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Abstract Background Solid splenic lesions may be the expression of a lymphoproliferative disease spreading to the spleen or appear as the only manifestation of possible neoplastic diseases, mainly hematologic malignancies. Therefore, biopsy is of uttermost importance in clarifying their nature. Patients and Methods Forty-four patients with splenic nodular lesions suspected of hematologic disease underwent spleen contrast-enhanced ultrasonography and contextual biopsy using an 18-gauge needle. All procedures were performed on an outpatient basis. Patients with inconclusive findings or with a diagnosis of unaffected splenic tissue were followed up to discriminate between true and false-negative results. Results All procedures ended up with sampling of splenic tissue without severe complications requiring hospitalization or supportive countermeasures. None was interrupted because of adverse event (AE)s. Out of 44 samples, a final diagnosis was accomplished in 39 cases, with a diagnostic yield of 88.6%. A diagnosis of lymphoma was made in 22 cases. Other diagnoses included: splenic metastases and splenic sarcoma (3 cases each), non-neoplastic lesions (3 cases), and unaffected splenic tissue (8 cases). Among the latter 8 patients, 1 received a diagnosis of Hodgkin lymphoma by marrow biopsy. All the other 7 patients never received a diagnosis of neoplasm and were true negative. Among the 5 patients with insufficient sampling, 3 were never diagnosed with a neoplasm during follow-up; 1 had myelofibrosis and 1 angiosarcoma. The sensitivity of the procedure was 96.6%; specificity was 100% and accuracy was 86.4%. Conclusions Ultrasound-guided core needle biopsy of splenic nodular lesions can be safely performed on an outpatient basis with no severe AEs. Graphical Abstract Graphical Abstract

The objectives of this study were to evaluate the risk and predictive factors of splenic malignancy and hemangiosarcoma in dogs undergoing splenectomy at a surgical specialty clinic. Medical records, hematologic results, surgical reports, and histopathologic results from 182 dogs that underwent splenectomy for the treatment of splenic masses or nodules were reviewed retrospectively. The majority of dogs (57.7%) had benign splenic diagnoses with no malignancy. Hemangiosarcoma was diagnosed in 32.4% of the dogs. A final multivariable model indicated that thrombocytopenia, anemia, and a smaller diameter of the largest splenic nodule were risk factors for hemangiosarcoma (P<0.001), and hemoperitoneum (P = 0.01) was an additional risk factor when nodule diameter was not evaluated. There were 91 dogs that had hemoperitoneum, and 60.4% of those dogs had malignant splenic lesions. Of the 33 dogs that underwent a splenectomy for incidentally identified splenic lesions, 93.9% had benign splenic lesions. Breed size was not a significant predictor of splenic malignancy risk; however, all 6 of the German shepherds included in the study had a hemangiosarcoma diagnosis. Overall prevalence of splenic malignancy including HSA may be overestimated in some canine populations.

The gut microbiota has recently been proposed as a novel component in the regulation of host homeostasis and immunity. We have assessed for the first time the role of the gut microbiota in a mouse model of leukemia (transplantation of BaF3 cells containing ectopic expression of Bcr-Abl), characterized at the final stage by a loss of fat mass, muscle atrophy, anorexia and inflammation. The gut microbial 16S rDNA analysis, using PCR-Denaturating Gradient Gel Electrophoresis and quantitative PCR, reveals a dysbiosis and a selective modulation of Lactobacillus spp. (decrease of L. reuteri and L. johnsonii/gasseri in favor of L. murinus/animalis) in the BaF3 mice compared to the controls. The restoration of Lactobacillus species by oral supplementation with L. reuteri 100-23 and L. gasseri 311476 reduced the expression of atrophy markers (Atrogin-1, MuRF1, LC3, Cathepsin L) in the gastrocnemius and in the tibialis, a phenomenon correlated with a decrease of inflammatory cytokines (interleukin-6, monocyte chemoattractant protein-1, interleukin-4, granulocyte colony-stimulating factor, quantified by multiplex immuno-assay). These positive effects are strain- and/or species-specific since L. acidophilus NCFM supplementation does not impact on muscle atrophy markers and systemic inflammation. Altogether, these results suggest that the gut microbiota could constitute a novel therapeutic target in the management of leukemia-associated inflammation and related disorders in the muscle.

