualitative synthesis and meta-analysis. Eligible studies included adult and pediatric patients with chronic and advanced phase (accelerated or blast) CML with ASXL1 mutation status assessed using validated molecular methods. Outcomes included molecular response, cytogenetic response, survival, and treatment resistance. Random-effects models were used to calculate pooled odds ratios (ORs) with 95% confidence intervals (CI). Statistical heterogeneity was assessed using the I² statistic. Results: Across included studies, ASXL1 mutations were detected in approximately 16% of patients. At 12 months, ASXL1-mutated patients had significantly lower odds of achieving major molecular response (MMR) compared with ASXL1–wildtype patients (OR 0.29; 95% CI 0.16–0.51; p< 0.0001; I²=30%). No statistically significant difference was observed in complete cytogenetic response (CCyR) (OR 0.30; 95% CI 0.02–5.31; p=0.41; I²=68%). Compared with patients harbouring other non-ASXL1 somatic mutations, ASXL1 mutation was not associated with a significant difference in MMR (OR 0.49; 95% CI 0.23–1.05; p=0.067; I²=0%). Conclusions: ASXL1 mutations are associated with inferior molecular response to TKI therapy in CML, supporting their role as an adverse prognostic biomarker. These findings highlight the potential value of incorporating myeloid mutation profiling into future CML risk-stratification strategies.

INPLASY202630075 Prevalence and Prognostic Impact of ASXL1 Somatic Mutation in Patients with Chronic Myeloid Leukemia: A Systemic Review and Meta-Analysis Keywords: chronic myeloid leukemia, CML, m…

Introduction Breast cancer is a major health concern and is the most common cancer in women according to the American Cancer Society with 1 in 3 women diagnosed each year. Breast cancer screening with annual or biennial mammography for women 40 years and older has significantly decreased mortality. Our aim in this study is to assess factors predicting and affecting adherence to breast cancer screening in the United States, consequently recognizing where and how an intervension is required. Methods A retrospective analysis was conducted of adult women using the 2021 National Health Interview Survey (NHIS). Data that was analyzed and recorded included age, race, anxiety, BMI, smoking status, region, education level, residence location, health insurance, self-rated health status, pay for mammogram, and mammogram within 2 years. Results Data from 6334 women between 50 and 74 of age was analyzed. 4583 women (72.8%) had a mammogram within the past two year while 1751 (27.2%) had notscreening was not affected by age as 27.8% of women between 50–64 and 26.2% of women between 65–74 did not have a mammogram (P value = 0.223), or by region (P value = 0.176). However, adherenece to screening varied significantly by race (P value < 0.0001), BMI (P value = 0.02), level of education (P value < 0.0001), insurance status (P value < 0.0001), smoking status (P value = 0.0001), and place of residence (P value = 0.002). Conclusion Breast cancer screening has substantial role in reducing morbidity and mortality from the disease. Further interventions are still needed to assess factors preventing women from undergoing screening and assist in addressing such factors.

Extramedullary hematopoiesis (EMH) is a well‐known complication of beta thalassemia major and frequently occurs in typical sites such as liver or spleen. However, when presenting in unusual sites as sacrum, other diagnosis should be excluded by histopathology prior to deciding on treatment plan.

Gastrointestinal manifestations of leukemias have been well recognized. Typically, acute leukemias cause typhlitis or appendicitis more commonly than chronic leukemias. Our case points to appendicitis as possible manifestation of chronic myelogenous leukemia.

To optimize care for patients with hemoglobinopathies, frequent screening for COVID‐19 is prudent as viral kinetics in asplenic patients are unknown and differentiating prolonged viral shedding versus reinfection remains a challenge.