Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress 2023 EHA Congress 2023 ASCO Annual Meeting
Clinical Collections
Advances in Alzheimer’s

Keynote webinar | Spotlight on sleep in brain health

LIVE: Thursday 2nd May 2024, 18:00-19:30 (CEST)

Quality sleep is essential for health. But what happens to our brains when sleep patterns are disturbed? Join our experts to explore the interplay between sleep disruption and neurological diseases, and the questions that you need to be asking your patients to help you prevent the harmful effects of sleep deprivation.
ADVANCED SEARCH
Log in
Top
Cancer and Metastasis Reviews
Published in: Cancer and Metastasis Reviews 2/2015

01-06-2015

Epigenetics in lung cancer diagnosis and therapy

Authors: Aditi Mehta, Stephanie Dobersch, Addi J. Romero-Olmedo, Guillermo Barreto

Published in: Cancer and Metastasis Reviews | Issue 2/2015

Login to get access

Abstract

Lung cancer is the leading cause of cancer-related deaths worldwide. The initiation and progression of lung cancer is the result of the interaction between permanent genetic and dynamic epigenetic alterations. DNA methylation is the best studied epigenetic mark in human cancers. Altered DNA methylation in cancer was identified in 1983. Within 30 years of this discovery, DNA methylation inhibitors are used clinically to treat a variety of cancers, highlighting the importance of the epigenetic basis of cancer. In addition, histone modifications, nucleosome remodeling, and micro RNA (miRNA)-mediated gene regulation are also fundamental to tumor genesis. Distinct chromatin alterations occur in all stages of lung cancer, including initiation, growth, and metastasis. Therefore, stage-specific epigenetic changes can be used as powerful and reliable tools for early diagnosis of lung cancer and to monitor patient prognosis. Moreover, since epigenetic changes are dynamic and reversible, chromatin modifiers are promising targets for the development of more effective therapeutic strategies against cancer. This review summarizes the chromatin alterations in lung cancer, focusing on the diagnostic and therapeutic approaches targeting epigenetic modifications that could help to reduce the high case-fatality rate of this dreadful disease.
Literature
1.
Balgkouranidou, I., Liloglou, T., & Lianidou, E. S. (2013). Lung cancer epigenetics: emerging biomarkers. Biomarkers in Medicine, 7(1), 49–58.PubMedCrossRef
2.
Molina, J. R., et al. (2008). Non-small cell lung cancer: epidemiology, risk factors, treatment, and survivorship. Mayo Clinic Proceedings, 83(5), 584–594.PubMedCentralPubMedCrossRef
3.
Herbst, R. S., Heymach, J. V., & Lippman, S. M. (2008). Lung cancer. New England Journal of Medicine, 359(13), 1367–1380.PubMedCrossRef
4.
5.
Nemeth, A., & Langst, G. (2004). Chromatin higher order structure: opening up chromatin for transcription. Briefings in Functional Genomics & Proteomics, 2(4), 334–343.CrossRef
6.
7.
Brzezianska, E., Dutkowska, A., & Antczak, A. (2013). The significance of epigenetic alterations in lung carcinogenesis. Molecular Biology Reports, 40(1), 309–325.PubMedCentralPubMedCrossRef
8.
Ozturk, N., Singh, I., Mehta, A., Braun, T., & Barreto, G. HMGA proteins as modulators of chromatin structure during transcriptional activation. Frontiers in Cell and Developmental Biology.
9.
10.
11.
