Intranodal palisaded myofibroblastoma: a case report

Intranodal palisaded myofibroblastoma is a rare benign soft tissue tumor, almost always arising from inguinal lymph nodes. It usually presents as a painless, slow-growing inguinal mass. We report herein a case of an intranodal palisaded myofibroblastoma occurring in a 36-year-old man. The salient clinicopathologic features of this unusual tumor are presented and the literature is briefly reviewed

A rare coexistence of adrenal cavernous hemangioma with extramedullar hemopoietic tissue: a case report and brief review of the literature

<p>Abstract</p> <p>Background</p> <p>Cavernous hemangiomas of the adrenal gland are rare, benign, non-functioning neoplastic tumors. To our knowledge, 55 cases have been reported in the literature to date.</p> <p>Case presentation</p> <p>We report the first case of a large, non-functioning adrenal cavernous hemangioma that was incidentally found during the preoperative staging workup of a 75 year old woman with left breast adenocarcinoma. Imaging with US, CT scan and MRI showed a heterogeneous 8 cm mass with non-specific radiological features that was located on the left adrenal gland. The mass was surgically excised and pathology revealed an adrenal hemangioma with areas of extramedullar hemopoiesis.</p> <p>Conclusion</p> <p>Although adrenal hemangiomas are rare and their preoperative diagnosis is difficult, they should always be included in the differential diagnosis of adrenal neoplasms.</p

Synchronous gastric adenocarcinoma and gastrointestinal stromal tumor (GIST) of the stomach: A case report

Gastrointestinal stromal tumors (GISTs) are rare mesenchymal neoplasms of the gastrointestinal tract (1%), and stomach is the most common location involved. However, the co-existence of gastric adenocarcinoma and GIST is very rare. A case of an 80-year-old male with a simultaneous presentation of a gastric adenocarcinoma and GIST is presented. Various hypotheses have been proposed in order to explain this rare simultaneous development, but even though it's cause has not been proven yet

Abscess formation mimicking disease progression, in a patient with metastatic renal cell carcinoma during sunitinib treatment

<p>Abstract</p> <p>Background</p> <p>Renal cell carcinoma (RCC) represents approximately 3% of all adult cancers and is more common in males. Systemic treatment for RCC has improved following the introduction of tyrosine kinase inhibitors, such as sunitinib. The molecular targets of sunitinib are receptor tyrosine kinases (RTKs). Moreover, sunitinib has an additional anti-angiogenic effect through its inhibition of the vascular endothelial growth factor receptor activation.</p> <p>Case presentation</p> <p>We present a case of intra-abdominal abscess formation mimicking disease progression, in a patient with metastatic renal cell carcinoma during sunitinib treatment.</p> <p>Conclusion</p> <p>In the advancing era of molecular therapy of solid tumours, sunitinib has demonstrated significant efficacy in the post-cytokine setting treatment of metastatic renal cancer. Concurrently, however, increasing evidence has emerged to indicate that this class of drugs exert profound immunomodulatory effects on T cells and play major roles in immune tumor surveillance.</p

The combined effect of erythropoietin and granulocyte macrophage colony stimulating factor on liver regeneration after major hepatectomy in rats

<p>Abstract</p> <p>Background</p> <p>The liver presents a remarkable capacity for regeneration after hepatectomy but the exact mechanisms and mediators involved are not yet fully clarified. Erythropoietin (EPO) and Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) have been shown to promote liver regeneration after major hepatectomy.</p> <p>Aim of this experimental study is to compare the impact of exogenous administration of EPO, GM-CSF, as well as their combination on the promotion of liver regeneration after major hepatectomy.</p> <p>Methods</p> <p>Wistar rats were submitted to 70% major hepatectomy. The animals were assigned to 4 experimental groups: a control group (n = 21) that received normal saline, an EPO group (n = 21), that received EPO 500 IU/kg, a GM-CSF group (n = 21) that received 20 mcg/kg of GM-CSF and a EPO+GMCSF group (n = 21) which received a combination of the above. Seven animals of each group were killed on the 1st, 3rd and 7th postoperative day and their remnant liver was removed to evaluate liver regeneration by immunochemistry for PCNA and Ki 67.</p> <p>Results</p> <p>Our data suggest that EPO and GM-CSF increases liver regeneration following major hepatectomy when administered perioperatively. EPO has a more significant effect than GM-CSF (p < 0.01). When administering both, the effect of EPO seems to fade as EPO and GM-CSF treated rats have decreased regeneration compared to EPO administration alone (p < 0.01).</p> <p>Conclusion</p> <p>EPO, GM-CSF and their combination enhance liver regeneration after hepatectomy in rats when administered perioperatively. However their combination has a weaker effect on liver regeneration compared to EPO alone. Further investigation is needed to assess the exact mechanisms that mediate this finding.</p

