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xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EThis article discusses the characterization of non-small cell lung cancer (NSCLC), including its histology, biology, and molecular classification, and an integrative approach to its management. Lung cancer was first characterized by Rudolf Virchow in the 1800s as a tumor in the lungs that could be diagnosed by examining a pathological sample. While this definition is still in use today, lung cancer is, in fact, the result of multiple molecular alterations underlying the phenotypic changes observed in the cells.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003ERespiratory Cancers\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ECancer\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EPulmonary Genomics\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EOncology Genomics\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EJean-Charles Soria, MD, PhD, Institut de Canc\u00e9rologie, Gustave Roussy, France, discussed the characterization of non-small cell lung cancer (NSCLC), including its histology, biology, and molecular classification, and an integrative approach to its management. Lung cancer was first characterized by Rudolf Virchow in the 1800s as a tumor in the lungs that could be diagnosed by examining a pathological sample. While this definition is still in use today, lung cancer is, in fact, the result of multiple molecular alterations underlying the phenotypic changes observed in the cells.\u003C\/p\u003E\u003Cp id=\u0022p-3\u0022\u003EProf. Soria explained the background of metastatic NSCLC. To define optimal therapy in daily clinical practice, NSCLC is primarily classified by histology as nonsquamous (adenocarcinoma and large cell carcinoma) or squamous cell carcinoma. He said that with appropriate treatment, the median overall survival for patients with these cancers is \u223c12 months, and patients with anaplastic lymphoma kinase (ALK), reactive oxygen species (ROS), and epidermal growth factor receptor (EGFR) mutations have a median survival of \u223c2 years. A better understanding of tumor biology is critical for selecting therapies that match a cancer\u0027s molecular features. As the cost of sequencing decreases (\u003Ca id=\u0022xref-fig-1-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F1\u0022\u003EFigure 1\u003C\/a\u003E) [MacConaill LE, Garraway LA. \u003Cem\u003EJ Clin Oncol\u003C\/em\u003E 2010], this goal is becoming more feasible.\u003C\/p\u003E\u003Cdiv id=\u0022F1\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/12\/15\/4\/F1.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022DNA Sequencing Costs.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-1965422162\u0022 data-figure-caption=\u0022DNA Sequencing Costs.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 1.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/12\/15\/4\/F1.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/12\/15\/4\/F1.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 1.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/12\/15\/4\/F1.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/14542\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption attrib\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 1.\u003C\/span\u003E \n            \u003Cp id=\u0022p-4\u0022 class=\u0022first-child\u0022\u003EDNA Sequencing Costs.\u003C\/p\u003E\n         \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-1\u0022\u003EReproduced from MacConaill and Garraway. Clinical implications of the Cancer Genome, \u003Cem\u003EJournal of Clinical Oncology\u003C\/em\u003E 2010; 28(35):5219\u20135228. With permission from the American Society of Clinical Oncology.\u003C\/q\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EMolecular Classification of NSCLC\u003C\/h2\u003E\n         \u003Cp id=\u0022p-5\u0022\u003EMost sequencing efforts have focused on adenocarcinomas. Mutations have been found in 67% of adenocarcinomas; KRAS mutations (28%) are the most common, followed by EGFR (13%), serine\/threonine kinase 11 (10%), and several others with an incidence of \u22642% [Planchard D et al. ELCC 2012]. Many of the identified mutations are not actionable, meaning no therapy has been developed to target them. For patients with EGFR and ALK mutations, erlotinib and crizotinib, respectively, have produced significant reductions in tumor burden [Rosell R et al. \u003Cem\u003ELancet Oncol\u003C\/em\u003E 2012; Kwak EL et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2010].\u003C\/p\u003E\n         \u003Cp id=\u0022p-6\u0022\u003ETargeted therapies are not yet available for squamous cell lung cancer. The Cancer Genome Atlas recently published molecular profiling results showing that squamous cell lung cancer is characterized by a high rate of genomic alterations [Cancer Genome Atlas Research Network. \u003Cem\u003ENature\u003C\/em\u003E 2012]. According to Prof. Soria, the fibroblast growth factor receptor 1 (FGFR1) mutation is one potential therapeutic driver in this cancer. FGFR1 mutations are found in 10% of squamous cell lung cancers by comparative genomic hybridization and 22% by fluorescence in situ hybridization [Weiss J et al. \u003Cem\u003ESci Transl Med\u003C\/em\u003E 2010]. FGFR has been targeted by selective (BJG398, AZD 4547, and JNJ-42756493) and nonselective inhibitors (EOS3810 and dovitinib). Potential therapeutic targets and their frequencies in squamous cell lung cancer include FGFR1 (22%), DDR2 (4%), PIK3CA (33%), MET (6%), and BRAF (2%) [Perez-Moreno P et al. \u003Cem\u003EClin Cancer Res\u003C\/em\u003E 2012]. FGFR1\/2, PIK3CA, and DDR2 inhibitor trials are ongoing. In the near future, patients with a lung nodule will not only undergo a tumor biopsy but also comprehensive molecular testing to determine the diagnosis, prognosis, chemotherapy sensitivity, and targeted therapy sensitivity, and to identify new targets.