Cedar, H., & Bergman, Y. (2009). Linking DNA methylation and histone modification: patterns and paradigms. Nature Reviews Genetics, 10(5), 295–304.PubMedCrossRef
12.
Wang, Y., et al. (2004). Beyond the double helix: writing and reading the histone code. Novartis Foundation Symposium, 259, 3–17. discussion 17–21, 163–9.PubMedCrossRef
13.
Knudson, A. G., Jr. (1971). Mutation and cancer: statistical study of retinoblastoma. Proceedings of the National Academy of Sciences of the United States of America, 68(4), 820–823.PubMedCentralPubMedCrossRef
14.
Kim, H., et al. (2006). Elevated mRNA levels of DNA methyltransferase-1 as an independent prognostic factor in primary nonsmall cell lung cancer. Cancer, 107(5), 1042–1049.PubMedCrossRef
15.
Lin, R. K., et al. (2007). Alteration of DNA methyltransferases contributes to 5′CpG methylation and poor prognosis in lung cancer. Lung Cancer, 55(2), 205–213.PubMedCrossRef
16.
Feinberg, A. P., & Vogelstein, B. (1983). Hypomethylation distinguishes genes of some human cancers from their normal counterparts. Nature, 301(5895), 89–92.PubMedCrossRef
17.
Weber, M., et al. (2005). Chromosome-wide and promoter-specific analyses identify sites of differential DNA methylation in normal and transformed human cells. Nature Genetics, 37(8), 853–862.PubMedCrossRef
18.
Rauch, T. A., et al. (2008). High-resolution mapping of DNA hypermethylation and hypomethylation in lung cancer. Proceedings of the National Academy of Sciences of the United States of America, 105(1), 252–257.PubMedCentralPubMedCrossRef
19.
Lander, E. S., et al. (2001). Initial sequencing and analysis of the human genome. Nature, 409(6822), 860–921.PubMedCrossRef
20.
Gaudet, F., et al. (2003). Induction of tumors in mice by genomic hypomethylation. Science, 300(5618), 489–492.PubMedCrossRef
21.
Gupta, P. K., et al. (1997). High frequency in vivo loss of heterozygosity is primarily a consequence of mitotic recombination. Cancer Research, 57(6), 1188–1193.PubMed
22.
23.
24.
Kim, M., et al. (2004). Dnmt1 deficiency leads to enhanced microsatellite instability in mouse embryonic stem cells. Nucleic Acids Research, 32(19), 5742–5749.PubMedCentralPubMedCrossRef
25.
26.
27.
28.
Dupuy, A. J., et al. (2005). Mammalian mutagenesis using a highly mobile somatic Sleeping Beauty transposon system. Nature, 436(7048), 221–226.PubMedCrossRef
29.
Collier, L. S., et al. (2005). Cancer gene discovery in solid tumours using transposon-based somatic mutagenesis in the mouse. Nature, 436(7048), 272–276.PubMedCrossRef
30.
31.
Lujambio, A., et al. (2010). CpG island hypermethylation-associated silencing of non-coding RNAs transcribed from ultraconserved regions in human cancer. Oncogene, 29(48), 6390–6401.PubMedCentralPubMedCrossRef
32.
Lin, S. H., et al. (2014). Genes suppressed by DNA methylation in non-small cell lung cancer reveal the epigenetics of epithelial-mesenchymal transition. BMC Genomics, 15, 1079.PubMedCentralPubMedCrossRef
33.
Thiery, J. P., et al. (2009). Epithelial-mesenchymal transitions in development and disease. Cell, 139(5), 871–890.PubMedCrossRef
34.
35.
Le Bras, G. F., Taubenslag, K. J., & Andl, C. D. (2012). The regulation of cell-cell adhesion during epithelial-mesenchymal transition, motility and tumor progression. Cell Adhesion & Migration, 6(4), 365–373.CrossRef
36.
Richardson, F., et al. (2012). The evaluation of E-Cadherin and vimentin as biomarkers of clinical outcomes among patients with non-small cell lung cancer treated with erlotinib as second- or third-line therapy. Anticancer Research, 32(2), 537–552.PubMed