Anal adenocarcinoma complicating chronic Crohn’s disease

Introduction: Colorectal adenocarcinoma and Crohn’s disease are known to be associated entities. However, a carcinoma arising within a chronic perianal fistulous tract in a patient with Crohn’s disease is a rare complication. Presentation of case: We present a case of a 40-year-old male patient with a long-standing perianal Crohn’s disease who developed an anal mucinous adenocarcinoma within the fistulous tracts. Discussion: Although, Crohn’s disease and colorectal carcinoma association is well established, few cases have been reported where the cancer has originated within a perianal fistula. Constant mucosal regeneration occurring within a fistula seems to be the predominant pathogenetic mechanism, while immunosuppressants and anti-TNF agents may also contribute to the malignant transformation. Unfortunately, the lack of suspicion and the inadequate physical examination or colonoscopy due to exacerbation of the perianal symptoms could lead to delayed diagnosis; and thus, a poor prognosis. Conclusion: Albeit a rare complication, clinicians should maintain a high degree of vigilance about the possible development of adenocarcinoma in patients with long-standing perianal Crohn’s disease. Thus, these patients should be kept under regular surveillance with examination under anaesthesia and biopsies or curettage of the tracts

Loss of Raf-1 kinase inhibitor protein (RKIP) is strongly associated with high-grade tumor budding and correlates with an aggressive phenotype in pancreatic ductal adenocarcinoma (PDAC)

BACKGROUND Raf-1 kinase inhibitor protein (RKIP) has emerged as a significant metastatic suppressor in a variety of human cancers and is known to inhibit Ras/Raf/MEK/ERK signaling. By suppressing the activation of the NFkB/SNAIL circuit, RKIP can regulate the induction of epithelial-mesenchymal transition (EMT). The aim of this study was to evaluate RKIP expression and to determine its association with clinicopathological features, including EMT in form of tumor budding in pancreatic ductal adenocarcinoma (PDAC). METHODS Staining for RKIP was performed on a multipunch Tissue Microarray (TMA) of 114 well-characterized PDACs with clinico-pathological, follow-up and adjuvant therapy information. RKIP-expression was assessed separately in the main tumor body and in the tumor buds. Another 3 TMAs containing normal pancreatic tissue, precursor lesions (Pancreatic Intraepithelial Neoplasia, PanINs) and matched lymph node metastases were stained in parallel. Cut-off values were calculated by receiver operating characteristic (ROC) curve analysis. RESULTS We found a significant progressive loss of RKIP expression between normal pancreatic ductal epithelia (average: 74%), precursor lesions (PanINs; average: 37%), PDAC (average 20%) and lymph node metastases (average 8%, p<0.0001). RKIP expression was significantly lower in tumor buds (average: 6%) compared to the main tumor body (average 20%; p<0.005). RKIP loss in the tumor body was marginally associated with advanced T-stage (p=0.0599) as well as high-grade peritumoral (p=0.0048) and intratumoral budding (p=0.0373). RKIP loss in the buds showed a clear association with advanced T stage (p=0.0089). CONCLUSIONS The progressive loss of RKIP seems to play a major role in the neoplastic transformation of pancreas, correlates with aggressive features in PDAC and is associated with the presence of EMT in form of tumor budding