Author
Giuseppe Pelosi
Other affiliations: European Institute of Oncology, Science for Life Laboratory
Bio: Giuseppe Pelosi is an academic researcher from University of Milan. The author has contributed to research in topics: Lung cancer & Neuroendocrine tumors. The author has an hindex of 62, co-authored 337 publications receiving 15785 citations. Previous affiliations of Giuseppe Pelosi include European Institute of Oncology & Science for Life Laboratory.
Topics: Lung cancer, Neuroendocrine tumors, Adenocarcinoma, Carcinoma, Cancer
Papers published on a yearly basis
Papers
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Memorial Sloan Kettering Cancer Center1, French Institute of Health and Medical Research2, Columbia University Medical Center3, Icahn School of Medicine at Mount Sinai4, Brigham and Women's Hospital5, University of Pittsburgh6, Fox Chase Cancer Center7, University of Mississippi Medical Center8, University of Colorado Boulder9, Aberdeen Royal Infirmary10, University of Tsukuba11, University of Texas MD Anderson Cancer Center12
TL;DR: The 2015 World Health Organization (WHO) Classification of Tumors of the Lung, Pleura, Thymus and Heart has just been published with numerous important changes from the 2004 WHO classification.
3,029 citations
Princess Margaret Cancer Centre1, University of Aberdeen2, Mount Sinai Hospital3, Cornell University4, Science for Life Laboratory5, University Hospital of Basel6, Brigham and Women's Hospital7, Fudan University8, Taipei Veterans General Hospital9, Seoul National University Bundang Hospital10, University of Pittsburgh11, Harvard University12, New York University13, National Institutes of Health14, University of Tsukuba15, University of Milan16, Memorial Sloan Kettering Cancer Center17, VU University Medical Center18, University of Texas MD Anderson Cancer Center19, Anschutz Medical Campus20
TL;DR: The Blueprint (BP) Programmed Death Ligand 1 (PD-L1) Immunohistochemistry Comparability Project is a pivotal academic/professional society and industrial collaboration to assess the feasibility of harmonizing the clinical use of five independently developed commercial PD-L 1 immunohistochemical assays.
550 citations
TL;DR: Analysis of circulating DNA in plasma can provide a useful marker for earlier lung cancer detection and identify patients with lung cancer and monitor their disease, and plasma DNA was a strong risk fact...
Abstract: Purpose: Analysis of circulating DNA in plasma can provide a useful marker for earlier lung cancer detection. This study was designed to assess the sensitivity and specificity of a quantitative molecular assay of circulating DNA to identify patients with lung cancer and monitor their disease. Materials and Methods: The amount of plasma DNA was determined through the use of real-time quantitative polymerase chain reaction (PCR) amplification of the human telomerase reverse transcriptase gene (hTERT) in 100 non–small-cell lung cancer patients and 100 age-, sex-, and smoking-matched controls. Screening performance of the assay was calculated through the receiver operating characteristic (ROC) curve. Odds ratios were calculated using conditional logistic regression analysis. Results: Median concentration of circulating plasma DNA in patients was almost eight times the value detected incontrols (24.3 v 3.1 ng/mL). The area under the ROC curve was 0.94 (95% CI, 0.907 to 0.973). Plasma DNA was a strong risk fact...
511 citations
Royal Free Hospital1, Institut Gustave Roussy2, University of Perugia3, University of Turin4, Imperial College London5, University of Milan6, University of Bern7, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico8, Memorial Sloan Kettering Cancer Center9, University of Marburg10, Autonomous University of Barcelona11, Erasmus University Rotterdam12, Uppsala University13, University of Genoa14, Churchill Hospital15, Kyushu University16, National Institutes of Health17, National and Kapodistrian University of Athens18, University of Reims Champagne-Ardenne19, University of Copenhagen20, Medical University of Silesia21, Curie Institute22, Aberdeen Royal Infirmary23, University College Dublin24, Charité25, Charles University in Prague26, University College London27, University of Freiburg28, Peking Union Medical College29
TL;DR: PCs are complex tumors which require a multidisciplinary approach and long-term follow-up, and may be considered as first-line systemic antiproliferative treatment in unresectable PCs, particularly of low-grade TC and AC.
505 citations
TL;DR: Combined use of low-dose spiral CT and selective PET effectively detects early lung cancer in high-risk individuals in a large cohort of high- risk volunteers.
447 citations
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TL;DR: Although the Ki‐67 protein is well characterized on the molecular level and extensively used as a proliferation marker, the functional significance still remains unclear; there are indications, however, that Ki‐ 67 protein expression is an absolute requirement for progression through the cell‐division cycle.