37.
Xiao, D., & He, J. (2010). Epithelial mesenchymal transition and lung cancer. Journal of Thoracic Disease, 2(3), 154–159.PubMedCentralPubMed
38.
Singh, A., & Settleman, J. (2010). EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer. Oncogene, 29(34), 4741–4751.PubMedCentralPubMedCrossRef
39.
40.
Yang, J., et al. (2004). Twist, a master regulator of morphogenesis, plays an essential role in tumor metastasis. Cell, 117(7), 927–939.PubMedCrossRef
41.
Tran, P. T., et al. (2012). Twist1 suppresses senescence programs and thereby accelerates and maintains mutant Kras-induced lung tumorigenesis. PLoS Genetics, 8(5), e1002650.PubMedCentralPubMedCrossRef
42.
De Craene, B., & Berx, G. (2013). Regulatory networks defining EMT during cancer initiation and progression. Nature Reviews Cancer, 13(2), 97–110.PubMedCrossRef
43.
Van’t Westeinde, S. C., & van Klaveren, R. J. (2011). Screening and early detection of lung cancer. Cancer Journal, 17(1), 3–10.CrossRef
44.
Mulshine, J. L. (2003). Screening for lung cancer: in pursuit of pre-metastatic disease. Nature Reviews Cancer, 3(1), 65–73.PubMedCrossRef
45.
Marshall, H. M., et al. (2013). Screening for lung cancer with low-dose computed tomography: a review of current status. Journal of Thoracic Disease, 5(Suppl 5), S524–S539.PubMedCentralPubMed
46.
Siegel, R., Naishadham, D., & Jemal, A. (2013). Cancer statistics, 2013. CA: A Cancer Journal for Clinicians, 63(1), 11–30.
47.
Ahrendt, S. A., et al. (1999). Molecular detection of tumor cells in bronchoalveolar lavage fluid from patients with early stage lung cancer. Journal of the National Cancer Institute, 91(4), 332–339.PubMedCrossRef
48.
Selamat, S. A., et al. (2011). DNA methylation changes in atypical adenomatous hyperplasia, adenocarcinoma in situ, and lung adenocarcinoma. PLoS One, 6(6), e21443.PubMedCentralPubMedCrossRef
49.
Yanagawa, N., et al. (2003). Promoter hypermethylation of tumor suppressor and tumor-related genes in non-small cell lung cancers. Cancer Science, 94(7), 589–592.PubMedCrossRef
50.
Pulling, L. C., et al. (2003). Promoter hypermethylation of the O6-methylguanine-DNA methyltransferase gene: more common in lung adenocarcinomas from never-smokers than smokers and associated with tumor progression. Cancer Research, 63(16), 4842–4848.PubMed
51.
Kim, J. S., et al. (2005). Aberrant methylation of H-cadherin (CDH13) promoter is associated with tumor progression in primary nonsmall cell lung carcinoma. Cancer, 104(9), 1825–1833.PubMedCrossRef
52.
Lin, Q., et al. (2009). RASSF1A, APC, ESR1, ABCB1 and HOXC9, but not p16INK4A, DAPK1, PTEN and MT1G genes were frequently methylated in the stage I non-small cell lung cancer in China. Journal of Cancer Research and Clinical Oncology, 135(12), 1675–1684.PubMedCrossRef
53.
Kneip, C., et al. (2011). SHOX2 DNA methylation is a biomarker for the diagnosis of lung cancer in plasma. Journal of Thoracic Oncology, 6(10), 1632–1638.PubMedCrossRef
54.
Tsou, J. A., et al. (2007). Identification of a panel of sensitive and specific DNA methylation markers for lung adenocarcinoma. Molecular Cancer, 6, 70.PubMedCentralPubMedCrossRef
55.
Niklinska, W., et al. (2009). Prognostic significance of DAPK and RASSF1A promoter hypermethylation in non-small cell lung cancer (NSCLC). Folia Histochemica et Cytobiologica, 47(2), 275–280.PubMedCrossRef
56.
