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BACKGROUND: Chemotherapy can induce cognitive impairment in cancer patients. The main goal of this longitudinal study was to determine the incidence, characteristics, and duration of cognitive dysfunction in patients treated with adjuvant chemotherapy for colon cancer. PATIENTS AND METHODS: We assessed cognitive function, quality of life, anxiety and depression, fatigue, and hemoglobin levels in colon cancer patients at three assessment points: pre-chemotherapy (n=81), post-chemotherapy (n=73), and after 6-month follow-up (n=54). All patients were treated with oxaliplatin plus 5-fluorouracil/leucovorin (FOLFOX4) for 6 months. RESULTS: Thirty patients (37%) had cognitive impairment in the pre-chemotherapy evaluation, mainly in processing speed and psychomotor executive function (Trail Making Test A and B). At the end of treatment, the main domain affected was the verbal memory, with an acute decline detected in 56% of patients. Fifty-four percent of the patients improved their dysfunction after 6 months of follow-up, whereas 18 (33%) of them showed worsening in at least one test. Cognitive impairment was most common in older patients and in those with less years of education. Quality of life, anxiety, depression, fatigue, and hemoglobin did not influence the results of the cognitive tests. CONCLUSIONS: Adjuvant FOLFOX4 in patients with colon cancer can have a negative effect on verbal memory. This deterioration is usually mild and transient., Depto. de Psicología Social, del Trabajo y Diferencial, Fac. de Psicología, TRUE, pub

According to recent guidelines for clinical practice published about the management of sarcoma during the coronavirus disease-2019 (COVID-19) pandemic, patients with a suspected infection should be screened for the presence of the virus. If confirmed or strongly suspected (clinically or by computed tomography [CT] scan), any cancer treatment must be postponed for at least 15 days after the start of symptoms and until the patient has recovered1. We present three clinical cases of patients with suspected COVID-19 in different situations.

[Background]: The promoter hypermethylation of the methylguanine-DNA methyltransferase gene is a frequently used biomarker in daily clinical practice as it is associated with a favorable prognosis in glioblastoma patients treated with temozolamide. Due to the absence of adequately standardized techniques, international harmonization of the MGMT methylation biomarker is still an unmet clinical need for the diagnosis and treatment of glioblastoma patients. [Results]: In this study we carried out a clinical validation of a quantitative assay for MGMT methylation detection by comparing a novel quantitative MSP using double-probe (dp_qMSP) with the conventional MSP in 100 FFPE glioblastoma samples. We performed both technologies and established the best cutoff for the identification of positive-methylated samples using the quantitative data obtained from dp_qMSP. Kaplan–Meier curves and ROC time dependent curves were employed for the comparison of both methodologies. [Conclusions]: We obtained similar results using both assays in the same cohort of patients, in terms of progression free survival and overall survival according to Kaplan–Meier curves. In addition, the results of ROC(t) curves showed that dp_qMSP increases the area under curve time-dependent in comparison with MSP for predicting progression free survival and overall survival over time. We concluded that dp_qMSP is an alternative methodology compatible with the results obtained with the conventional MSP. Our assay will improve the therapeutic management of glioblastoma patients, being a more sensitive and competitive alternative methodology that ensures the standardization of the MGMT-biomarker making it reliable and suitable for clinical use.

