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Introduction: Myeloid sarcoma (MS) is also known as chloroma, extramedullary acute myeloid leukemia (AML), or granulocytic sarcoma. MS is a rare extramedullary infiltration of myeloid cells, most commonly collecting in the skin and causing a small number of localized lesions. It is strongly associated with AML; however, MS more commonly occurs after diagnosis of AML is previously established or after previous treatment of AML. Case Presentation: This case describes a patient with an atypical presentation of MS with no known history of AML and up to 18 lesions identified on CT scan that were previously being monitored for months by her primary care physician. She presented with sepsis attributed to choledocholithiasis versus bacteremia from scattered abscesses versus osteomyelitis of her left knee; nonetheless, lactic acid failed to improve after common bile duct stent with biliary sphincterotomy/dilation or with incision and drainage and empiric antibiotics. Core needle biopsy of her left abdominal sidewall was eventually positive for MS, but she unfortunately developed multiorgan failure with symptomatic hypercalcemia refractory to treatment and ultimately decided to go to comfort care rather than pursue further workup and treatment. Although bone marrow biopsy was ultimately not performed to rule out synchronous AML, this is likely a case of isolated MS due to her scattered skin lesions being present for months prior to hospitalization and acute illness. Conclusion: This case highlights the importance of maintaining MS in the differential diagnosis and the importance of early diagnostic core needle biopsy for patients with persistent skin lesions of unknown origin.
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Introduction: Earlier, patients with advanced ovarian cancer were treated with a combination of cytoreductive surgery and platinum-based chemotherapy, which had significant outcomes in the past until an increase in relapse and resistance to treatment, which led to the use or development of bevacizumab (a vascular endothelial growth factor inhibitor) in the treatment of primary or relapsed ovarian cancer. Method and Methodology: This study includes five-phase three randomized controlled clinical trials designed to study the impact of bevacizumab in combination with platinum-based chemotherapy compared with platinum-based chemotherapy alone. Results: This study demonstrated significant improvement in the progression-free span but no improvement in overall survival in the treatment group when compared with the control group. Also, adverse effects reported with combination therapy were tolerable and easily manageable by decreasing the infusion rate or by decreasing the frequency of infusion.
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Current strategies to suppress graft-versus-host disease (GVHD) also compromise graft-versus-tumor (GVT) responses. Furthermore, most experimental strategies to separate GVHD and GVT responses merely spare GVT function without actually enhancing it. We have previously shown that endogenously expressed TNF-related apoptosis-inducing ligand (TRAIL) is required for optimal GVT activity against certain malignancies in recipients of allogeneic hematopoietic stem cell transplantation (allo-HSCT). In order to model a donor-derived cellular therapy, we genetically engineered T cells to overexpress TRAIL and adoptively transferred donor-type unsorted TRAIL+ T cells into mouse models of allo-HSCT. We found that murine TRAIL+ T cells induced apoptosis of alloreactive T cells, thereby reducing GVHD in a DR5-dependent manner. Furthermore, murine TRAIL+ T cells mediated enhanced in vitro and in vivo antilymphoma GVT response. Moreover, human TRAIL+ T cells mediated enhanced in vitro cytotoxicity against both human leukemia cell lines and against freshly isolated chronic lymphocytic leukemia (CLL) cells. Finally, as a model of off-the-shelf, donor-unrestricted antitumor cellular therapy, in vitro-generated TRAIL+ precursor T cells from third-party donors also mediated enhanced GVT response in the absence of GVHD. These data indicate that TRAIL-overexpressing donor T cells could potentially enhance the curative potential of allo-HSCT by increasing GVT response and suppressing GVHD.