Risse, E. K., et al. (1985). Sputum cytology by the Saccomanno method in diagnosing lung malignancy. Diagnostic Cytopathology, 1(4), 286–291.PubMedCrossRef
57.
Hubers, A. J., et al. (2014). Combined sputum hypermethylation and eNose analysis for lung cancer diagnosis. Journal of Clinical Pathology, 67(8), 707–711.PubMedCrossRef
58.
Leng, S., et al. (2012). Defining a gene promoter methylation signature in sputum for lung cancer risk assessment. Clinical Cancer Research, 18(12), 3387–3395.PubMedCentralPubMedCrossRef
59.
Wang, Y. C., et al. (2003). Inactivation of hMLH1 and hMSH2 by promoter methylation in primary non-small cell lung tumors and matched sputum samples. Journal of Clinical Investigation, 111(6), 887–895.PubMedCentralPubMedCrossRef
60.
Liu, Y., et al. (2003). Hypermethylation of p16INK4a in Chinese lung cancer patients: biological and clinical implications. Carcinogenesis, 24(12), 1897–1901.PubMedCrossRef
61.
Destro, A., et al. (2004). K-ras and p16(INK4A)alterations in sputum of NSCLC patients and in heavy asymptomatic chronic smokers. Lung Cancer, 44(1), 23–32.PubMedCrossRef
62.
Belinsky, S. A., et al. (2007). Predicting gene promoter methylation in non-small-cell lung cancer by evaluating sputum and serum. British Journal of Cancer, 96(8), 1278–1283.PubMedCentralPubMedCrossRef
63.
Cirincione, R., et al. (2006). Methylation profile in tumor and sputum samples of lung cancer patients detected by spiral computed tomography: a nested case–control study. International Journal of Cancer, 118(5), 1248–1253.CrossRef
64.
Ammanagi, A. S., et al. (2012). Sputum cytology in suspected cases of carcinoma of lung (Sputum cytology a poor man’s bronchoscopy!). Lung India, 29(1), 19–23.PubMedCentralPubMedCrossRef
65.
Hsu, H. S., et al. (2007). Characterization of a multiple epigenetic marker panel for lung cancer detection and risk assessment in plasma. Cancer, 110(9), 2019–2026.PubMedCrossRef
66.
Suga, Y., et al. (2008). Quantitative p16 and ESR1 methylation in the peripheral blood of patients with non-small cell lung cancer. Oncology Reports, 20(5), 1137–1142.PubMed
67.
Bearzatto, A., et al. (2002). p16(INK4A) Hypermethylation detected by fluorescent methylation-specific PCR in plasmas from non-small cell lung cancer. Clinical Cancer Research, 8(12), 3782–3787.PubMed
68.
Russo, A. L., et al. (2005). Differential DNA hypermethylation of critical genes mediates the stage-specific tobacco smoke-induced neoplastic progression of lung cancer. Clinical Cancer Research, 11(7), 2466–2470.PubMedCrossRef
69.
Hanahan, D., & Weinberg, R. A. (2011). Hallmarks of cancer: the next generation. Cell, 144(5), 646–674.PubMedCrossRef
70.
Boedeker, E., Friedel, G., & Walles, T. (2012). Sniffer dogs as part of a bimodal bionic research approach to develop a lung cancer screening. Interactive Cardiovascular and Thoracic Surgery, 14(5), 511–515.PubMedCentralPubMedCrossRef
71.
Rattray, N. J., et al. (2014). Taking your breath away: metabolomics breathes life in to personalized medicine. Trends in Biotechnology, 32(10), 538–548.PubMedCrossRef
72.
Dent, A. G., Sutedja, T. G., & Zimmerman, P. V. (2013). Exhaled breath analysis for lung cancer. Journal of Thoracic Disease, 5(Suppl 5), S540–S550.PubMedCentralPubMed
73.
Xiao, P., et al. (2014). Methylation of P16 in exhaled breath condensate for diagnosis of non-small cell lung cancer. Lung Cancer, 83(1), 56–60.PubMedCrossRef
74.