Transcription factor NRF2 orchestrates a cellular defense against oxidative stress and, so far, has been involved in tumor progression by providing a metabolic adaptation to tumorigenic demands and resistance to chemotherapeutics. In this study, we discover that NRF2 also propels tumorigenesis in gliomas and glioblastomas by inducing the expression of the transcriptional co-activator TAZ, a protein of the Hippo signaling pathway that promotes tumor growth. The expression of the genes encoding NRF2 (NFE2L2) and TAZ (WWTR1) showed a positive correlation in 721 gliomas from The Cancer Genome Atlas database. Moreover, NRF2 and TAZ protein levels also correlated in immunohistochemical tissue arrays of glioblastomas. Genetic knock-down of NRF2 decreased, while NRF2 overexpression or chemical activation with sulforaphane, increased TAZ transcript and protein levels. Mechanistically, we identified several NRF2-regulated functional enhancers in the regulatory region of WWTR1. The relevance of the new NRF2/TAZ axis in tumorigenesis was demonstrated in subcutaneous and intracranial grafts. Thus, intracranial inoculation of NRF2-depleted glioma stem cells did not develop tumors as determined by magnetic resonance imaging. Forced TAZ overexpression partly rescued both stem cell growth in neurospheres and tumorigenicity. Hence, NRF2 not only enables tumor cells to be competent to proliferate but it also propels tumorigenesis by activating the TAZ-mediated Hippo transcriptional program.

Often patients treated with chemotherapy and/or radiotherapy suffer memory and attention problems. The exact mechanisms of action are unknown, although several explanations have been proposed. Both chemotherapy and radiotherapy have a direct toxic effect in the CNS, especially neural progenitor cells and the glia, which are responsible for maintaining neurogenesis in the hippocampus and white matter integrity. Besides the treatments can induce vascular damage in the brain, altering the immune response mediated by cytokines, and hormonal changes secondary to either chemotherapy or hormone therapy itself. The intensity of these effects would be modulated by several genetic factors that influence the ability of neuronal repair, pharmacodynamics and activity of neurotransmitters., A menudo los pacientes que reciben tratamiento con quimioterapia y/o radioterapia presentan problemas de memoria y de atención. Se desconocen los mecanismos exactos por los que esto se produce, aunque se han propuesto diversas explicaciones. Tanto la quimioterapia como la radioterapia poseen una acción tóxica directa en el SNC, especialmente sobre las células progenitoras neurales y las de la glía, que son las responsables de mantener la neurogénesis del hipocampo y la integridad de la sustancia blanca. A ello cabe añadir el daño que pueden inducir los tratamientos en la vascularización cerebral, la alteración de la respuesta inmune mediada por citoquinas, y los cambios hormonales ya sean secundarios a la quimioterapia o a la propia hormonoterapia. La intensidad de estos efectos estaría modulada por diversos factores genéticos que influyen sobre la capacidad de reparación neuronal, la farmacodinamia y la actividad de los neurotransmisores.

Often patients treated with chemotherapy and/or radiotherapy suffer memory and attention problems. The exact mechanisms of action are unknown, although several explanations have been proposed. Both chemotherapy and radiotherapy have a direct toxic effect in the CNS, especially neural progenitor cells and the glia, which are responsible for maintaining neurogenesis in the hippocampus and white matter integrity. Besides the treatments can induce vascular damage in the brain, altering the immune response mediated by cytokines, and hormonal changes secondary to either chemotherapy or hormone therapy itself. The intensity of these effects would be modulated by several genetic factors that influence the ability of neuronal repair, pharmacodynamics and activity of neurotransmitters., A menudo los pacientes que reciben tratamiento con quimioterapia y/o radioterapia presentan problemas de memoria y de atención. Se desconocen los mecanismos exactos por los que esto se produce, aunque se han propuesto diversas explicaciones. Tanto la quimioterapia como la radioterapia poseen una acción tóxica directa en el SNC, especialmente sobre las células progenitoras neurales y las de la glía, que son las responsables de mantener la neurogénesis del hipocampo y la integridad de la sustancia blanca. A ello cabe añadir el daño que pueden inducir los tratamientos en la vascularización cerebral, la alteración de la respuesta inmune mediada por citoquinas, y los cambios hormonales ya sean secundarios a la quimioterapia o a la propia hormonoterapia. La intensidad de estos efectos estaría modulada por diversos factores genéticos que influyen sobre la capacidad de reparación neuronal, la farmacodinamia y la actividad de los neurotransmisores.