Long-term Transcatheter Aortic Valve Durability

Transcatheter aortic valve implantation (TAVI) has become the standard of care for high-risk and inoperable surgical patients and a valid alternative to surgery for low- and intermediate-risk patients with severe, symptomatic aortic stenosis. It is increasingly being used for younger, lower-risk patients, so it is important to ensure the durability for long-term transcatheter aortic valves. The lack of standard definitions of structural valve degeneration (SVD) had made comparison among studies on prosthetic valve durability problematic. The 2017 standardised definitions of SVD by the European Association of Percutaneous Cardiovascular Intervention), the European Society of Cardiology and the European Association for Cardio-Thoracic Surgery, and the 2018 definitions by the Valve In Valve International Data group, has generated an increased uniformity in evaluations. This article examines the potential mechanisms and rates of SVD of transcatheter bioprostheses and the role of redo TAVI as a treatment option

Author Correction: Antineoplastic activity of products derived from cellulose‑containing materials: levoglucosenone and structurally‑related derivatives as new alternatives for breast cancer treatment

Fe de erratas del artículo Antineoplastic activity of products derived from cellulose-containing materials: levoglucosenone and structurally-related derivatives as new alternatives for breast cancer treatment.Fil: Delbart, Damian Ignacio. Universidad de Buenos Aires. Instituto de Oncología Ángel H. Roffo. Área Investigación; Argentina.Fil: Giri, Germán Francisco. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Química Rosario (IQUIR-CONICET); Argentina.Fil: Cammarata, Agostina. Comisión Nacional de Energía Atómica. Gerencia de Investigación y Aplicaciones; Argentina.Fil: Pan, Melisa Denise. Universidad de Buenos Aires. Instituto de Oncología Ángel H. Roffo. Unidad de Transferencia Genética; Argentina.Fil: Bareño, Lizeth Ariza. Universidad de Buenos Aires. Instituto de Oncología Ángel H. Roffo. Área Investigación; Argentina.Fil: Amigo, Natalia Loreley. Universidad de Buenos Aires. Instituto de Oncología Ángel H. Roffo. Área Investigación; Argentina.Fil: Bechis, Andrés. Universidad de Buenos Aires. Instituto de Oncología Ángel H. Roffo. Área Investigación; Argentina.Fil: Suarez, Alejandra Graciela. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Química Rosario (IQUIR-CONICET); Argentina.Fil: Spanevello, Rolando Ángel. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Química Rosario (IQUIR-CONICET); Argentina.Fil: Spanevello, Rolando Ángel. Consejo Nacional de Investigaciones Científicas y Técnicas. Scientific Research Career; Argentina.Fil: Villaverde, Marcela Solange. Universidad de Buenos Aires. Instituto de Oncología Ángel H. Roffo. Unidad de Transferencia Genética; Argentina.Fil:Villaverde, Marcela Solange. Consejo Nacional de Investigaciones Científicas y Técnicas. Scientific Research Career; Argentina.Fil: Todaro, Laura Beatriz. Universidad de Buenos Aires. Instituto de Oncología Ángel H. Roffo. Área Investigación; Argentina.Fil: Todaro, Laura Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Scientific Research Career; Argentina.Fil: Urtreger, Alejandro Jorge. Universidad de Buenos Aires. Instituto de Oncología Ángel H. Roffo. Área Investigación; Argentina.Fil: Urtreger, Alejandro Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas. Scientific Research Career; Argentina

Role of 1q21 in Multiple Myeloma: From Pathogenesis to Possible Therapeutic Targets

Multiple myeloma (MM) is characterized by an accumulation of malignant plasma cells (PCs) in the bone marrow (BM). The amplification of 1q21 is one of the most common cytogenetic abnormalities occurring in around 40% of de novo patients and 70% of relapsed/refractory MM. Patients with this unfavorable cytogenetic abnormality are considered to be high risk with a poor response to standard therapies. The gene(s) driving amplification of the 1q21 amplicon has not been fully studied. A number of clear candidates are under investigation, and some of them (IL6R, ILF2, MCL-1, CKS1B and BCL9) have been recently proposed to be potential drivers of this region. However, much remains to be learned about the biology of the genes driving the disease progression in MM patients with 1q21 amp. Understanding the mechanisms of these genes is important for the development of effective targeted therapeutic approaches to treat these patients for whom effective therapies are currently lacking. In this paper, we review the current knowledge about the pathological features, the mechanism of 1q21 amplification, and the signal pathway of the most relevant candidate genes that have been suggested as possible therapeutic targets for the 1q21 amplicon

Lenalidomide increases human dendritic cell maturation in multiple myeloma patients targeting monocyte differentiation and modulating mesenchymal stromal cell inhibitory properties

The use of Lenalidomide (LEN), to reverse tumor-mediated immune suppression and amplify multiple myeloma-specific immunity is currently being explored. Particularly, LEN effects on dendritic cells (DCs) are still unclear. In this study, we investigated the potential effect of LEN on DC differentiation and activity. DCs were differentiated either from CD14(+) cells obtained from patients with multiple myeloma or from a human monocytic cell line. LEN, at the concentration range reached in vivo, significantly increased the median intensity expression of HLA-DR, CD86 and CD209 by DCs derived from both bone marrow and peripheral myeloma monocytes and enhanced the production of Interleukin-8, C-C motif chemokine ligand (CCL) 2, CCL5 and tumor necrosis factor-α. Consistently, LEN pre-treated DCs showed an increased ability to stimulate autologous CD3(+) cell proliferation. LEN effect on dendritic differentiation was associated with the degradation of the Cereblon-related factors Ikaros and Aiolos. Moreover, we showed that LEN also blunted mesenchymal stromal cell inhibitory effect on dendritic differentiation, inhibiting Casein Kinase-1α levels. Finally, in vitro data were confirmed in ex vivo cultures obtained from relapsed myeloma patients treated with LEN, showing a significant increase of DC differentiation from peripheral blood monocytes. In conclusion, LEN increased the expression of mature dendritic markers both directly and indirectly and enhanced DC ability to stimulate T cell proliferation and to release chemokines. This suggests a new possible mechanism by which LEN could exert its anti-myeloma activity