Active study: undetected prevalence and clinical inertia in the treatment of breakthrough cancer pain (BTcP).

AIMS: To prove if there is clinical inertia in the identification and treatment of episodes of breakthrough cancer pain (BTcP), comparing actual results from clinical practice with clinical oncologists' prior perception. DESIGN: Observational and descriptive study, using information collected by practising medical oncologists, at three moments: (a) questionnaire regarding their professional judgement of the handling of patients with BTcP in their practice, (b) cross-sectional clinical screening, to detect possible existing cases of BTcP in a representative sample of their patients, (c) retrospective self-audit of clinical case histories of patients diagnosed with BTcP to find out about how it has been handled. PARTICIPANTS AND STUDY PERIOD: A random sample on a state level of 108 specialists in medical oncology. 540 patients who suffer some type of cancer pain on the designated study date for each specialist (July-December 2016). RESULTS: The global prevalence of BTcP in the study sample covered 91.3% of the patients who were suffering some type of cancer pain. Barely 2% of the doctors surveyed suspected figures around this mark. 40.9% of the cases had not been previously detected as BTcP by their doctors. Although 90% of the patients who had previously been diagnosed with BTcP received a specific analgesic treatment for the symptoms, 42% of those patients with known BTcP were not able to control their episodes of pain. CONCLUSIONS: Clinical inertia is a serious problem in the handling of BTcP in medical oncology services, where it is the subject of a significantly low level of detection and treatment, despite the contrasting perception of specialists.

[Stem cells and cancer: elucidating the origin of the cancer stem cell]. / Células madre y cáncer: dilucidando el origen de la célula madre tumoral.

Stem cell therapy is currently at the frontier of biomedical research. A considerable volume of evidence indicates that cancer stem cells are responsible for the development of different types of tumors. Malignant transformation of stem cells may be due to the loss of normal asymmetric division processes, cell fusion, microenviromental factors, generic and epigenetic mechanisms or carcinogenics already implicated in cancer development. A better understanding of these transforming events will allow more rational design of new specific therapeutic strategies targeting the cancer stem cell.

Células madre y cáncer: dilucidando el origen de la célula madre tumoral / No disponible

La terapia con células madre está en la vanguardia de la investigación biomédica actual. Cada vez hay más evidencias de que la célula madre tumoral puede estar implicada en el origen del cáncer como se propone en el modelo jerárquico. La célula madre puede transformarse en maligna por procesos de pérdida de la división asimétrica, transferencia genética horizontal, fusión celular, factores microambientales y los agentes carcinógenos ya descritos para las células diferenciadas. Conocer mejor cómo se produce esta transformación permitirá diseñar abordajes de terapia celular más seguros y nuevos tratamientos específi cos contra estas células madre tumorales

Stem cell therapy is currently at the frontier of biomedical research. A considerable volume of evidence indicates that cancer stem cells are responsible for the development of different types of tumors. Malignant transformation of stem cells may be due to the loss of normal asymmetric division processes, cell fusion, microenviromental factors, generic and epigenetic mechanisms or carcinogenics already implicated in cancer development. A better understanding of these transforming events will allow more rational design of new specifi c therapeutic strategies targeting the cancer stem cell

[Gene sequence analysis of suppressor oncogene p53 in bladder carcinoma]. / Análisis por secuenciación genómica del oncogen supresor p53 en el carcinoma vesical.

A prospective study which analyzes the presence of mutations in the suppressor oncogene p53 through automated genome sequentiation in 75 specimens of transitional cell carcinoma. The presence of mutations correlated to the pathological stage and cellular grade. Also, both the different types of mutations detected and the diversity of their location indicate the heterogeneity of bladder transitional cells carcinoma. The automated genome sequentiation method allows to detect both the type of mutation and the exact location. The detection of suppressor oncogene p53 mutations allows to identify those patients who may be at higher risk of disease progression and therefore those who should undergo a more intense follow-up.