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Berlin Brandenburg

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  • 1
    Language: English
    In: Cancer and Metastasis Reviews, 2010, Vol.29(1), pp.23-36
    Description: Considerable knowledge has accumulated about mutations of the epidermal growth factor receptor (EGFR)-tyrosine kinase domain since these were first identified in 2004. Patients with nonsmall cell lung cancer with this mutation show dramatic clinical responses to treatment with EGFR-tyrosine kinase inhibitors, whose effectiveness has been established recently in large clinical trials. Most of the mechanisms responsible for resistance to treatment, which most responders experience eventually, have been elucidated, and methods to overcome resistance have been developed. In addition to the clinical benefit, understanding EGFR mutations sheds new light on the molecular and pathological aspects of this adenocarcinoma subset, which include frequent development in nonsmokers or females, and particular clusters within the molecular classification in lung cancer. In contrast to the involvement of EGFR mutations in the early stage of lung adenocarcinoma development, EGFR amplification is superimposed on the progression to invasive cancer. In this review, I summarize the clinicopathological characteristics of EGFR mutations in lung cancer. I also provide an overview of the current understanding of the lung adenocarcinoma subset harboring EGFR mutations with special reference to the molecular classification of lung cancer and the novel concept of the “terminal respiratory unit.”
    Keywords: EGFR mutation ; Lung cancer ; Adenocarcinoma ; Molecular classification ; Terminal respiratory unit
    ISSN: 0167-7659
    E-ISSN: 1573-7233
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  • 2
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 11 September 2001, Vol.98(19), pp.10839-10844
    Description: The stem cells that maintain human colon crypts are poorly characterized. To better determine stem cell numbers and how they divide, epigenetic patterns were used as cell fate markers. Methylation exhibits somatic inheritance and random changes that potentially record lifelong stem cell division histories as binary strings or tags in adjacent CpG sites. Methylation tag contents of individual crypts were sampled with bisulfite sequencing at three presumably neutral loci. Methylation increased with aging but varied between crypts and was mosaic within single crypts. Some crypts appeared to be quasi-clonal as they contained more unique tags than expected if crypts were maintained by single immortal stem cells. The complex epigenetic patterns were more consistent with a crypt niche model wherein multiple stem cells were present and replaced through periodic symmetric divisions. Methylation tags provide evidence that normal human crypts are long-lived, accumulate random methylation errors, and contain multiple stem cells that go through "bottlenecks" during life.
    Keywords: Arts -- Applied arts -- Architecture ; Biological sciences -- Biology -- Cytology ; Physical sciences -- Chemistry -- Chemical reactions ; Physical sciences -- Physics -- Microphysics ; Biological sciences -- Biology -- Genetics ; Arts -- Applied arts -- Decorative arts ; Mathematics -- Pure mathematics -- Algebra ; Biological sciences -- Biology -- Zoology ; Mathematics -- Applied mathematics -- Statistics ; Biological sciences -- Biology -- Cytology
    ISSN: 00278424
    E-ISSN: 10916490
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  • 3
    Language: English
    In: Lung Cancer, 2011, Vol.74(1), pp.7-11
    Description: Similar to the adenoma–carcinoma sequence of colorectal cancer, lung adenocarcinoma is thought to follow a linear multistep progression, in which a precursor lesion progresses to adenocarcinoma , which is followed by invasive adenocarcinoma. However, lung adenocarcinoma can no longer be considered as a single type of tumor but rather a group of distinct subsets of tumors that arise from different molecular pathways. Consistent with this concept, recent findings revealed that this linear progression might not occur in all lung adenocarcinomas. First, according to the molecular classification based on expression profiling, lung cancer can be divided into at least two subsets; precancerous and lesions share characteristics of molecular expression and clinical features with only one of the two subsets, suggesting that the linear progression is only applicable to the subset in the molecular classification. Second, when EGFR and KRAS were examined based on the progression steps, the mutation rate of KRAS was disproportionally distributed; however, according to the progression schema, gene alterations should be evenly accumulated along the entire progression. Third, by means of comparative genomic hybridization analysis, some adenocarcinoma revealed gene alterations discontinuous to invasive adenocarcinoma. Finally, there were some clinical observations that support that some lesions escape from the progression. In this review, we hypothesize a novel scenario for the progression of lung adenocarcinoma, which does not support a linear progression schema.
    Keywords: Precancerous Lesion ; Carcinoma in Situ ; Cancer Progression ; Lung Cancer ; Adenocarcinoma ; Tumor ; Medicine
    ISSN: 0169-5002
    E-ISSN: 1872-8332
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  • 4
    Language: English
    In: The Journal of Urology, April 2013, Vol.189(4), pp.e791-e791
    Keywords: Medicine
    ISSN: 0022-5347
    E-ISSN: 1527-3792
    Source: ScienceDirect Journals (Elsevier)
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  • 5
    Language: English
    In: Journal of Thoracic Oncology, April 2015, Vol.10(4), pp.548-550
    Keywords: Medicine
    ISSN: 1556-0864
    E-ISSN: 1556-1380
    Source: ScienceDirect Journals (Elsevier)
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  • 6
    Language: Japanese
    In: Rinsho byori. The Japanese journal of clinical pathology, April 2013, Vol.61(4), pp.328-33
    Description: Patients with SCLC (Small cell lung cancer) have been treated differently from those with NSCLC (New-small cell lung cancer) as a different disease. Recently, even patients with NSCLC are treated differently according to histological subtypes. This change is associated with the development of new drugs, particularly molecular-targeted drugs. Because Bevacizumab can cause serious adverse effects, patients with squamous cell carcinoma histology and a history of hemoptysis are contraindicated for this drug. Pemetrexed has been approved with an anti-mesothelioma drug and was confirmed to be effective for NSCLC. However, its efficacy was not equally proved among the histological subtypes; only adenocarcinoma patients showed shorter progression-free and prolonged survival periods. Regarding tyrosine kinase inhibitors, the targeted gene alterations occur specifically in adenocarcinoma. Based on these findings, the current therapeutic strategy for NSCLC is based on the histological subtype and mutational status of EGFR and ALK. In this article, transition of the therapeutic strategy for NSCLC, characteristics of targeted gene alterations and efficacies of the targeted therapy are reviewed.
    Keywords: Antineoplastic Agents -- Therapeutic Use ; Carcinoma, Non-Small-Cell Lung -- Drug Therapy ; Erbb Receptors -- Genetics ; Lung Neoplasms -- Drug Therapy ; Mutation -- Genetics ; Receptor Protein-Tyrosine Kinases -- Genetics
    ISSN: 0047-1860
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 7
    Language: Japanese
    In: Gan to kagaku ryoho. Cancer & chemotherapy, November 2018, Vol.45(11), pp.1582-1586
    Description: MSI-H tumors are drove with molecular mechanism different from ordinary carcinoma, and thus the morphological features could be distinct. Particularly, MSI-H colorectal carcinoma has peculiar morphological characteristics, which are listed as one of the criteria to recommend MSI-testing. In this article, morphological characteristics and immunohistological detection of MSI-H colorectal cancer are reviewed, with contrasting to those of gynecological tumors.
    Keywords: Microsatellite Instability ; Neoplasms -- Pathology
    ISSN: 0385-0684
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 8
    Language: English
    In: Cancer Research, 07/01/2018, Vol.78(13 Supplement), pp.84-84
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 9
    Language: English
    In: Cancer Research, 04/15/2011, Vol.71(8 Supplement), pp.718-718
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 10
    Language: English
    In: Cancer Research, 04/15/2011, Vol.71(8 Supplement), pp.1120-1120
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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