in this species ( Langoni et al., 2009; Milanelo et al., 2009 ), but spontaneous neoplasms are rarely described ( Reppas et al., 2001; Skorinsky et al., 2008 ), with only one reported case of epitheliotropic lymphoma in the skin ( Skorinsky et al
A follikuláris lymphoma B-sejt eredetű, indolens, ritkán gyógyítható, de döntő többségben jól kezelhető betegség, melyre remissziókkal és relapszusokkal tarkított lefolyás jellemző, bár a klinikai spektrum heterogén [ 1 ]. A betegek kezelési
The aim of this study was to evaluate the epidemiology, clinical and laboratory characteristics of canine lymphomas as well as some aspects of treatment outcomes. The study was conducted on Boxer dogs with lymphoma diagnosed by cytology and immunocytochemistry (CD3 and CD79 alpha). During the study period, lymphoma was diagnosed in 63 Boxers; 86.8% were T-cell (based on the Kiel classification: small clear cell lymphoma, pleomorphic small cell lymphoma, pleomorphic mixed T-cell lymphoma, pleomorphic large T-cell lymphoma, lymphoblastic lymphoma/acute lymphoblastic leukaemia) and 13.2% were B-cell lymphomas (according to the Kiel classification: B-cell chronic lymphocytic leukaemia, centroblastic/centroblastic polymorphic lymphoma). Overall survival (OS) was significantly longer in dogs with low-grade than with high-grade lymphoma (median OS of 6.8 and 4.7 months, respectively; P = 0.024). OS was not influenced by WHO clinical stage, WHO clinical substage, presence of splenomegaly, early administration of glucocorticoids or the time from the first presentation to the beginning of chemotherapy. There are no significant differences in clinical and laboratory parameters between low-grade and high-grade lymphomas. Boxer dogs are predisposed to T-cell lymphoma, with a predominance of high-grade tumour, especially pleomorphic, mixed small and large T-cell subtype. It is possible that Boxer dogs may respond less favourably to chemotherapy than patients of other breeds.
Lymphomas are solid tumors consisting of lymphoid cells; they form a heterogeneous group of less or more malignant disorders. A portion of lymphomas develop due to latent herpesvirus infections established in B and/or T-lymphocytes. The basis for latency is a lifelong presence of the circularized covalently linked viral genome within nuclei of carrier lymphocytes. In certain cases, however, the essential event leading to tumor formation is the integration of a portion(s) of viral DNA into the host cell DNA. This leads to rearrangements within the host cell genome on one hand, and, on other hand, to unregulated expression of oncoproteins encoded by the integrated fragment. Our review deals with mechanisms of lymphoma formation regarding to the role of non-structural herpesvirus oncoproteins interfering with the regulation of cell division and/or exerting anti-apoptotic effects. In addition, the authors wish to highlight the common procedures, which allowed isolation and/or identification of lymphoma-associated viruses in cell cultures derived from tumors and/or proliferating lymphatic tissues.
Heteroduplex polymerase chain reaction for antigen receptor rearrangements (hPARR) was developed to monitor minimal residual disease (MRD) in canine B- and T-cell lymphomas treated with the modified L-COP or L-CHOP protocol. Thirty-five dogs were recruited in this study and their neoplastic lineages were determined by immunophenotyping with Pax5 and CD3. Peripheral blood leukocytes were collected prior to and during chemotherapy in weeks 4, 9 and 13 to detect MRD by hPARR. Twenty-eight dogs (80%) had B-cell lymphoma while seven dogs (20%) had T-cell lymphoma. A monoclonal band was detected in 11 cases that showed complete or partial remission before tumour relapse and no response to the current treatment without statistical difference in clinical outcomes; however, the treatment response had an association with the MRD result (P < 0.05). Modified L-CHOP prolonged median progression-free survival as compared to modified L-COP (215 days vs. 93 days; P < 0.05). Substage b had shorter progression-free survival than substage a (90 days vs. 215 days; P < 0.05). Clinical stage III affected median overall survival time when compared to clinical stages IV and V (432, 173 and 118 days, respectively; P < 0.05). hPARR could be used for screening refractory lymphoma together with lymph node measurement in routine clinical cases.