Han, W., et al. (2009). Gene promoter methylation assayed in exhaled breath, with differences in smokers and lung cancer patients. Respiratory Research, 10, 86.PubMedCentralPubMedCrossRef
75.
Filipowicz, W., Bhattacharyya, S. N., & Sonenberg, N. (2008). Mechanisms of post-transcriptional regulation by microRNAs: are the answers in sight? Nature Reviews Genetics, 9(2), 102–114.PubMedCrossRef
76.
77.
Calin, G. A., et al. (2004). MicroRNA profiling reveals distinct signatures in B cell chronic lymphocytic leukemias. Proceedings of the National Academy of Sciences of the United States of America, 101(32), 11755–11760.PubMedCentralPubMedCrossRef
78.
Lu, J., et al. (2005). MicroRNA expression profiles classify human cancers. Nature, 435(7043), 834–838.PubMedCrossRef
79.
80.
Johnson, S. M., et al. (2005). RAS is regulated by the let-7 microRNA family. Cell, 120(5), 635–647.PubMedCrossRef
81.
Takamizawa, J., et al. (2004). Reduced expression of the let-7 microRNAs in human lung cancers in association with shortened postoperative survival. Cancer Research, 64(11), 3753–3756.PubMedCrossRef
82.
Hayashita, Y., et al. (2005). A polycistronic microRNA cluster, miR-17-92, is overexpressed in human lung cancers and enhances cell proliferation. Cancer Research, 65(21), 9628–9632.PubMedCrossRef
83.
84.
Boeri, M., et al. (2011). MicroRNA signatures in tissues and plasma predict development and prognosis of computed tomography detected lung cancer. Proceedings of the National Academy of Sciences of the United States of America, 108(9), 3713–3718.PubMedCentralPubMedCrossRef
85.
86.
Nair, V. S., Maeda, L. S., & Ioannidis, J. P. (2012). Clinical outcome prediction by microRNAs in human cancer: a systematic review. Journal of the National Cancer Institute, 104(7), 528–540.PubMedCentralPubMedCrossRef
87.
Cagle, P. T., & Chirieac, L. R. (2012). Advances in treatment of lung cancer with targeted therapy. Archives of Pathology and Laboratory Medicine, 136(5), 504–509.PubMedCrossRef
88.
(2011) In The diagnosis and treatment of lung cancer (Update). Cardiff (UK).
89.
Schuchert, M. J., et al. (2010). Sublobar resection for early-stage lung cancer. Seminars in Thoracic and Cardiovascular Surgery, 22(1), 22–31.PubMedCrossRef
90.
Sonke, J. J., & Belderbos, J. (2010). Adaptive radiotherapy for lung cancer. Seminars in Radiation Oncology, 20(2), 94–106.PubMedCrossRef
91.
Pfister, D. G., et al. (2004). American Society of Clinical Oncology treatment of unresectable non-small-cell lung cancer guideline: update 2003. Journal of Clinical Oncology, 22(2), 330–353.PubMedCrossRef
92.
Simone, C. B., 2nd, et al. (2013). Stereotactic body radiation therapy for lung cancer. Chest, 143(6), 1784–1790.PubMedCrossRef
93.
94.
Ma, P.C. (2012). Personalized targeted therapy in advanced non-small cell lung cancer. Cleveland Clinic Journal of Medicine, (79 Electronic Suppl 1), eS56–60.
95.
Sandler, A., et al. (2006). Paclitaxel-carboplatin alone or with bevacizumab for non-small-cell lung cancer. New England Journal of Medicine, 355(24), 2542–2550.PubMedCrossRef
96.
97.
98.
99.
Chuang, J. C., & Jones, P. A. (2007). Epigenetics and microRNAs. Pediatric Research, 61(5 Pt 2), 24R–29R.PubMedCrossRef
100.
Dawson, M. A., & Kouzarides, T. (2012). Cancer epigenetics: from mechanism to therapy. Cell, 150(1), 12–27.PubMedCrossRef
101.
