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Publicaciones científicas más recientes (desde 2010)

Autores: Alfaro, Carlos; et al.
Revista: CANCER TREATMENT REVIEWS
ISSN 0305-7372  Vol. 60  2017  págs. 24 - 31
Interleukin-8 (CXCL8) was originally described asa chemokine whose main function is the attraction of a polymorphonuclear inflammatory leukocyte infiltrate acting on CXCR1/2. Recently, it has been found that tumors very frequently coopt the production of this chemokine, which in this malignant context exerts different pro-tumoral functions. Reportedly, these include angiogenesis, survival signaling for cancer stem cells and attraction of myeloid cells endowed with the ability to immunosuppress and locally provide growth factors. Given the fact that in cancer patients IL-8 is mainly produced by tumor cells themselves, its serum concentration has been shown to correlate with tumor burden. Thus, IL-8 serum concentrations have been shown to be useful asa pharmacodynamic biomarker to early detect response to immunotherapy. Finally, because of the roles that IL-8 plays in favoring tumor progression, several therapeutic strategies are being developed to interfere with its functions. Such interventions hold promise, especially for therapeutic combinations in the field of cancer immunotherapy.
Autores: Vallejo, A.; Guruceaga, Elisabet; et al.
Revista: NATURE COMMUNICATIONS
ISSN 2041-1723  Vol. 21  Nº 8  2017  págs. 14294
KRAS mutated tumours represent a large fraction of human cancers, but the vast majority remains refractory to current clinical therapies. Thus, a deeper understanding of the molecular mechanisms triggered by KRAS oncogene may yield alternative therapeutic strategies. Here we report the identification of a common transcriptional signature across mutant KRAS cancers of distinct tissue origin that includes the transcription factor FOSL1. High FOSL1 expression identifies mutant KRAS lung and pancreatic cancer patients with the worst survival outcome. Furthermore, FOSL1 genetic inhibition is detrimental to both KRAS-driven tumour types. Mechanistically, FOSL1 links the KRAS oncogene to components of the mitotic machinery, a pathway previously postulated to function orthogonally to oncogenic KRAS. FOSL1 targets include AURKA, whose inhibition impairs viability of mutant KRAS cells. Lastly, combination of AURKA and MEK inhibitors induces a deleterious effect on mutant KRAS cells. Our findings unveil KRAS downstream effectors that provide opportunities to treat KRAS-driven cancers.
Autores: Marquez Rodas, I.; López-Tarruella Cobo, S.; et al.
Revista: ANNALS OF ONCOLOGY
ISSN 0923-7534  Vol. 28  Nº Suppl. 5  2017  págs.  LBA20
Autores: Pérez, José Luis; et al.
Revista: ANNALS OF ONCOLOGY
ISSN 0923-7534  Vol. 28  Nº Supl. 11  2017  págs. 48P
Autores: Sola, Jesús Javier; Diaz-Gonzalez, JA; et al.
Revista: BRITISH JOURNAL OF CANCER
ISSN 0007-0920  Vol. 115  Nº 6  2016  págs. 655-663
Preoperative chemoradiation increases the likelihood of achieving favourable histopathological features that correlate with a 5-year OS>70% in GC patients.
Autores: Ponz-Sarvise, Mariano; Corbo, V.; Frese, K.; et al.
Revista: ANNALS OF ONCOLOGY
ISSN 0923-7534  Vol. 27  Nº Supl. 6  2016  págs. 1523P
Autores: Ponz-Sarvise, Mariano; Castañón, Eduardo; et al.
Revista: CLINICAL GENITOURINARY CANCER
ISSN 1558-7673  Vol. 12  Nº 2  2014  págs. 87 - 93
Inhibitor of differentiation-1 (Id1) might constitute a novel prognostic factor able to differentiate indolent from aggressive prostate tumors. In this study, 2 cohorts of 52 and 79 prostate cancer patients were selected for Id1 expression analysis. Higher levels of Id1 protein in advanced poor-prognosis patients and a correlation of higher Id1 mRNA expression levels with a lower survival in stage I to III patients were observed. Background: In the prostate-specific antigen era, potentially indolent prostate tumors are radically treated, causing overtreatment. Molecular prognostic factors might differentiate indolent from aggressive tumors, allowing avoidance of unnecessary treatment. Patients and Methods: Fifty-two prostate cancer patients (20 organ-confined and 32 metastatic) were selected. All formalin-fixed and paraffin-embedded primary biopsies and matched metastases of 15 of them were evaluated for tumor and endothelial cell Id1 protein expression. Seventy-nine additional patients with organ-confined prostate cancer were selected for Id1 mRNA in silico analysis. Results: Among metastatic cancer subjects, 48% of primary tumors and 38% of metastases showed Id1 tumor cell expression, and 79% of primary tumors and 81% of metastases showed endothelial immunoreactivity. In the organ-confined group none of them showed Id1 protein tumor cell expression and 50% displayed endothelial expression. In the metastatic patients group, lower levels of Id1 protein predicted a nonsignificant longer overall survival (13 months vs. 7 months; P = .79). In the in silico analysis, however, lower levels of Id1 mRNA predicted a longer disease-free survival (61 months vs. not-reached; P = .018) and the hazard ratio for progression was 0.451 (P = .022) in favor of patients showing lower levels. Conclusion: In our cohort, it seems to be a differential epithelial expression of Id1 protein according to the prognostic features (metastatic/poor prognosis vs. organ-confined/good prognosis). In localized tumors treated with radical prostatectomy, higher Id1 mRNA expression levels might predict a higher hazard ratio for progression and a shorter disease-free survival. Further validation of these results in larger prospective series is warranted.
Autores: Ponz-Sarvise, Mariano; Nguewa, Paul; Pajares, María Josefa; et al.
Revista: CLINICAL CANCER RESEARCH
ISSN 1078-0432  Vol. 17  Nº 12  2011  págs. 4155 -4166
Autores: Centeno, Carlos; Carvajal Valcarcel, A; et al.
Revista: Journal of Palliative Medicine
ISSN 1096-6218  Vol. 14  Nº 1  2011  págs. 4 - 5
Autores: Zarate, Ruth Noemí; Rodriguez, J.; et al.
Revista: Cancer Research
ISSN 0008-5472  Vol. 102  Nº 6  2010  págs. 987 - 994
Autores: Pajares, María Josefa; Agorreta, J; et al.
Revista: Molecular Cancer
ISSN 1476-4598  Vol. 28  Nº 9  2010  págs. 130