11 results match your criteria: "University and Fondazione IRCCS Policlinico San Matteo[Affiliation]"

The presence of activating mutations of the epidermal growth factor receptor (EGFR)-gene identifies a distinct and clinically relevant molecular subset of non-small-cell lung cancer. It is now well demonstrated that EGFR tyrosine kinase inhibitors (TKIs) gefitinib and erlotinib are superior to standard chemotherapy in this subset of tumors. Nevertheless, in many cases, responses are not durable and last for 6-12 months due to the occurrence of secondary or acquired resistance.

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Brain metastases develop in one-third of patients with non-small-cell lung cancer and are associated with a dismal prognosis, irrespective of surgery or chemo-radiotherapy. Pathological markers for predicting outcomes after surgical resection and radiotherapy responsiveness are still lacking. Caveolin 1 has been associated with chemo- and radioresistance in various tumors, including non-small-cell lung cancer.

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Background: Malignant Pleural Mesothelioma (MPM) is an aggressive tumor arising from mesothelial cells lining the pleural cavities characterized by resistance to standard therapies. Most of the molecular steps responsible for pleural transformation remain unclear; however, several growth factor signaling cascades are known to be altered during MPM onset and progression. Transducers of these pathways, such as PIK3CA-mTOR-AKT, MAPK, and ezrin/radixin/moesin (ERM) could therefore be exploited as possible targets for pharmacological intervention.

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Activation of oncogenic pathways in idiopathic pulmonary fibrosis.

Transl Oncol

October 2014

Laboratory of Biochemistry and Genetics, Pneumology Unit, Department of Molecular Medicine, University and Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.

Idiopathic pulmonary fibrosis (IPF) is defined as a specific form of chronic, progressive fibrosing interstitial pneumonia of unknown cause. The most recent hypotheses on IPF pathogenesis suggest a central role of epithelial cell damage, followed by a dysregulated molecular cross talk between epithelial cells and fibroblasts. Thus, IPF progression has often been assimilated to that of cancer, and several signaling patterns appear to be disrupted in both diseases.

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Lung cancer is among the most common cancers in the world. Despite advances in defining the molecular mechanisms involved in lung oncogenesis and the remarkable efforts made to improve screening programs for secondary cancer prevention, patients' prognosis remains poor. Moreover, wide international inequalities remain apparent, even among developed countries.

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In the airway tract acetylcholine (ACh) is known to be the mediator of the parasympathetic nervous system. However ACh is also synthesized by a large variety of non-neuronal cells. Strongest expression is documented in neuroendocrine and in epithelial cells (ciliated, basal and secretory elements).

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Background & Objectives: Kidney transplantation is the best option for patients with end-stage renal disease (ESRD) failure. Prolonged use of immunosuppressive drugs often causes opportunistic infections and malignancies of skin and mucosae, but due to lack of a careful dermatological screening in several transplantation centers the diagnosis and the treatment of dermatological lesions in kidney transplant patients are underestimated. In addition after the introduction of interleukin (IL)-2 -receptor antagonists (basiliximab/daclizumab), mTOR inhibitors and mycophenolate mofetil (MMF)/mycophenolic acid (MPA) in new immunosuppressive protocols only a few studies have analyzed the skin and mucosal lesions in kidney transplant patients.

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EGFR and KRAS mutational profiling in fresh non-small cell lung cancer (NSCLC) cells.

J Cancer Res Clin Oncol

August 2013

Laboratory of Biochemistry and Genetics, Division of Pneumology, Department of Molecular Medicine, University and Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy.

Purpose: Knowledge of tumor mutational status has become a priority for effective NSCLC-tailored treatment. NSCLC diagnosis is more often reached through biopsy; thus, there is a clear need to implement for routine tumor molecular profiling on small cytological samples. This work aims to screen and compare the EGFR and KRAS mutational prevalence in fresh tumor cells and in corresponding routinely processed samples derived from trans-thoracic fine-needle aspiration.

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Lung cancer is the leading cause of death for solid tumors worldwide with an annual mortality of over one million. Lung carcinoma includes a series of different diseases which are roughly divided into two groups based on clinical and histo-pathological features: non-small cell lung cancer (NSCLC), accounting for almost 80% of lung cancer diagnosis and small cell lung cancer (SCLC) responsible for the remaining 20%. The NSCLC molecular profile has been deeply investigated; alterations in several oncogenes, tumor suppressor genes and transcription factors have been detected, mainly in adenocarcinomas.

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We discuss the case of synchronous bilateral lung cancers which feature the same histological phenotype and a different EGFR mutational profile. Both histological and molecular characterizations were performed on specimens derived thorough CT-guided fine needle aspiration. A first-line chemotherapy was unsuccessful.

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Background: Peritoneal dialysis (PD) is associated with a depression of T cell function, as suggested by the impaired production of cytokines by Th cells collected from PD patients. Although treatment biocompatibility could be implicated in this immune dysfunction, it has been poorly investigated, thus far. Therefore, we undertook a study aiming to analyze the effects of different peritoneal dialysis fluids on the Th1/Th2 balance in PD patients.

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