Keohane, C., Mesa, R., & Harrison, C. (2013). The role of JAK1/2 inhibitors in the treatment of chronic myeloproliferative neoplasms. American Society of Clinical Oncology Educational Book, 301–305.
102.
103.
Lyko, F., & Brown, R. (2005). DNA methyltransferase inhibitors and the development of epigenetic cancer therapies. Journal of the National Cancer Institute, 97(20), 1498–1506.PubMedCrossRef
104.
105.
Christman, J. K. (2002). 5-Azacytidine and 5-aza-2′-deoxycytidine as inhibitors of DNA methylation: mechanistic studies and their implications for cancer therapy. Oncogene, 21(35), 5483–5495.PubMedCrossRef
106.
Komashko, V. M., & Farnham, P. J. (2010). 5-azacytidine treatment reorganizes genomic histone modification patterns. Epigenetics, 5(3), 229–240.PubMedCrossRef
107.
Kim, H. J., & Bae, S. C. (2011). Histone deacetylase inhibitors: molecular mechanisms of action and clinical trials as anti-cancer drugs. American Journal of Translational Research, 3(2), 166–179.PubMedCentralPubMed
108.
Brazelle, W., et al. (2010). Histone deacetylase inhibitors downregulate checkpoint kinase 1 expression to induce cell death in non-small cell lung cancer cells. PLoS One, 5(12), e14335.PubMedCentralPubMedCrossRef
109.
Tang, Y. A., et al. (2010). A novel histone deacetylase inhibitor exhibits antitumor activity via apoptosis induction, F-actin disruption and gene acetylation in lung cancer. PLoS One, 5(9), e12417.PubMedCentralPubMedCrossRef
110.
Perrino, E., et al. (2008). New sulfurated derivatives of valproic acid with enhanced histone deacetylase inhibitory activity. Bioorganic and Medicinal Chemistry Letters, 18(6), 1893–1897.PubMedCrossRef
111.
Tesei, A., et al. (2012). Organosulfur derivatives of the HDAC inhibitor valproic acid sensitize human lung cancer cell lines to apoptosis and to cisplatin cytotoxicity. Journal of Cellular Physiology, 227(10), 3389–3396.PubMedCrossRef
112.
Zhang, W., et al. (2009). Histone deacetylase inhibitor romidepsin enhances anti-tumor effect of erlotinib in non-small cell lung cancer (NSCLC) cell lines. Journal of Thoracic Oncology, 4(2), 161–166.PubMedCentralPubMedCrossRef
113.
Karthik, S., et al. (2014). Romidepsin induces cell cycle arrest, apoptosis, histone hyperacetylation and reduces matrix metalloproteinases 2 and 9 expression in bortezomib sensitized non-small cell lung cancer cells. Biomedicine and Pharmacotherapy, 68(3), 327–334.PubMedCrossRef
114.
Papeleu, P., et al. (2003). Trichostatin A induces differential cell cycle arrests but does not induce apoptosis in primary cultures of mitogen-stimulated rat hepatocytes. Journal of Hepatology, 39(3), 374–382.PubMedCrossRef
115.
Mukhopadhyay, N. K., et al. (2006). Effectiveness of trichostatin A as a potential candidate for anticancer therapy in non-small-cell lung cancer. Annals of Thoracic Surgery, 81(3), 1034–1042.PubMedCrossRef
116.
Platta, C. S., et al. (2007). The HDAC inhibitor trichostatin A inhibits growth of small cell lung cancer cells. Journal of Surgical Research, 142(2), 219–226.PubMedCrossRef
117.
Juergens, R.A., & Rudin, C.M. (2013). Aberrant epigenetic regulation: a central contributor to lung carcinogenesis and a new therapeutic target. American Society of Clinical Oncology Educational Book.
118.
Petta, V., et al. (2013). Histones and lung cancer: are the histone deacetylases a promising therapeutic target? Cancer Chemotherapy and Pharmacology, 72(5), 935–952.PubMedCrossRef
119.