Modulation of the cellular response by the administration of probiotic bacteria may be an effective strategy for preventing or inhibiting tumour growth. We orally pre-inoculated mice with probiotics Lactobacillus acidophilus NCFM (La) for 14 d. Subcutaneous dorsal-flank tumours and segmental orthotopic colon cancers were implanted into mice using CT-26 murine colon adenocarcinoma cells. On day 28 after tumour initiation, the lamina propria of the colon, mesenteric lymph nodes (MLN) and spleen were harvested and purified for flow cytometry and mRNA analyses. We demonstrated that La pre-inoculation reduced tumour volume growth by 50·3 %, compared with untreated mice at 28 d after tumour implants (2465·5 (sem 1290·4) v. 4950·9 (sem 1689·3) mm3, P < 0·001). Inoculation with La reduced the severity of colonic carcinogenesis caused by CT-26 cells, such as level of colonic involvement and structural abnormality of epithelial/crypt damage. Moreover, La enhanced apoptosis of CT-26 cells both in dorsal-flank tumour and segmental orthotopic colon cancer, and the mean counts of apoptotic body were higher in mice pre-inoculated with La (P < 0·05) compared with untreated mice. La pre-inoculation down-regulated the CXCR4 mRNA expressions in the colon, MLN and extra-intestinal tissue, compared with untreated mice (P < 0·05). In addition, La pre-inoculation reduced the mean fluorescence index of MHC class I (H-2Dd, -Kd and -Ld) in flow cytometry analysis. Taken together, these findings suggest that probiotics La may play a role in attenuating tumour growth during CT-26 cell carcinogenesis. The down-regulated expression of CXCR4 mRNA and MHC class I, as well as increasing apoptosis in tumour tissue, indicated that La may be associated with modulating the cellular response triggered by colon carcinogenesis.

Background Extraskeletal osteosarcoma is an extremely rare malignancy that accounts for 1% of soft tissue sarcoma and 4.3% of all osteosarcoma. Extraskeletal osteosarcoma can develop in a patient between the ages of 48 and 60 years. The incidence of extraskeletal osteosarcoma is slightly higher in male patients than in females. Case presentation A 50-year-old Caucasian male patient presented with a 6-month history of intermittent lower-left back pain that limits his activity. Prior ultrasonography and abdominal computed tomography scan showed a diagnosis of kidney stone and tumor in the lower-left abdomen. The computed tomography urography with contrast revealed a mass suspected as a left retroperitoneal malignant tumor. Hence, the tumor was resected through laparotomy and the patient continued with histopathological and immunohistochemistry examination with the result of extraskeletal osteosarcoma. Conclusion Extraskeletal osteosarcoma presents diagnostic challenges requiring multimodal examination, including histological and immunohistochemistry analyses. This case underscores the aggressive nature and poor prognosis despite undergoing the current suggested treatment.

The spleen is the target of numerous non-neoplastic and uncommon neoplastic lesions. Our study’s objective was to evaluate the main indications and clinicopathologic features of a large number of splenectomy specimens from southern Iran, with a focus on splenic neoplasms. This five-year retrospective cross-sectional study was carried out on all splenectomy specimens from two referring centers. The hospital-recorded files and hematoxylin and eosin histopathology slides were reviewed in order to collect demographic information, the primary causes of splenectomy, and histopathological findings. Immunohistochemistry was performed in cases of splenic neoplasms. Of the 803 splenectomy cases, splenic rupture from accidents accounted for 36.3% and hematologic diseases for 31.1% of the procedures. Splenectomies were performed in 24% of cases as a result of staging and surgery for other cancers of the abdominal organs; in general, 3.4% were involved by direct tumor invasion or metastasis. Hydatid cysts, epithelial cysts, pseudocysts, granulomatous inflammation, and storage diseases, in order, accounted for 6.6% of spleens with the non-neoplastic lesions. The 1.8% of cases that were primary splenic neoplasms included 10 vascular tumor cases (including 4 hamartomas, 3 littoral cell angiomas, 1 hemangioma, 1 lymphangioma, and 1 sclerosing angiomatoid nodular transformation) and 4 lymphoma instances, all of which were DLBCL. As the spleen has numerous physiologic functions, it has the capacity to cause numerous traumatic, hematologic, infectious, benign, or malignant primary or metastatic neoplastic lesions. Many different pathologies should therefore be considered when evaluating the pathologic status of splenectomy cases.

