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2.
Biomed Res Int ; 2015: 432479, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-26161400

RESUMEN

Mucosal melanoma is a rare disease, which differs from its cutaneous counterpart genetically and for its clinical behaviour. Moreover this is a heterogeneous disease based on the tissue of origin. As CT7 and CT10 are highly expressed in cutaneous melanoma and are immunogenic in this disease, we analysed their expression throughout the different subtypes of mucosal melanoma and tumor development. We detected a frequent expression of CT7 in primaries and corresponding metastases (55%) as well as for CT10 (30%). This expression resulted to be heterogeneous in the same tumor specimen and moreover influenced by the tissue of origin. Our results support the role of these antigens in immunotherapy for mucosal melanoma.


Asunto(s)
Antígenos de Neoplasias/metabolismo , Heterogeneidad Genética , Melanoma/patología , Membrana Mucosa/metabolismo , Membrana Mucosa/patología , Proteínas de Neoplasias/metabolismo , Neoplasias Cutáneas/patología , Humanos , Melanoma/metabolismo , Recurrencia Local de Neoplasia/metabolismo , Recurrencia Local de Neoplasia/patología , Neoplasias Cutáneas/metabolismo
4.
Ann Oncol ; 24(1): 193-201, 2013 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-22967991

RESUMEN

BACKGROUND: Aggressive mature B-cell non-Hodgkin's lymphomas (BCL) sharing features of Burkitt's lymphoma (BL) and diffuse large B-cell lymphoma (DLBCL) (intermediate BL/DLBCL) but deviating with respect to one or more characteristics are increasingly recognized. The limited knowledge about these biologically heterogeneous lymphomas hampers their assignment to a known entity, raising incertitude about optimal treatment approaches. We therefore searched for discriminative, prognostic, and predictive factors for their better characterization. PATIENTS AND METHODS: We analyzed 242 cytogenetically defined aggressive mature BCL for differential protein expression. Marker selection was based on recent gene-expression profile studies. Predictive models for diagnosis were established and validated by a different set of lymphomas. RESULTS: CSE1L- and inhibitor of DNA binding-3 (ID3)-overexpression was associated with the diagnosis of BL and signal transduction and transcription-3 (STAT3) with DLBCL (P<0.001 for all markers). All three markers were associated with patient outcome in DLBCL. A new algorithm discriminating BL from DLBCL emerged, including the expression of CSE1L, STAT3, and MYC translocation. This 'new classifier' enabled the identification of patients with intermediate BL/DLBCL who benefited from intensive chemotherapy regimens. CONCLUSION: The proposed algorithm, which is based on markers with reliable staining properties for routine diagnostics, represents a novel valid tool in separating BL from DLBCL. Most interestingly, it allows segregating intermediate BL/DLBCL into groups with different treatment requirements.


Asunto(s)
Algoritmos , Biomarcadores de Tumor/genética , Linfoma de Burkitt/diagnóstico , Proteína de Susceptibilidad a Apoptosis Celular/genética , Genes myc , Linfoma de Células B Grandes Difuso/diagnóstico , Factor de Transcripción STAT3/genética , Western Blotting , Linfoma de Burkitt/genética , Femenino , Humanos , Inmunohistoquímica , Hibridación Fluorescente in Situ , Linfoma de Células B Grandes Difuso/genética , Masculino , Persona de Mediana Edad , Pronóstico
5.
Ann Oncol ; 23 Suppl 10: x83-8, 2012 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-22987998

RESUMEN

The current diagnosis of lymphoid neoplasias is based on the criteria of the World Health Organization (WHO) classification. This framework is built on two major principles: the stratification of neoplasms according to their derivation from precursor or mature cells and the definition of clinically relevant nonoverlapping diseases. The diagnosis is established by integrating the clinical, morphological, phenotypic, genetic and molecular characteristics of the tumors. This approach is reproducible, clinically relevant and scientifically sound. The elucidation of the human genome a decade ago and the development of high-throughput technologies have opened the possibility to search for comprehensive views of the genomic alterations of the tumors that are starting to influence our current approach to diagnosis. The new generation of sequencing technologies and their systematic application to human cancer and in particular to lymphoid neoplasms are revealing a landscape of somatic mutations of unprecedented complexity. These studies have already provided a number of important findings with functional and clinical implications. The translation of all this knowledge into the clinic is challenging and offers relevant perspectives.


