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Introduction: Burkitt lymphoma (BL) is a rare and aggressive subtype of non-Hodgkin's lymphoma. Several studies have identified prognostic factors (PFs) for disease progression and mortality among adults with BL. However, there is no consensus on risk stratification based on PFs.

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Klippel-Feil syndrome (KFS) is a rare congenital disorder characterized by the fusion of cervical vertebrae, with a clinical presentation that can vary widely due to genetic and phenotypic diversity. While KFS can occur as an isolated anomaly, it is often associated with other congenital conditions, such as Sprengel deformity, which may present with or without an omovertebral bone, complicating diagnosis and management. This particular case also involves diffuse large B-cell lymphoma (DLBCL), the most common subtype of non-Hodgkin lymphoma.

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Immunity suffers a function deficit during aging, and the incidence of cancer is increased in the elderly. However, most cancer models employ young mice, which are poorly representative of adult cancer patients. We have previously reported that Triple-Therapy (TT), involving antigen-presenting-cell activation by vinorelbine and generation of TCF1-stem-cell-like T cells (scTs) by cyclophosphamide significantly improved anti-PD-1 efficacy in anti-PD1-resistant models like Triple-Negative Breast Cancer (TNBC) and Non-Hodgkin's Lymphoma (NHL), due to T-cell-mediated tumor killing.

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Background: CAR T-cell therapy (CAR-T) is leading to durable responses in patients with cancer but there is concern that cytokine release syndrome (CRS) and neurotoxicity may impact survivors' cognitive function. We assessed long-term cognitive function in CAR-T recipients and examine factors associated with change in cognition over time.

Methods: We assessed perceived cognition (Functional Assessment of Cancer Therapy - Cognition) and neurocognitive performance (standardized neuropsychological battery) in adult patients prior to receiving CAR-T and at 6 month follow-up.

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Unlabelled: Immune escape is a critical hallmark of cancer progression and underlies resistance to multiple immunotherapies. However, it remains unclear when the genetic events associated with immune escape occur during cancer development. Here, we integrate functional genomics studies of immunomodulatory genes with a tumor evolution reconstruction approach to infer the evolution of immune escape across 38 cancer types from the Pan-Cancer Analysis of Whole Genomes dataset.

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