Cytology represents a useful diagnostic tool in the preliminary clinical approach to canine splenic lesions, and may prevent unnecessary splenectomy. However, few studies have evaluated diagnostic accuracy of cytology in the diagnosis of canine splenic neoplasms. The aim of this study was to determine overall accuracy, sensitivity, specificity, positive and negative predictive values (i.e. diagnostic accuracy indexes) of cytology for canine splenic neoplasms following Standards for the Reporting of Diagnostic Accuracy Studies (STARD) guidelines. A consecutive series of canine splenic cytological samples was retrospectively retrieved from the database of the Diagnostic Pathology Service of the Department of Veterinary Medicine (DIMEVET-University of Milan). Histopathology was set as the diagnostic reference standard. Cytological cases were enrolled when slides were available for review and when the same lesion was submitted for histopathology. Seventy-eight (78) lesions were included in the study. By histopathology, 56 were neoplastic and 22 were non-neoplastic. Cytology had an overall accuracy of 73.08% (95% C.I. 61.84%-82.50%), sensitivity of 64.29% (95% C.I. 50.36%-76.64%), specificity of 95.45% (95% C.I. 77.16%-99.88%), and positive and negative predictive values of 97.3% (95% C.I. 84.01%-99.60%) and 51.22% (95% C.I. 42.21%-60.15%), respectively. Low sensitivity and negative predictive value were balanced by very high specificity and positive predictive value. When positive for neoplasia, cytology represents a useful diagnostic tool to rule in splenic neoplasia, prompting surgery independently from other diagnostic tests. Conversely, a negative cytological result requires additional investigations to confirm the dog to be disease free.

ObjectivesSplenic lesions might exhibit overlapping imaging features, varying from benign entities like cysts and hemangiomas to malignancies such as lymphoma and angiosarcoma. This meta-analysis aims to delineate imaging characteristics that distinguish malignant from benign splenic lesions.MethodsAdhering to PRISMA guidelines, we searched PubMed, Scopus, and Web of Science for studies on imaging features differentiating malignant from benign splenic lesions. We extracted data on splenic pathology and imaging characteristics and assessed the methodological quality via QUADAS-2. Odds ratio meta-analyses were performed using STATA (Version 17.0, Stata Corp, College Station, TX).ResultsPortal phase hypoenhancement, hypovascular enhancement pattern, diffusion restriction, and late phase hypoenhancement, with odds ratios above 10, highly indicate malignancy. Other features suggestive of malignancy include solid morphology, lymphadenopathy, presence of perisplenic fluid, arterial hypoenhancement, hypoechogenicity on ultrasound, splenomegaly, and presence of multiple lesions. In contrast, cystic morphology, hypervascular-washout and hypervascular-persistent pattern of enhancement, late phase hyperenhancement, anechogenicity on ultrasound, portal phase hyperenhancement, well-defined borders, and calcification are in favour of benign pathology.ConclusionThe study underscores the critical role of contrast-enhanced and diffusion-weighted imaging in distinguishing malignant from benign splenic lesions, emphasizing the role of features like portal phase hypoenhancement and restricted diffusion in diagnosing malignancies. Additionally, the study emphasizes the value of contrast-enhanced ultrasound, which allows for the visualization of key contrast-enhancement patterns without the risk of ionizing radiation exposure.

Splenic marginal zone lymphoma (SMZL) is one of the most common B-cell lymphomas that affect the spleen. We report a case with splenomegaly and lymphocytosis that showed a clonal B-cell population lacking CD5 and CD10 expression. Notably, the atypical lymphoid cells showed prolymphocytoid morphology and expressed cyclin D1. Fluorescence in-situ hybridization was negative for CCND1/IgH rearrangement. The prolymphocytoid morphology and cyclin D1 expression present a diagnostic pitfall. The clinical presentation, morphology, immunophenotype, and molecular genetic findings are most consistent with a diagnosis of SMZL with prolymphocytic transformation and cyclin D1 expression. Here, we present this case along with a review of the literature, and summarize the clinicopathological characteristics of SMZL with prolymphocytic transformation.

The pathogenesis of splenic marginal zone lymphoma (SMZL) remains largely unknown. Recent high-throughput sequencing studies have identified recurrent mutations in key pathways, most notably NOTCH2 mutations in >25% of patients. These studies are based on small, heterogeneous discovery cohorts, and therefore only captured a fraction of the lesions present in the SMZL genome. To identify further novel pathogenic mutations within related biochemical pathways, we applied whole exome sequencing (WES) and copy number (CN) analysis to a biologically and clinically homogeneous cohort of seven SMZL patients with 7q abnormalities and IGHV1-2*04 gene usage. We identified 173 somatic non-silent variants, affecting 160 distinct genes. In additional to providing independent validation of the presence of mutation in several previously reported genes (NOTCH2, TNFAIP3, MAP3K14, MLL2 and SPEN), our study defined eight additional recurrently mutated genes in SMZL; these genes are CREBBP, CBFA2T3, AMOTL1, FAT4, FBXO11, PLA2G4D, TRRAP and USH2A. By integrating our WES and CN data we identified three mutated putative candidate genes targeted by 7q deletions (CUL1, EZH2 and FLNC), with FLNC positioned within the well-characterized 7q minimally deleted region. Taken together, this work expands the reported directory of recurrently mutated cancer genes in this disease, thereby expanding our understanding of SMZL pathogenesis. Ultimately, this work will help to establish a stratified approach to care including the possibility of targeted therapy.