Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
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A new theory about the development of solid tumours is emerging from the idea that solid tumours, like normal adult tissues, contain stem cells (called cancer stem cells) and arise from them. Genetic mutations encoding for proteins involved in critical signalling pathways for stem cells such as BMP, Notch, Hedgehog and Wnt would allow stem cells to undergo uncontrolled proliferation and form tumours. ⋯ In the present paper we will review the molecular basis of the Notch signalling pathway. Additionally, we will pay attention to their role in adult stem cell self-renewal, and cell fate specification and differentiation, and we will also review evidence that supports their implication in cancer.
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Cancer is a heritable disorder of somatic cells: environment and heredity are both important in the carcinogenic process. The primal force is the "two hits" of Knudson's hypothesis, which has proved true for many tumours, including renal cell carcinoma. Knudson et al. [1, 2] recognised that familial forms of cancer might hold the key to the identification of important regulatory elements known as tumour-suppressor genes. ⋯ Families with hereditary predisposition to cancer continue to provide a unique opportunity for the identification and characterisation of genes involved in carcinogenesis. A surprising number of genetic syndromes predispose to the development of renal cell carcinoma, and genes associated with five of these syndromes have been already identified: VHL, MET, FH, BHD and HRPT2. Few cancers have as many different types of genetic predisposition as renal cancer, although to date only a small proportion of renal cell cancers can be explained by genetic predisposition.
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Multicenter Study
Sensivity to change of the Spanish validated Memorial Pain Assessment Card in cancer patients.
Pain intensity is a good parameter to assess effective treatment of cancer and palliative care. The Memorial Pain Assessment Card (MPAC) is a quick, easy and reliable measure of quality of life in cancer patients. The MPAC was validated in Spanish in 2004. This study evaluated the sensitivity to change Spanish version of the MPAC. ⋯ The present study showed sensitivity to change among the different MPAC subscales of the Spanish version. Moreover, the MPAC Spanish version has proven to be a good tool accepted by health-care-professionals and patients. Due to its facility of administration, it may allow a useful and quick evaluation of cancer-related pain in the clinical practice.
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Spain's radiation oncology infrastructure has evolved in terms of both quantity and structure since the last analysis was carried out in 1999. The purpose of this paper is to describe the current facilities, basically consisting of external radiotherapeutic units, and to present a calculation model for estimating the number of irradiation units required to guarantee equitable cover for radiotherapeutic treatment. An electronic questionnaire was designed to be accessed via a link on the Spanish Association of Radiotherapy and Oncology Web page. ⋯ Forty-five of these were cobalt units and 132 were accelerators. The rate of radiotherapy use in Spain based on the best scientific evidence available and on its rate of use with cancer has been estimated at 61%. The number of external irradiation units available in 2004 (177) is clearly lower than the number desirable (266-316).
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Retinoblastoma (Rb), the most common intraocular tumor in childhood, is caused by the loss of function of both retinoblastoma susceptibility gene (RB1 or Rb1) alleles. In 1971, Alfred Knudson proposed his "two-hit" theory based upon empiric observations of the clinical genetics of Rb, revealing the role of tumor-suppressor genes in human cancer. Knudson proposed that: "In the dominant inherited form of Rb, one mutation is inherited via germ line and the second occurs in somatic cells. ⋯ A few years later, Harbour extended these findings to small-cell lung cancer, showing that the RB1 locus was disrupted in tumors other than Rb and osteosarcoma. Since then, it has been found that most, if not all, tumors have defects in their RB1 pathway through genetic lesions in the RB1 gene itself or other genes in the pathway. The history of Rb research highlights how basic research on a rare childhood cancer can have a much broader effect on a disease that affects millions of people each year worldwide.