Introduction: Tumors of salivary glands constitute 3% of neoplasms of the body. Clinical signs and symptoms usually occur in tumors at advance stages. Dynamic-contrast-enhanced and diffusion-weighted MR sequences have been described as useful diagnostic tools in other locations. Our goal is to evaluate the utility of these techniques for parotid tumors.
Material and methods:We retrospectively reviewed the Parotid tumors operated by our department whit Dynamic-contrast-enhanced and diffusion-weighted MR sequences between 2012 and 2015. We correlate the results with the final histopathological diagnosis.Results: From 44 parotid tumors studied, Warthin tumors were the most common (43%). They showed high enhancement and high washout in perfusion series, so as low ADC values. Pleomorphic adenomas (41%) are hyperintense tumors in T2, with moderate constant enhancement in perfusion and high Apparent Diffusion Coefficient values. It is not possible to establish consistent results for malignant tumors given their underrepresentation in this sample.
Conclusion:Advanced MRI techniques contribute to the differential diagnosis of parotid tumors. Perfusion is useful in diagnosis of Warthin tumors and Pleomorphic adenomas. There is greater overlap in other tumors, for which diffusion-weighted MR sequences can help in discriminating malignancies. Both malignancies and Warthins show low Apparent Diffusion Coefficient values.
Ruxolitinib is the front-line non-palliative treatment for myelofibrosis (MF). However, a significant number of patients lose or present suboptimal response, are resistant or have unacceptable toxicity. In an attempt to improve response and avoid the adverse effects of this drug, we evaluated the combination of 17 drugs with ruxolitinib in
ex vivo
models of peripheral blood mononuclear cells from MF patients and cell lines. We found that the combination ruxolitinib and nilotinib had a synergistic effect against MF cells (ΔEC
50
nilotinib, −21.6%). Moreover, the addition of prednisone to combined ruxolitinib/nilotinib improved the synergistic effect in all MF samples studied. We evaluated the molecular mechanisms of combined ruxolitinib/nilotinib/prednisone and observed inhibition of JAK/STAT (STAT5, 69.2+11.8% inhibition) and MAPK (ERK, 29.4+4.5% inhibition) signaling pathways. Furthermore, we found that the triple therapy combination inhibited collagen protein and
COL1A1
gene expression in human bone marrow mesenchymal cells. Taken together, we provide evidence that combined ruxolitinib/nilotinib/prednisone is a potential therapy for MF, possibly through the anti-fibrotic effect of nilotinib, the immunomodulatory effect of ruxolitinib and prednisone, and the anti-proliferative effect of ruxolitinib. This combination will be further investigated in a phase Ib/II clinical trial in MF.
Eosinophilic fasciitis (EF) is a rare entity characterized by symmetrical and painful thickness and induration of the skin, especially localized on forearms and thorax and generally accompanied by eosinophilia. Although several reports indicate the relationship between EF and hematological disorders such as aplastic anemia, polycythemia vera, or myelomonocytic leukemia, the association with lymphomas is extremely rare. Only a few cases of EF have been previously described preceding or concomitant to the Hodgkin disease, peripheral T-cell lymphoma, B-cell lymphoma, and mycosis fungoides. We report for the first time a 76-year-old man with an EF associated with a peripheral T-cell lymphoma not otherwise specified. We review the relationship between both conditions. In conclusion, we present a unique case of EF as a manifestation of a T-cell lymphoma not otherwise specified. The present case demonstrates the importance of clinical and radiological studies in those cases of EF to rule out a visceral, lymph node, or cutaneous lymphoma.
Precision medicine can significantly improve outcomes for cancer patients, but implementation requires comprehensive characterization of tumor cells to identify therapeutically exploitable vulnerabilities. Here we describe somatic biallelic TET2 mutations in an elderly patient with acute myeloid leukemia (AML) that was chemoresistant to anthracycline and cytarabine (Ara-C), but acutely sensitive to 5'-azacitidine (5'-Aza) hypomethylating monotherapy resulting in longterm morphological remission. Given the role of TET2 as a regulator of genomic methylation, we hypothesized that mutant TET2 allele dosage affects response to 5'-Aza. Using an isogenic cell model system and an orthotopic mouse xenograft, we demonstrate that biallelic TET2 mutations confer sensitivity to 5'-Aza compared to cells with monoallelic mutation. Our data argue in favor of using hypomethylating agents for chemoresistant disease or as first line therapy in patients with biallelic TET2-mutated AML and demonstrate the importance of considering mutant allele dosage in the implementation of precision medicine for cancer patients.
Owing to predictable or unpredictable causes, interruptions may arise during therapy. On average, the extension of fractionated radiotherapy treatments is prone to be delayed by several weeks and interruptions can come up extending overall treatment time (OTT). Clonogenic cells of aggressive tumors might benefit from this situation, modifying local control (LC). Preserving treatment quality in radiotherapy is an essential issue for the treatment outcome, and our institution is increasingly concerned about this line of work. Establishing some objective criteria to schedule patients that have suffered interruptions along their treatments is of capital importance and not a trivial issue. Publications strongly encourage departments to minimize the effect of lag periods during treatments. Therefore, in July 2017, our facility implemented the so called 'Protocol to Manage Interruptions in Radiotherapy', based on a scoring system for patient categorization that considers not only histology but also associated comorbidity and sequence of the therapy.
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