Li, C. T., et al. (2011). Vorinostat, SAHA, represses telomerase activity via epigenetic regulation of telomerase reverse transcriptase in non-small cell lung cancer cells. Journal of Cellular Biochemistry, 112(10), 3044–3053.PubMedCrossRef
120.
Forde, P. M., Brahmer, J. R., & Kelly, R. J. (2014). New strategies in lung cancer: epigenetic therapy for non-small cell lung cancer. Clinical Cancer Research, 20(9), 2244–2248.PubMedCentralPubMedCrossRef
121.
Belinsky, S. A., et al. (2011). Combination therapy with Vidaza and entinostat suppresses tumor growth and reprograms the epigenome in an orthotopic lung cancer model. Cancer Research, 71(2), 454–462.PubMedCentralPubMedCrossRef
122.
Noro, R., et al. (2007). PTEN inactivation in lung cancer cells and the effect of its recovery on treatment with epidermal growth factor receptor tyrosine kinase inhibitors. International Journal of Oncology, 31(5), 1157–1163.PubMed
123.
Peipp, M., et al. (2002). A recombinant CD7-specific single-chain immunotoxin is a potent inducer of apoptosis in acute leukemic T cells. Cancer Research, 62(10), 2848–2855.PubMed
124.
Deng, X. K., Nesbit, L. A., & Morrow, K. J., Jr. (2003). Recombinant single-chain variable fragment antibodies directed against Clostridium difficile toxin B produced by use of an optimized phage display system. Clinical and Diagnostic Laboratory Immunology, 10(4), 587–595.PubMedCentralPubMed
125.
126.
Wang, R., et al. (2013). Engineering production of functional scFv antibody in E. coli by co-expressing the molecule chaperone Skp. Frontiers in Cellular and Infection Microbiology, 3, 72.PubMedCentralPubMed
127.
128.
Xu, X., et al. (2012). Evidence for type II cells as cells of origin of K-Ras-induced distal lung adenocarcinoma. Proceedings of the National Academy of Sciences of the United States of America, 109(13), 4910–4915.PubMedCentralPubMedCrossRef
129.
Oh, Y. K., & Park, T. G. (2009). siRNA delivery systems for cancer treatment. Advanced Drug Delivery Reviews, 61(10), 850–862.PubMedCrossRef
Metadata
Title
Epigenetics in lung cancer diagnosis and therapy
Authors
Aditi Mehta
Stephanie Dobersch
Addi J. Romero-Olmedo
Guillermo Barreto
Publication date
01-06-2015
Publisher
Springer US
Published in
Cancer and Metastasis Reviews / Issue 2/2015
Print ISSN: 0167-7659
Electronic ISSN: 1573-7233
DOI
https://doi.org/10.1007/s10555-015-9563-3

Other articles of this Issue 2/2015

Cancer and Metastasis Reviews 2/2015 Go to the issue

OriginalPaper

Application of clinical bioinformatics in lung cancer-specific biomarkers

OriginalPaper

Radiation therapy for oligometastatic non-small cell lung cancer

OriginalPaper

Targeting roles of inflammatory microenvironment in lung cancer and metastasis

OriginalPaper

New strategies to develop new medications for lung cancer and metastasis

Erratum

Erratum to: Association of chromosome 19 to lung cancer genotypes and phenotypes

OriginalPaper

Nanomedicine as an emerging platform for metastatic lung cancer therapy
Webinar | 19-02-2024 | 17:30 (CET)

Keynote webinar | Spotlight on antibody–drug conjugates in cancer

Watch now

Antibody–drug conjugates (ADCs) are novel agents that have shown promise across multiple tumor types. Explore the current landscape of ADCs in breast and lung cancer with our experts, and gain insights into the mechanism of action, key clinical trials data, existing challenges, and future directions.

Dr. Véronique Diéras
Prof. Fabrice Barlesi
Developed by: Springer Medicine
Image Credits