The association between hypocholesterolemia and lung cancer risk has been confirmed in some studies. The purpose of the study was to determine whether preoperative hypocholesterolemia (below normal range) is a prognostic factor for survival after nonsmall cell lung cancer (NSCLC) resection. Two hundred and sixty-two consecutive cases of resected NSCLC with a followup period for more than 5 years were reviewed retrospectively. In our results, there were only 13/262 patients having hypocholesterolemia. A significant association was observed between preoperative hypocholesterolemia and patients' survival. However, we failed to find the prognostic significance of preoperative hypocholesterolemia by univariate analysis. No statistical differences were also found by the comparison between 5-year survivors and the others. Our data indicates a trend toward an association between preoperative hypocholesterolemia and poorer survival in NSCLC; however, it did not reach statistical significance.

Masaki Tomita

Takanori Ayabe

Tetsuya Shimizu

Kunihide Nakamura

Preoperative Total Serum Cholesterol and Patients' Survival in Resected Nonsmall Cell Lung Cancer

Objective. Gefitinib often induces liver damage. A few reports have described that the subsequent administration of erlotinib was associated with less hepatotoxicity, but the safety and efficacy of this treatment are still not fully investigated. Therefore, we evaluated retrospectively the patients with erlotinib following gefitinib-induced hepatotoxicity. Methods and Patients. We retrospectively reviewed the medical records between December 2007 and March 2010. The patients were evaluated including the following information: age, gender, histology of lung cancer, performance status, smoking status, epidermal growth factor receptor (EGFR) mutation status, liver metastasis, viral hepatitis, alcoholic liver injury, clinical response, and hepatotoxicity due to EGFR tyrosine kinase inhibitors. Results. We identified 8 patients with erlotinib following gefitinib-induced hepatotoxicity. All achieved disease control by gefitinib. Hepatotoxicity was grades 2 and 3 in 3 and 5 patients, respectively. The median duration of treatment with gefitinib was 112.5 days and the median time to gefitinib-induced hepatotoxicity was 51.5 days. The median duration of treatment with erlotinib was 171.5 days. Grade 1 and 2 erlotinib-induced hepatotoxicity was observed in 2 and 1 patient, respectively. Conclusions. Erlotinib administration with careful monitoring is thought to be a good alternative strategy for patients who respond well to gefitinib treatment but experience hepatotoxicity.

Yukihiro Yano

Yoshinobu Namba

Masahide Mori

Yukie Nakazawa

Ayumi Nashi

Shinichi Kagami

Manabu Niinaka

Tsutomu Yoneda

Hiromi Kimura


							Toshihiko Yamaguchi

Soichiro Yokota

Treatment of Non-Small-Cell Lung Cancer with Erlotinib following Gefitinib-Induced Hepatotoxicity: Review of 8 Clinical Cases

Lung cancer accounts for the majority of cancer-related deaths worldwide of which non-small-cell lung carcinoma alone takes a toll of around 85&#x25;. Platinum-based therapy is the stronghold for lung cancer at present. The discovery of various molecular alterations that underlie lung cancer has contributed to the development of specifically targeted therapies employing specific mutation inhibitors. Targeted chemotherapy based on molecular profiling has shown great promise in lung cancer treatment. Various molecular markers with predictive and prognostic significance in lung cancer have evolved as a result of advanced research. Testing of EGFR and Kras mutations is now a common practice among community oncologists, and more recently, ALK rearrangements have been added to this group. This paper discusses various predictive and prognostic markers that are being investigated and have shown significant relevance which can be exploited for targeted treatment in lung cancer.

Alphy Rose-James

Sreelekha TT

Molecular Markers with Predictive and Prognostic Relevance in Lung Cancer

Background. The main attention regarding prognostic and predictive markers in NSCLC directs towards the EGFR-targeted pathway, where the most studied genetic alterations include EGFR mutations, EGFR copy number, and KRAS mutations. We wanted to explore the prognostic impact of mutated KRAS in the stage III setting treated with high-dose radiochemotherapy. Methods. Samples were obtained from patients participating in two prospective studies of locally advanced NSCLC receiving combined radiochemotherapy: the RAKET study, a randomized phase II study where patients were treated with induction chemotherapy (carboplatin/paclitaxel) followed by concurrent radiochemotherapy, and the Satellite trial, a phase II study with induction chemotherapy (cisplatin/docetaxel) followed by radiotherapy concurrent cetuximab. The samples were analysed regarding KRAS mutations, EGFR mutations, and EGFR FISH positivity. Results. Patients with mutated KRAS had a significantly inferior survival, which maintained its significance in a multivariate analysis when other possible prognostic factors were taken into account. The prevalence of KRAS mutations, EGFR mutations, and EGFR FISH positivity were 28.8&#x25;, 7.5&#x25;, and 19.7&#x25;, respectively. Conclusion. Mutated KRAS is an independent negative prognostic factor for survival in NSCLC stage III disease treated with combined radiochemotherapy. The prevalence of KRAS mutations and EGFR mutations are as expected in this Scandinavian population.

A. Hallqvist

F. Enlund

C. Andersson

H. Sj&#xf6;gren

A. Hussein

E. Holmberg

J. Nyman

Mutated KRAS Is an Independent Negative Prognostic Factor for Survival in NSCLC Stage III Disease Treated with High-Dose Radiotherapy

A vast array of data suggests that early age of smoking onset enhances the risk for development of lung cancer in adulthood. Initiation of smoking at a young age may influence the development of lung cancer because of its effect on duration of smoking. Early onset of smoking also may serve as an independent risk factor. It may increase the likelihood that smoking occurs during a critical period of development that enhances susceptibility to the adverse effects of cancer causing agents in cigarette smoke, thereby facilitating the initiation of the carcinogenic process. While evidence for the latter hypothesis derives from a variety of sources, definitive proof has proven elusive. Whether or not early age of smoking serves as an independent risk factor for lung carcinogenesis, the consensus of the public health community is that prevention of smoking onset at a young age and early cessation are keys to stemming the current lung cancer pandemic. Population approaches to tobacco prevention and control, such as measures contained in the World Health Organization Framework Convention Tobacco Control Treaty, offer the best opportunity, on the scale needed, to create a smoke-free world and bring an end to the pandemic of tobacco-related disease.

Norman Hymowitz

Cigarette Smoking and Lung Cancer: Pediatric Roots

Tobacco smoke and radioactive radon gas impose a high risk for lung cancer. The radon-derived ionizing radiation and some components of cigarette smoke induce oxidative stress by generating reactive oxygen species (ROS). Respiratory lung cells are subject to the ROS that causes DNA breaks, which subsequently bring about DNA mutagenesis and are intimately linked with carcinogenesis. The damaged cells by oxidative stress are often destroyed through the active apoptotic pathway. However, the ROS also perform critical signaling functions in stress responses, cell survival, and cell proliferation. Some molecules enhance radiation-induced tumor cell killing via the reduction in DNA repair levels. Hence the DNA repair levels may be a novel therapeutic modality in overcoming drug resistance in lung cancer. Either survival or apoptosis, which is determined by the balance between DNA damage and DNA repair levels, may lender the major problems in cancer therapy. The purpose of this paper is to take a closer look at risk factor and at therapy modulation factor in lung cancer relevant to the ROS.

Naoko Okumura

Hitomi Yoshida

Yasuko Kitagishi

Yuri Nishimura

Shio Iseki

Satoru Matsuda

Against Lung Cancer Cells: To Be, or Not to Be, That Is the Problem

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Lung Cancer International