The Network That Unites a Qualitative Study on Clinical Psychological Intervention for Women with a History of Breast Cancer and Chronic Pain.

The aim of this qualitative research is to deepen the knowledge in the field of psycho-oncology and the consequences of chronic and persistent pain by listening to patients' experiences, their emotions and difficulties in facing this hard condition, and assessing their perception of the role of the psychologist in pain management. In this qualitative study, a semistructured interview was used, designed from three research questions: chronic pain and quality of life; chronic pain and psychological well-being; and the role and perception of the psychologist in pain management. The sample consists of 29 women who suffered or have recovered from breast carcinoma, and who currently report having chronic pain due either to the presence of the cancer or as a result of surgery or treatment. Three themes emerged from the thematic analysis: quality of life and psychological well-being, relational well-being, and perception and role of the psychologist. Two subthemes have been identified for each theme: common features of chronic pain and consequences and resilience for the first theme; not feeling understood and willingness to protect loved ones for the second theme; and improvements perceived by users and reasons for not making use of the service for the last theme. In conclusion, the results obtained from the literature and those from the analysis of the interviews are discussed and compared, and reflections are made on possible future implications.

Overexpression of Fgfr2c causes craniofacial bone hypoplasia and ameliorates craniosynostosis in the Crouzon mouse.

FGFR2c regulates many aspects of craniofacial and skeletal development. Mutations in the FGFR2 gene are causative of multiple forms of syndromic craniosynostosis, including Crouzon syndrome. Paradoxically, mouse studies have shown that the activation (Fgfr2cC342Y; a mouse model for human Crouzon syndrome), as well as the removal (Fgfr2cnull), of the FGFR2c isoform can drive suture abolishment. This study aims to address the downstream effects of pathogenic FGFR2c signalling by studying the effects of Fgfr2c overexpression. Conditional overexpression of Fgfr2c (R26RFgfr2c;ßact) results in craniofacial hypoplasia as well as microtia and cleft palate. Contrary to Fgfr2cnull and Fgfr2cC342Y, Fgfr2c overexpression is insufficient to drive onset of craniosynostosis. Examination of the MAPK/ERK pathway in the embryonic sutures of Fgfr2cC342Y and R26RFgfr2c;ßact mice reveals that both mutants have increased pERK expression. The contrasting phenotypes between Fgfr2cC342Y and R26RFgfr2c;ßact mice prompted us to assess the impact of the Fgfr2c overexpression allele on the Crouzon mouse (Fgfr2cC342Y), in particular its effects on the coronal suture. Our results demonstrate that Fgfr2c overexpression is sufficient to partially rescue craniosynostosis through increased proliferation and reduced osteogenic activity in E18.5 Fgfr2cC342Y embryos. This study demonstrates the intricate balance of FGF signalling required for correct calvarial bone and suture morphogenesis, and that increasing the expression of the wild-type FGFR2c isoform could be a way to prevent or delay craniosynostosis progression.

Vinorelbine and prednisone in older cancer patients with hormone-refractory metastatic prostate cancer. A phase II study.

AIMS AND BACKGROUND: Prostate cancer is a common disease in older men. Since it is hormone resistant, no treatment may improve survival. In patients with hormone-refractory prostate cancer, clinical benefit is an important treatment end point. STUDY DESIGN: This study evaluated the efficacy and toxicity of a vinorelbine and prednisone combination in hormone-refractory prostate cancer patients. Vinorelbine was administered at the dose of 25 mg/m2 on days 1 and 8, every three weeks; prednisone was administered orally at the dose of 12 mg/day. Thirty consecutive patients, 65 years or older, with progressive (PSA increase or increase in bidimensionally measurable lesion) metastatic prostate adenocarcinoma were enrolled. Four patients (13%) had a partial response and 14 (46%) stable disease. Time to progression for the entire group was 4.5 months (range, 2-13) and 7.5 months for the group of responders (range, 3-13). A PSA decrease >50% was registered in 36% of the patients. Pain reduction was recorded in 44.4% of the patients and stability in 14.8%. RESULTS: The treatment was well tolerated and grade 3 toxicity was found in 2 cases of anemia and 2 cases of leukopenia without fever. CONCLUSIONS: The schedule is able to control the evolution of hormone-refractory prostate cancer and to give a clinical benefit. These results provide information for further clinical trials in a large series of elderly cancer patients.