Systemic and Targeted Therapies for Early-Stage Lung Cancer

Byron, Elizabeth; Pinder-Schenck, Mary

doi:10.1177/107327481402100104

Cited by 23 publications

(24 citation statements)

References 90 publications

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“…NSCLC (almost exclusive to AC) is also related to somatic mutations in BRAF gene [2,40] and V600E, G469A, and D549G are considered the most relevant BRAF mutations for the accurate selection of a targeted therapy [55,85]. Generally, BRAF mutations in NSCLC are non-overlapping with other NSCLC-related oncogenic mutations, including EGFR mutations.…”

Section: Mutations In Brafmentioning

confidence: 97%

“…Moreover, BRAF mutations are associated to an increased resistance to EGFR-TKIs treatment [104,105]. The BRAF V600E mutation is usually associated to a lower sensitivity to gefitinib [68], but some studies report that these patients respond to vemurafenib [85,106]. The BRAF inhibitor dabrafenib is also being tested in phase II clinical trials [57,107].…”

Section: Mutations In Brafmentioning

confidence: 97%

“…Currently, there are no FDA-approved anti-KRAS therapies. Several trials have been directed at the specific inhibition of mutant KRAS [40,83,84], where others focused on the inhibition of downstream MAPK and AKT/ PI3K pathways [40,[85][86][87]. Kinase inhibitors (such as MEK or MTOR inhibitors) that target kinases in pathways downstream of RAS may thus be effective against KRAS mutant cells [88].…”

Section: Kras Mutationsmentioning

confidence: 99%

“…Kinase inhibitors (such as MEK or MTOR inhibitors) that target kinases in pathways downstream of RAS may thus be effective against KRAS mutant cells [88]. In particular, the MEK inhibitor, selumetinib combined with docetaxel, demonstrated improved rate of survival at clinical trials [31,85,89].…”

Section: Kras Mutationsmentioning

confidence: 99%

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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

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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

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Section: Mutations In Brafmentioning

confidence: 97%

Section: Mutations In Brafmentioning

confidence: 97%

Section: Kras Mutationsmentioning

confidence: 99%

Section: Kras Mutationsmentioning

confidence: 99%

See 2 more Smart Citations

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

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“…Given the limitations in cisplatin dosing, several clinical trials have been or are currently being conducted to improve lung cancer outcomes using cisplatin in conjunction with other agents such as 5-fluorouracil,[13] gemcitabine,[14] and targeted therapies involving small-molecule inhibitors or monoclonal antibodies. [15-18]…”

Section: Introductionmentioning

confidence: 99%

Prevention of lung cancer recurrence using cisplatin-loaded superhydrophobic nanofiber meshes

Kaplan¹,

et al. 2016

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For early stage lung cancer patients, local cancer recurrence after surgical resection is a significant concern and stems from microscopic disease left behind after surgery. Here we apply a local drug delivery strategy to combat local lung cancer recurrence after resection using non-woven, biodegradable nanofiber meshes loaded with cisplatin. The meshes are fabricated using a scalable electrospinning process from two biocompatible polymers—polycaprolactone and poly(glycerol monostearate-co-caprolactone)—to afford favorable mechanical properties for use in a dynamic tissue such as the lung. Owing to their rough nanostructure and hydrophobic polymer composition, these meshes exhibit superhydrophobicity, and it is this non-wetting nature that sustains the release of cisplatin in a linear fashion over ~90 days, with anti-cancer efficacy demonstrated using an in vitro Lewis Lung carcinoma (LLC) cell assay. The in vivo evaluation of cisplatin-loaded superhydrophobic meshes in the prevention of local cancer recurrence in a murine model of LLC surgical resection demonstrated a statistically significant increase (p = 0.0006) in median recurrence-free survival to >23 days, compared to standard intraperitoneal cisplatin therapy of equivalent dose. These results emphasize the importance of supplementing cytoreductive surgery with local drug delivery strategies to improve prognosis for lung cancer patients undergoing tumor resection.

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SPARC acts as a mediator of TGF‐β1 in promoting epithelial‐to‐mesenchymal transition in A549 and H1299 lung cancer cells

et al. 2018

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Migration and metastasis of tumor cells greatly contributes to the failure of cancer treatment. Recently, the extracellular protein secreted protein acidic and rich in cysteine (SPARC) has been reported closely related to tumorigenesis. Some articles have suggested that SPARC promoted metastasis in several highly metastatic tumors. However, there are also some studies shown that SPARC acted as an antitumor factor. SPARC-induced epithelial-tomesenchymal transition (EMT) in melanoma cells and promoted EMT in hepatocellular carcinoma. Therefore, the role of SPARC in tumorigenesis and its relationship with EMT is still unclear. In this study, we investigated the expression change of SPARC in A549 and H1299 lung cancer cells undergoing EMT process. Our study indicated that SPARC was upregulated in A549 and H1299 cells EMT process. We further investigated the function of SPARC on proliferation, migration, and EMT process of A549 and H1299 cells. Overexpression of SPARC promoted the migration and EMT of A549 and H1299 cells. Knockdown SPARC inhibited the EMT of A549 cells. Overexpression of SPARC induced the increased expression of p-Akt and P-ERK. Furthermore, exogenous SPARC peptide promoted transforming growth factor (TGF)-β1-induced EMT of A549 and H1299 cells. SPARC knockdown partially eliminated TGF-β1 function in inducing EMT of A549 cells. SPARC follistatin-like functional domain reduced the expression of E-cadherin, but had no effect on the expression of p-Akt and p-ERK. In conclusion, we elucidated that SPARC contributes to tumorigenesis by promoting migration and EMT of A549 and H1299 lung cancer cells. These results will provide some new suggestion for lung cancer treatment. © 2018 BioFactors, 44(5):453-464, 2018Abbreviations: A549, A human lung adenocarinoma epithelial cell line; Akt, A serine/threonine-specific protein kinase; BSA, bovine serum albumin; CCK-8, cell counting kit-8; DMEM, Dulbecco's modified Eagle's Medium; EC, extracellular calcium-binding domain; EDTA, ethylenediaminetetraacetic acid; EGFP, enhancer green fluorescent protein; EGF, epidermal growth factor; EMT, epithelial-to-mesenchymal transition; ERK, extracellular signal-regulated kinases; FBS, fetal bovine serum; FS, follistatin-like functional domain; Fyn, Fyn proto-oncogene, Src family tyrosine kinase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; H1299, A human non-small cell lung carcinoma cell line; ILK, integrin-linked kinase; MDM2, mouse double minute 2 homolog; NF-κB, nuclear factor kappa B subunit 1; Nab-PTX, nanoparticle albumin bound paclitaxel; NSCLC, nonsmall cell lung cancer; NT, N terminal acidic domain; PBS, phosphate-buffered saline; PARP, poly (ADP-ribose) polymerase 1; PMSF, phenylmethane sulfonyl fluoride; RIPA, radioimmunoprecipitation assay buffer; SDS, sodium dodecyl sulfate; SPARC, secreted protein acidic and rich in cysteine; TGF-β, transforming growth factor; TBST, a mixture of tris-buffered saline and Tween 20 Additional Supporting Information may be found in the online version of this article.

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Systemic and Targeted Therapies for Early-Stage Lung Cancer

Cited by 23 publications

References 90 publications

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

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

Prevention of lung cancer recurrence using cisplatin-loaded superhydrophobic nanofiber meshes

SPARC acts as a mediator of TGF‐β1 in promoting epithelial‐to‐mesenchymal transition in A549 and H1299 lung cancer cells

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