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ETowards an Integrative Approach\u003C\/h2\u003E\n         \u003Cp id=\u0022p-7\u0022\u003EIndividual tumor heterogeneity presents a limitation to developing molecular targets [Meric-Bernstam F, Mills GB. \u003Cem\u003ENat Rev Clin Oncol\u003C\/em\u003E 2012]. Treatment with a drug targeted at a specific alteration will eliminate that particular clone; however, other clones will remain. Further, as a cancer progresses and metastasizes, additional biopsies will need to be performed to identify and target emerging gene alterations. Another issue pertains to the one third of patients without an identified alteration. For these patients, it is important to optimize the use of chemotherapy and radiotherapy, and develop a better understanding of DNA repair. These patients also present an opportunity to develop new immunomodulatory checkpoints and to define predictive biomarkers.\u003C\/p\u003E\n         \u003Cp id=\u0022p-8\u0022\u003EDNA repair pathways are crucial to cell survival. Normal cells have 6 interindependent DNA repair pathways; recent studies have shown that when 1 pathway fails, another takes over. These pathways include base excision repair, nucleotide excision repair, direct repair, mismatch repair, homologous recombination repair, and nonhomologous end-joining repair [Postel-Vinay S et al. \u003Cem\u003ENat Rev Clin Oncol\u003C\/em\u003E 2012].\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003EIn cancer cells, there is at least 1 repair pathway that is often defective [Shaheen M et al. \u003Cem\u003EBlood\u003C\/em\u003E 2011; Postel-Vinay S et al. \u003Cem\u003ENat Rev Clin Oncol\u003C\/em\u003E 2012]. Adenocarcinomas and squamous cell cancers contain different levels of molecules involved in DNA repair. For example, adenocarcinomas express low levels of poly [ADP-ribose] polymerase 1 and breast cancer 1\/2 compared with squamous cell cancers. This is also true for checkpoint kinase 1 expression. These differences can be exploited in the development of DNA repair modulators.\u003C\/p\u003E\n         \u003Cp id=\u0022p-10\u0022\u003EImmunohistochemistry has not been sufficient to identify the presence of a deficient DNA repair pathway in tumor specimens. Prof. Soria has been working on developing a functional DNA repair assay for use on fresh lung tumor specimens, which he believes is necessary for developing and optimizing therapeutics in this area.\u003C\/p\u003E\n         \u003Cp id=\u0022p-11\u0022\u003EImmunogenic modulation is another area with potential for therapeutic development in lung cancer. In addition to cytotoxic T-lymphocyte antigen 4, the programmed death-1 (PD-1) protein and its ligand, PD-L1, are potential targets for which antibodies are currently in development in at least six Phase 1 and 2 trials (\u003Ca id=\u0022xref-table-wrap-1-1\u0022 class=\u0022xref-table\u0022 href=\u0022#T1\u0022\u003ETable 1\u003C\/a\u003E).\u003C\/p\u003E\n         \u003Cdiv id=\u0022T1\u0022 class=\u0022table pos-float\u0022\u003E\u003Cdiv class=\u0022table-inline\u0022\u003E\u003Cdiv class=\u0022callout\u0022\u003E\u003Cspan\u003EView this table:\u003C\/span\u003E\u003Cul class=\u0022callout-links\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022\/\u0022 class=\u0022table-expand-inline\u0022 data-table-url=\u0022\/highwire\/markup\/14543\/expansion?postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media%2Chighwire_embed\u0026amp;table-expand-inline=1\u0022 html=\u00221\u0022 fragment=\u0022#\u0022 external=\u00221\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView inline\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022\/highwire\/markup\/14543\/expansion?width=1000\u0026amp;height=500\u0026amp;iframe=true\u0026amp;postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media\u0022 class=\u0022colorbox colorbox-load table-expand-popup\u0022 rel=\u0022gallery-fragment-tables\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView popup\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/14543\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022table-caption\u0022\u003E\u003Cspan class=\u0022table-label\u0022\u003ETable 1.\u003C\/span\u003E \n               \u003Cp id=\u0022p-12\u0022 class=\u0022first-child\u0022\u003EStudies of Antibodies Targeting PD-1 and PD-L1 Pathways.\u003C\/p\u003E\n            \u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-14\u0022\u003EThe PD-1 antibody BMS-936558 has demonstrated objective response rates of 33% (95% CI, 13% to 59%) in squamous cell cancer and 12.5% (95% CI, 5% to 24%) in NSCLC [Brahmer JR et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2012]. Other recent evidence has shown a correlation between PD-L1 expression in pretreatment tumor biopsies with clinical outcomes in 16 of 42 patients, including those with NSCLC (n=10), melanoma (n=18), colorectal cancer (n=7), renal cell cancer (n=5), or castration-resistant prostate cancer (n=2) [Soliman HH et al. ASCO 2012. Abstract 2501].\u003C\/p\u003E\n         \u003Cp id=\u0022p-15\u0022\u003EProf. Soria concluded that the future of patients with lung cancer depends on the ability to offer them a molecular portrait revealing the specific mutations and amplifications that can then be targeted with existing therapies, such as gefitinib, erlotinib, and afatinib (EGFR inhibitors), crizotinib (ALK and ROS inhibitor), trastuzumab (human epidermal growth factor receptor 2 inhibitor), and BJG398, AZD4547, and EOS3810 (FGFR1 inhibitors). For patients with no identified genetic alterations, treatment relies on standard chemotherapy and radiotherapy. DNA dysfunctionality analysis and new immune checkpoint identification should be pursued in these patients with the goal of entering them into appropriate clinical trials.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2012 MD Conference Express\u00ae\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/12\/15\/4.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_figures.js?nzn7ke\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzn7ke\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_tables.js?nzn7ke\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}