决定异体 CAR T 细胞排斥与扩增的细胞和分子机制
Cellular and molecular mechanisms determining allogeneic CAR T cell rejection and expansion.
我们评估了11例接受单一批次cemacabtagene ansegedleucel(cema-cel)治疗的大B细胞淋巴瘤患者,cemacabtagene ansegedleucel是一种异体抗CD19 CAR T产品。
英文原题:Navigating Diagnostic and Therapeutic Challenges in Primary Cutaneous Gamma/Delta T-Cell Lymphoma: A Case Study of Fatal Outcomes Within Two Months.
原发性皮肤γ/δ T细胞淋巴瘤(PCGD-TCL)是一种罕见但高度侵袭性的原发性皮肤淋巴瘤亚型。
原发性皮肤γ/δ T细胞淋巴瘤(PCGD-TCL)是一种罕见但高度侵袭性的原发性皮肤淋巴瘤亚型。PCGD-TCL以诊断困难、预后差为特征,具有独特的临床和组织病理学特征,可与其他原发性皮肤淋巴瘤亚型相区分。在此,我们报告一例75岁男性患者,最初表现为背部和双下肢多发红斑性硬化性斑块。初次活检提示原发性皮肤T细胞淋巴瘤(PCTCL),呈CD30阴性表型。然而,在2个月的时间内,疾病迅速进展,表现为胸部和上肢广泛的皮肤受累。再次行皮肤活检,显示真皮非典型淋巴细胞,无嗜表皮现象。免疫组化分析显示CD3、CD5和CD4阳性,以及T细胞受体δ(TCR delta)表达,同时CD8和CD30表达缺失。这些发现与PCGD-TCL的诊断一致。尽管采取了包括全身治疗在内的治疗干预,患者病情仍迅速恶化,最终在确诊PCGD-TCL后一个月内死亡。本病例突出了PCGD-TCL相关的诊断复杂性,强调了仔细的组织病理学检查和免疫表型特征分析的重要性。鉴于其侵袭性本质和快速播散倾向,早期识别PCGD-TCL对于启动适当的治疗干预至关重要。然而,PCGD-TCL的有效治疗选择仍然有限,该病通常预后不良。需要进一步研究以阐明驱动PCGD-TCL发病机制的潜在分子机制,识别新的治疗靶点,并改善患者预后。此外,提高临床医生和病理学家对PCGD-TCL临床表现和诊断标准的认识,对于促进这一具有挑战性的恶性肿瘤的及时诊断和管理至关重要。
Primary cutaneous gamma/delta T-cell lymphoma (PCGD-TCL) is a rare yet highly aggressive subtype of primary cutaneous lymphoma. Characterized by its challenging diagnosis and poor prognosis, PCGD-TCL presents unique clinical and histopathological features that distinguish it from other primary cutaneous lymphoma subtypes. Here, we report the case of a 75-year-old man who initially presented with multiple erythematous indurated plaques over his back and bilateral lower extremities. The initial biopsy suggested primary cutaneous T-cell lymphoma (PCTCL) with a CD30-negative phenotype. However, within a 2-month interval, the disease progressed rapidly, manifesting as extensive skin involvement across the chest and upper extremities. A repeat skin biopsy was performed, revealing dermal atypical lymphocytes without epidermotropism. Immunohistochemical analysis demonstrated positivity for CD3, CD5, and CD4, as well as T-cell receptor delta (TCR delta) expression, along with the loss of CD8 and CD30 expression. These findings were consistent with a diagnosis of PCGD-TCL. Despite therapeutic interventions, including systemic treatments, the patient's condition deteriorated rapidly, ultimately leading to his demise within a month of receiving the PCGD-TCL diagnosis. This case highlights the diagnostic complexities associated with PCGD-TCL, emphasizing the importance of careful histopathological examination and immunophenotypic characterization. Given its aggressive nature and propensity for rapid dissemination, early recognition of PCGD-TCL is paramount for initiating appropriate therapeutic interventions. However, effective treatment options for PCGD-TCL remain limited, and the disease typically carries an unfavorable prognosis. Further research is needed to elucidate the underlying molecular mechanisms driving the pathogenesis of PCGD-TCL, to identify novel therapeutic targets, and to improve patient outcomes. In addition, increased awareness among clinicians and pathologists regarding the clinical presentation and diagnostic criteria of PCGD-TCL is crucial for facilitating timely diagnosis and management of this challenging malignancy.
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