Search

De novo immune responses to myeloid and other blood-borne tumors are notably limited and ineffective, making our ability to promote immune responses with vaccines a major challenge. While focus has been largely on cytotoxic cell-mediated tumor eradication, B-cells and the antibodies they produce also have roles in anti-tumor responses. Indeed, therapeutic antibody-mediated tumor cell killing is routinely employed in patients with hematolymphoid cancers, but whether endogenous antibody responses can be incited to blood-born tumors remains poorly studied. A major limitation of immunoglobulin therapies is that cell surface expression of tumor-associated antigen (TAA) targets is dynamic and varied, making promotion of polyclonal, endogenous B cell responses appealing. Since many TAAs are self-antigens, developing tumor vaccines that enable production of antibodies to non-polymorphic antigen targets remains a challenge. As B cell responses to RNA vaccines are known to occur, we employed the Viral Replicon Particles (VRP) which was constructed to encode mouse FLT3. The VRP-FLT3 vaccine provoked a rapid IgG B-cell response to this self-antigen in leukemia and lymphoma mouse models. In addition, IgGs to other TAAs were also produced. Our data suggest that vaccination with RNA viral particle vectors incites a loss of B-cell tolerance that enables production of anti-tumor antibodies. This proof of principle work provides impetus to employ such strategies that lead to a break in B-cell tolerance and enable production of broadly reactive anti-TAA antibodies as potential future therapeutic agents for patients with hematolymphoid cancers. [ABSTRACT FROM AUTHOR]

De novo immune responses to myeloid and other blood-borne tumors are notably limited and ineffective, making our ability to promote immune responses with vaccines a major challenge. While focus has been largely on cytotoxic cell-mediated tumor eradication, B-cells and the antibodies they produce also have roles in anti-tumor responses. Indeed, therapeutic antibody-mediated tumor cell killing is routinely employed in patients with hematolymphoid cancers, but whether endogenous antibody responses can be incited to blood-born tumors remains poorly studied. A major limitation of immunoglobulin therapies is that cell surface expression of tumor-associated antigen (TAA) targets is dynamic and varied, making promotion of polyclonal, endogenous B cell responses appealing. Since many TAAs are self-antigens, developing tumor vaccines that enable production of antibodies to non-polymorphic antigen targets remains a challenge. As B cell responses to RNA vaccines are known to occur, we employed the Viral Replicon Particles (VRP) which was constructed to encode mouse FLT3. The VRP-FLT3 vaccine provoked a rapid IgG B-cell response to this self-antigen in leukemia and lymphoma mouse models. In addition, IgGs to other TAAs were also produced. Our data suggest that vaccination with RNA viral particle vectors incites a loss of B-cell tolerance that enables production of anti-tumor antibodies. This proof of principle work provides impetus to employ such strategies that lead to a break in B-cell tolerance and enable production of broadly reactive anti-TAA antibodies as potential future therapeutic agents for patients with hematolymphoid cancers.

Non-Hodgkin lymphomas (NHLs) in the head and neck region are malignant lymphoid neoplasms that usually originate from B-lymphocytic cell lines. Primary extranodal manifestations of this hematolymphoid tumor in the oral cavity are rare and involve the maxillary jaw including the palatal soft tissues, the mandible, and gingival tissues in patients between 60 and 70 years of age without sex predilection. This case report of an extranodal NHL in the palate of a 75-year-old patient emphasizes the importance of accurate clinical, radiographic, and histologic diagnostic procedures to avoid delayed diagnosis or inappropriate treatment strategies. Chemotherapy, radiotherapy, or a combination of the two with a regular clinical and hemic follow-up is recommended. [ABSTRACT FROM AUTHOR]

Sarcomas comprise a heterogeneous and biologically diverse group of malignant neoplasms having as a common denominator their origin from mesenchymal cells. Head and neck sarcomas account for 4 to less than 20% of total body sarcomas depending on the criteria, such as age of patients (pediatric vs adult population), type of sarcomas (soft-tissue vs bony sarcomas) and site of location. Although head and neck sarcomas occur infrequently in adults, in the pediatric population one in three sarcomas will occur in the head and neck region. Most head and neck sarcomas are of the soft-tissue type, with only 20% being of bony or cartilaginous origin. Sarcomas display a diverse array of histologies and a wide spectrum of clinical behavior, ranging from relatively slow growing lesions to aggressive locally and regionally destructive tumors with the potential for systemic metastases Osteosarcomas, rhabdomyosarcomas, pleomorphic sarcomas (malignant fibrous histiocytomas), fibrosarcomas and angiosarcomas are among the most common histologic types of sarcoma found in the head and neck. Surgery has been the primary therapeutic approach for the management of head and neck sarcomas. Survival rates for head and neck sarcomas suggest worse outcomes than for their extremity counterparts. Lymph node metastasis only occurs in 3-10% of sarcomas of the head and neck. An improvement in local disease control has recently been suggested with the combined use of surgery and radiotherapy. Conflicting results have been regimen, especially for high-grade sarcomas in long-term survival or local disease control. Encouraging results have recently been reported with the use of molecular targeted therapies with tyrosine kinase inhibitors and antiangiogenetic agents. [ABSTRACT FROM AUTHOR]