Abstract: The expression of the human Ki-67 protein is strictly associated with cell proliferation. During interphase, the antigen can be exclusively detected within the nucleus, whereas in mitosis most of the protein is relocated to the surface of the chromosomes. The fact that the Ki-67 protein is present during all active phases of the cell cycle (G(1), S, G(2), and mitosis), but is absent from resting cells (G(0)), makes it an excellent marker for determining the so-called growth fraction of a given cell population. In the first part of this study, the term proliferation marker is discussed and examples of the applications of anti-Ki-67 protein antibodies in diagnostics of human tumors are given. The fraction of Ki-67-positive tumor cells (the Ki-67 labeling index) is often correlated with the clinical course of the disease. The best-studied examples in this context are carcinomas of the prostate and the breast. For these types of tumors, the prognostic value for survival and tumor recurrence has repeatedly been proven in uni- and multivariate analysis. The preparation of new monoclonal antibodies that react with the Ki-67 equivalent protein from rodents now extends the use of the Ki-67 protein as a proliferation marker to laboratory animals that are routinely used in basic research. The second part of this review focuses on the biology of the Ki-67 protein. Our current knowledge of the Ki-67 gene and protein structure, mRNA splicing, expression, and cellular localization during the cell-division cycle is summarized and discussed. Although the Ki-67 protein is well characterized on the molecular level and extensively used as a proliferation marker, the functional significance still remains unclear. There are indications, however, that Ki-67 protein expression is an absolute requirement for progression through the cell-division cycle.
4,359 citations
TL;DR: This new adenocarcinoma classification is needed to provide uniform terminology and diagnostic criteria, especially for bronchioloalveolar carcinoma (BAC), the overall approach to small nonresection cancer specimens, and for multidisciplinary strategic management of tissue for molecular and immunohistochemical studies.
3,850 citations
TL;DR: It is shown that the tumour type is characterized by complex genomic alterations, with a mean of 360 exonic mutations, 165 genomic rearrangements, and 323 segments of copy number alteration per tumour.
Abstract: Lung squamous cell carcinoma is a common type of lung cancer, causing approximately 400,000 deaths per year worldwide. Genomic alterations in squamous cell lung cancers have not been comprehensively characterized, and no molecularly targeted agents have been specifically developed for its treatment. As part of The Cancer Genome Atlas, here we profile 178 lung squamous cell carcinomas to provide a comprehensive landscape of genomic and epigenomic alterations. We show that the tumour type is characterized by complex genomic alterations, with a mean of 360 exonic mutations, 165 genomic rearrangements, and 323 segments of copy number alteration per tumour. We find statistically recurrent mutations in 11 genes, including mutation of TP53 in nearly all specimens. Previously unreported loss-of-function mutations are seen in the HLA-A class I major histocompatibility gene. Significantly altered pathways included NFE2L2 and KEAP1 in 34%, squamous differentiation genes in 44%, phosphatidylinositol-3-OH kinase pathway genes in 47%, and CDKN2A and RB1 in 72% of tumours. We identified a potential therapeutic target in most tumours, offering new avenues of investigation for the treatment of squamous cell lung cancers.
3,356 citations
Memorial Sloan Kettering Cancer Center1, French Institute of Health and Medical Research2, Columbia University Medical Center3, Icahn School of Medicine at Mount Sinai4, Brigham and Women's Hospital5, University of Pittsburgh6, Fox Chase Cancer Center7, University of Mississippi Medical Center8, University of Colorado Boulder9, Aberdeen Royal Infirmary10, University of Tsukuba11, University of Texas MD Anderson Cancer Center12
TL;DR: The 2015 World Health Organization (WHO) Classification of Tumors of the Lung, Pleura, Thymus and Heart has just been published with numerous important changes from the 2004 WHO classification.
3,029 citations
TL;DR: Somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B are found.
Abstract: Determining the genetic basis of cancer requires comprehensive analyses of large collections of histopathologically well-classified primary tumours. Here we report the results of a collaborative study to discover somatic mutations in 188 human lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are probably involved in carcinogenesis. The frequently mutated genes include tyrosine kinases, among them the EGFR homologue ERBB4; multiple ephrin receptor genes, notably EPHA3; vascular endothelial growth factor receptor KDR; and NTRK genes. These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers--including NF1, APC, RB1 and ATM--and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B. The observed mutational profiles correlate with clinical features, smoking status and DNA repair defects. These results are reinforced by data integration including single nucleotide polymorphism array and gene expression array. Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.
2,615 citations