Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Radiation recall dermatitis is characterized by an inflammatory reaction within a previously irradiated volume after administration of a drug. Antineoplastic drugs have mainly been involved in radiation recall reactions. This phenomenon is well known but poorly understood. Many hypotheses as stem-cell depletion in the radiotherapy field, heritable mutations within surviving stem cells, local vascular changes as well as a drug hypersensitivity reaction have been proposed to explain these reactions. In this report, we describe a non-small cell lung cancer patient treated with a carboplatin plus gemcitabine combination chemotherapy as first line followed by pemetrexed as second line therapy. Twenty-five years ago, she completed radiation therapy for breast cancer. Three days after the first cycle of pemetrexed, she presented with a radiation recall dermatitis. As EGFR-staining was negative, we rechallenged the patient with pemetrexed. Unfortunately, although less intense, we faced a recurrence of the skin reaction and pemetrexed was no longer continued.
Lung Cancer 2006 Dec
PMID:Unsuccessful rechallenge with pemetrexed after a previous radiation recall dermatitis. 1704 69

Lung cancer is the most common cause of cancer-related deaths worldwide, and the discovery and implementation of more effective therapy remains challenging. The development of agents that target the epidermal growth factor receptor/human epidermal growth factor receptor 1 (EGFR/HER1) signal transduction pathway have provided a class of novel targeted therapies that are applicable in the treatment of non-small-call lung cancer (NSCLC). Current challenges include the determination of how best these promising new agents can be integrated into current methods of treatment for patients with NSCLC, and clarification of the extent to which early lines of treatment can influence outcome in the later stages.
Lung Cancer 2006 Dec
PMID:Integrating new targeted agents into the treatment of non-small-cell lung cancer. 1705 50

We have investigated 26 adenosquamous lung cancer tissues and found that four EGFR mutations were mainly in female and non-smoker lung cancer. However, EGFR mutation at kinase domain was exclusive with K-ras mutation. However, smoking and gender status could affect the occurrence of EGFR mutation. There was no difference in EGFR mutation status if analysis was performed in never smoker female subgroup.
Lung Cancer 2007 Jan
PMID:Mutation of epidermal growth factor receptor gene in adenosquamous carcinoma of the lung. 1650 85

Erlotinib, a potent inhibitor of the tyrosine-kinase (TK) activity of human epidermal growth factor receptor (HER1/EGFR), produces significant survival and quality of life benefits in patients with previously treated advanced-stage non-small-cell lung cancer. Although the survival benefit from erlotinib was observed in varied subgroups of patients, the radiographic responses were more common in certain patient subgroups, such as women, never-smokers, patients with adenocarcinoma histology, patients of Asian ethnicity, and patients with presence of HER1/EGFR TK domain mutations. Herein, we describe a white male former smoker with advancedstage squamous cell non-small-cell lung cancer, who responded to first-line erlotinib. A molecular analysis of the tumor did not reveal HER1/EGFR TK mutations. This case study, along with subgroup analyses of the BR.21 phase III study, suggests that patients should not be selected for erlotinib treatment based only on characteristics, such as smoking status, tumor histology, HER1/EGFR TK mutation status, sex, or ethnicity.
Clin Lung Cancer 2006 Nov
PMID:Response to erlotinib in first-line treatment of non-small-cell lung cancer in a white male smoker with squamous-cell histology. 1723 98

Biphasic pulmonary blastoma is a rare lung tumor with epithelial and mesenchymal components. Genetic alterations in this tumor are largely unknown, except for the presence of beta-catenin and p53 mutations and the absence of KRAS mutation. To understand the molecular process of histogenesis of this tumor, a whole genome allelic imbalance (AI) scanning using a high-resolution single nucleotide polymorphism array as well as mutational analysis of the p53, EGFR, KRAS and beta-catenin genes were performed against the epithelial and mesenchymal components in the primary tumor and a metastatic tumor in a case of pulmonary blastoma. AI at chromosome regions 14q24-q32 and 17p11-p13 and beta-catenin mutation were commonly detected in all tumors. On the other hand, AI at chromosome regions 3p11-p14 and 9p21-p24 and p53 mutation were detected only in the mesenchymal component in the primary tumor but not in the epithelial component in the primary tumor and the brain metastasis. Likewise, AI at chromosome regions 6p24-p25 and 6q14-q27 was detected in the epithelial component in the primary tumor and the brain metastasis but not in the mesenchymal component in the primary tumor. Furthermore, the genetic alterations detected in the metastatic tumor were completely the same as those in the epithelial component in the primary tumor, indicating that a tumor cell(s) in the epithelial component in the primary tumor selectively metastasized to the brain. These results indicate that this biphasic tumor is of monoclonal origin and the phenotypic heterogeneity of the tumor is due to the differences in the accumulated genetic alterations in each component of the tumor.
Lung Cancer 2007 Jul
PMID:Clonality and heterogeneity of pulmonary blastoma from the viewpoint of genetic alterations: a case report. 1735 Jan 38

