Beyond EGFR and ALK inhibition: Unravelling and exploiting novel genetic alterations in advanced non small-cell lung cancer

Califano, Raffaele; Abidin, Aidalena Z; Tariq, Noor-ul-Ain; Economopoulou, Panagiota; Metro, Giulio; Mountzios, Giannis

doi:10.1016/j.ctrv.2015.03.009

Cited by 43 publications

(34 citation statements)

References 126 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have identified a number of molecularly distinct subsets of lung cancer characterized by different oncogenes [17][18][19]. Researchers have found tumor mutational frequencies and spectra differences between smokers and nonsmokers, as indicated by the reported differences in the frequency of somatic mutations of EGFR and KRAS observed between smoking and nonsmoking lung cancer patients [20].…”

Section: Discussionmentioning

confidence: 99%

“…Total RNA samples were reverse transcribed into complementary DNA (cDNA) using RevertAid First Strand cDNA Synthesis Kit (Fermentas, St Leon-Rot, Germany). EGFR (exons [18][19][20][21][22], KRAS (exons 2-3), HER2 (exons 18-21), and BRAF (exons [11][12][13][14][15] were amplified by polymerase chain reaction (PCR) using cDNA. Amplified products were analyzed by direct dideoxynucleotide sequencing.…”

Section: Mutation Analysesmentioning

confidence: 99%

See 1 more Smart Citation

Former smokers with non‐small‐cell lung cancers: a comprehensive investigation of clinicopathologic characteristics, oncogenic drivers, and prognosis

et al. 2016

View full text Add to dashboard Cite

The aim of this present investigation was to evaluate the clinicopathologic characteristics, oncogenic drivers, and prognosis of former smokers with non-smallcell lung cancer (NSCLC), and to compare them with those of the current and never smokers. This investigation was a single-institution retrospective study of 2289 NSCLC patients, who were classified as former, current, or never smokers. A collection was made of the clinicopathological characteristics, spectra of wellidentified driver genes and survival rates. The survival rates were compared using log-rank test, and independent prognostic factors, identified using Cox regression analysis. Of 2289 NSCLC patients, 257 (11.2%) were former smokers; 868 (37.9%), current smokers; and 1164 (50.9%), never smokers. Compared with the current, the former were characterized by older age at diagnosis (64.3y vs. 59.9y; P < 0.001), earlier TNM stage (stage I, 47.9% vs. 39.5%; P = 0.017), fewer solid predominance in adenocarcinomas (16.2% vs. 29.5%; P = 0.005), and more EGFR mutation (33.2% vs. 20.7%; P < 0.001) but less KRAS mutation (6.7% vs. 11.9%, P = 0.041). No statistically significant survival differences were observed between the former and current. However, the light former smokers presented favorable overall survival when compared with the light current and heavy former or current (the light former vs. the heavy former, P = 0.028; the light former vs. the light current, P = 0.048; and the light former vs. the heavy current, P = 0.048). Our findings suggest that the former smokers with NSCLCs can have distinctive clinicopathologic characteristics, oncogenic drivers, and prognosis, and they, especially the light former, can benefit from smoking cessation. Cancer Medicine Open Access 2118

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Mutation Analysesmentioning

confidence: 99%

Former smokers with non‐small‐cell lung cancers: a comprehensive investigation of clinicopathologic characteristics, oncogenic drivers, and prognosis

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Vandetanib showed promising results when combined with docetaxel over docetaxel monotherapy (ZODIAC trial -advanced NSCLC), but not when combined with pemetrexed over pemetrexed monotherapy (ZEAL trial) or as monotherapy against erlotinib (ZEST trial) or as second line (after gefitinib or erlotinib (ZEPHYR trial)) compared to placebo [115][116][117][118]. Recently, the interest on vandetanib increased due to the finding of its mechanism of action against RET rearrangements [119].…”

Section: Ret Rearrangementsmentioning

confidence: 99%

Non-small cell lung cancer biomarkers and targeted therapy - two faces of the same coin fostered by nanotechnology

Mendes

Carreira

Baptista

et al. 2016

Expert Review of Precision Medicine and Drug Development

View full text Add to dashboard Cite

Lung cancer is the leading cause of cancer-related mortality in the world, non-small lung cancer (NSCLC) is the most frequent subtype (85% of the cases). Within this subtype, adenocarcinoma and squamous cell carcinoma are the most frequent. New therapeutic strategies based on targeted delivery of drugs have relied on the use of biomarkers derived from the patients' molecular profiling. Several biomarkers have been found to be useful for use as targets for precision therapy in NSCLC, such as mutations in the epidermal growth factor receptor, v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog, anaplastic lymphoma kinase, mesenchymal-epithelial transition factor receptor tyrosine kinase, BRAF, c-ros oncogene 1, P53 and phosphatase with tensin homology. Current developments in Nanomedicine have allowed for multifunctional systems capable of delivering therapeutics with increased precision to the target site/tissue, while simultaneously assisting in diagnosis. Here, we review the use of biomarkers in nanotechnology translation in NSCLC management. ARTICLE HISTORY

show abstract

“…Patients harboring ALK fusions are now standardly treated using TKIs, crizotinib and alectinib, and also have yielded a good therapeutic outcome. Based on these significant successful therapy as with EGFR mutations and ALK fusions, clinical trials have been started for other driver genes, such as RET and ROS1 fusions and HER2 and BRAF mutations 10,16) . Oncogenic RET fusions were identified in a small subset of LADC (1-2%) by us and others [17][18][19] .…”

Section: Ladcmentioning

confidence: 99%

Advances in targeted therapy and immunotherapy for treatment of lung cancer

Saito

Takenoshita

2016

Ann. Cancer Res. Therap.

View full text Add to dashboard Cite

Personalized therapy based on targetable genetic aberrations has become a standard therapy for cases of lung adenocarcinoma (LADC) harboring EGFR mutations and ALK fusions. The effects of such personalized therapy are significantly positive with a higher response rate and longer survival compared to conventional chemotherapy. Therefore, further identification of druggable genetic aberrations and the development of molecular targeting drugs for them are required. For LADC, several new targeted drugs against driver mutations in EGFR, KRAS, HER2, and BRAF; and driver fusions involving ALK, RET, and ROS1 have been developed, and clinical trials of these new targeted drugs are currently being conducted. On the other hand, personalized therapy against driver mutations has not well progressed in squamous cell lung cancer and small cell lung cancer. For those subtypes, immunotherapy might be an effective treatment strategy.

show abstract

Beyond EGFR and ALK inhibition: Unravelling and exploiting novel genetic alterations in advanced non small-cell lung cancer

Cited by 43 publications

References 126 publications

Former smokers with non‐small‐cell lung cancers: a comprehensive investigation of clinicopathologic characteristics, oncogenic drivers, and prognosis

Former smokers with non‐small‐cell lung cancers: a comprehensive investigation of clinicopathologic characteristics, oncogenic drivers, and prognosis

Non-small cell lung cancer biomarkers and targeted therapy - two faces of the same coin fostered by nanotechnology

Advances in targeted therapy and immunotherapy for treatment of lung cancer

Contact Info

Product

Resources

About