Asunto(s)
Biomarcadores de Tumor , Linfoma , Biomarcadores de Tumor/genética , Biomarcadores de Tumor/metabolismo , Regulación Neoplásica de la Expresión Génica , Humanos , Linfoma/clasificación , Linfoma/diagnóstico , Linfoma/genética , Linfoma/patología , Análisis de Secuencia por Matrices de Oligonucleótidos/métodos , Investigación Biomédica Traslacional , Organización Mundial de la Salud
6.
Qual Saf Health Care ; 18(3): 205-8, 2009 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-19468003

RESUMEN

BACKGROUND: Limited information exists in regard to drug omissions and unjustified medications in the hospital discharge summary (DS). OBJECTIVE: To evaluate the incidence and types of drug omissions and unjustified medications in the DS, and to assess their potential impact on patient health. METHODS: A prospective observational review of the DSs of all patients discharged from our Internal Medicine Department over a 3-month period. Data assessment was made by internists using a structured form. RESULTS: Of the 577 evaluated DSs, 66% contained at least one inconsistency accounting for a total of 1012 irregularities. There were 393 drug omissions affecting 251 patients, 32% of which were potentially harmful. Seventeen per cent of all medications (619/3691) were unjustified, affecting 318 patients. The unjustified medication was potentially harmful in 16% of cases, occurred significantly more frequent in women than in men (61% vs 50%; p = 0.008) and increased linearly with the number of drugs prescribed (p<0.001). Drug omission had a twofold higher potential to cause harm than unjustified medication. CONCLUSIONS: Drug omissions and unjustified medications are frequent, and systemic changes are required to substantially reduce these inconsistencies.


Asunto(s)
Registros Médicos/normas , Errores de Medicación , Alta del Paciente/estadística & datos numéricos , Medicamentos bajo Prescripción , Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Suiza
7.
Ann Oncol ; 20(4): 628-35, 2009 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-19074747

RESUMEN

BACKGROUND: Breast cancer may be classified into distinct molecular subtypes based on gene expression profiling and/or immunophenotypic characteristics. Aim of the study was to investigate prevalence, clinicopathologic features and overall survival (OS) of molecular subtypes, in a large European population-based study. PATIENTS AND METHODS: All invasive breast cancers from 2003 to 2007 were selected from the files of Ticino Cancer Registry. Molecular subtypes were defined by immunohistochemical markers. Clinicopathological characteristics and short-term OS were analyzed. RESULTS: Of 1214 invasive breast cancers, 73.2% were luminal A subtype, 13.8% luminal B, 7.4% basal like and 5.6% Her2/neu. Basal like presented largely in premenopausal women and displayed aggressive features, such as large tumor size, poorly differentiated cancers, high Ki-67 proliferation index and the worst 24-month OS. Luminal A included the highest percentage of patients >70, the highest proportion of stage I tumors and well/moderately differentiated lesions. Her2/neu was more frequent in postmenopausal women and showed the highest percentage of positive lymph nodes and stage IV cases. CONCLUSION: This is a comprehensive European population-based study on breast cancer molecular subtypes. We provide strong evidence that the molecular classification is useful for clinical management and superior to World Health Organization classification in terms of short-term prognostic value.


Asunto(s)
Neoplasias de la Mama/clasificación , Vigilancia de la Población , Análisis de Supervivencia , Adulto , Anciano , Neoplasias de la Mama/metabolismo , Neoplasias de la Mama/patología , Femenino , Humanos , Inmunohistoquímica , Persona de Mediana Edad , Pronóstico , Suiza
8.
Bone Marrow Transplant ; 42(11): 749-55, 2008 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-18711347

RESUMEN

Epithelial cancers can arise from BM-derived cells (BMCs) in animal models. We studied whether the same phenomenon can occur in humans. Biopsy specimens from carcinomas and healthy adjacent tissues were obtained from three women who had undergone allogeneic BMT from an HLA-matched brother. Complete donor hematopoietic chimerism was verified by cytogenetic analysis, RFLP analysis or by reverse transcription-PCR analysis. Biopsies were studied for the presence of the Y chromosome derived from BM-derived cells by combined FISH and immunohistochemical staining. In our studies, we showed that human epithelial neoplastic and adjacent non-neoplastic tissues incorporate the Y chromosome at low and comparable rates. The lack of enrichment in malignancies argues against the possibility that BM-derived cells represent a direct source of carcinomas, and we suggest that these cells randomly contribute to neoplastic and non-neoplastic epithelial cells. On the basis of the absence of a fusion karyotype, we favor a model in which the differentiation of BM-derived cells is largely determined by the microenvironment encountered.


Asunto(s)
Células de la Médula Ósea/citología , Trasplante de Médula Ósea/métodos , Carcinoma/patología , Epitelio/metabolismo , Neoplasias/metabolismo , Adolescente , Adulto , Animales , Células de la Médula Ósea/metabolismo , Carcinoma/metabolismo , Citogenética , Femenino , Antígenos HLA/química , Humanos , Hibridación Fluorescente in Situ , Masculino , Cromosoma Y
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