In lung adenocarcinomas, genetic alterations of PTEN are relatively rare and little has been reported concerning the relationship between PTEN transcriptional level and clinicopathologic features or genetic changes. This study was conducted to gain insight into clinicopathologic correlations. The transcriptional levels of PTEN were examined using real time RT-PCR and analyzed for correlations with clinicopathologic features and the mutation status of EGFR and KRAS. After confirming significant correlation for PTEN levels between macrodissected and microdissected materials (p<0.01), macrodissected samples from 115 lung adenocarcinomas were examined. There were no significant difference between the PTEN levels, divided into three ranges, and the mutation status of EGFR or KRAS. Noteworthy clinicopathologic correlations between PTEN transcriptional up/down-regulation and young age (p=0.0081, 61.7+/-8.7years versus 66.1+/-8.1years), smoking (p=0.032) and less differentiated adenocarcinomas (p=0.013) were identified. Whereas male patients demonstrated no prognostic association with PTEN levels, female cases with up-regulated PTEN expression had significantly worse survival compared with those with normal PTEN levels (p=0.0027). This study revealed distinct clinicopathologic correlations with PTEN transcriptional up/down-regulation.
Lung Cancer 2007 Aug
PMID:Up-regulation of PTEN at the transcriptional level is an adverse prognostic factor in female lung adenocarcinomas. 1745 61

We report a case of small cell lung cancer (SCLC) developing after prolonged treatment (more than 2 years) for primary adenocarcinoma of the lung, and we show that both the SCLC and non-small cell lung cancer (NSCLC) tissues obtained from the same site share the same deletion in exon 19 of EGFR. This case suggests that the activating EGFR mutations may confer the pathogenesis of a subset of SCLC.
Lung Cancer 2007 Dec
PMID:Sequential occurrence of non-small cell and small cell lung cancer with the same EGFR mutation. 1760 31

It has been proposed that reduced let-7 expression causes RAS expression and correlates with poor survival of lung cancer cases, but little is known about correlations with clinicopathologic features. In this study, we examined 15 early bronchioloalveolar carcinomas (BACs), usually considered as adenocarcinomas in situ, as well as 26 well-differentiated and 25 less-differentiated invasive adenocarcinomas, to assess the association between tumor progression and let-7 expression levels. Additionally, we investigated 47 invasive lung adenocarcinomas for EGFR and KRAS mutations and correlations with let-7 levels. Relative to the corresponding normal lung tissue, reduced let-7 expression was observed in 13 of 15 BACs (87%) and totally in 52 of the 66 adenocarcinomas (79%), suggesting a link with early occurrence in carcinogenesis. On classification of adenocarcinomas into two groups according to let-7 expression, no prognostic or genetic differences were observed. Interestingly, some differences between histological subtypes were observed, such as lower let-7 expression levels in acinar adenocarcinomas and mucinous BACs.
Lung Cancer 2007 Dec
PMID:let-7 microRNA expression is reduced in bronchioloalveolar carcinoma, a non-invasive carcinoma, and is not correlated with prognosis. 1839 92

It has been proposed that stepwise progression occurs from atypical adenomatous hyperplasia (AAH) through bronchioloalveolar carcinoma (BAC) to invasive lung adenocarcinoma. However, the underlying molecular mechanisms have not been identified. We report a patient with a mixed adenocarcinoma of the lung that had different EGFR mutations in the papillary subtype, the acinar subtype, and the surrounding AAH and BAC areas. EGFR mutations may accumulate during tumor progression and lead to heterogeneity of EGFR mutations within the tumor.
Lung Cancer 2008 Apr
PMID:Heterogeneity of epidermal growth factor receptor mutations within a mixed adenocarcinoma lung nodule. 1788 60

This review is focused on "new drugs" that might be developed for thyroid cancer treatment. Thyroid cancer is frequently associated to the activation of specific protein (RET, BRAF) and lipid [PI(3)K] kinases. There is good evidence that these genetic lesions are causative events in thyroid cancer initiation or progression. Therefore, novel compounds able to target these kinases might be useful for thyroid cancer treatment. The power of this approach is witnessed by the examples of BCR-ABL, c-KIT and EGFR inhibitors in the treatment of chronic myelogenous leukemia (CML), gastro-intestinal stromal tumors (GIST) and non-small cell lung carcinoma (NSCLC).
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PMID:New drugs in thyroid cancer. 1789 Dec 51


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