Serum HDL cholesterol concentration in patients with squamous cell and small cell lung cancer.

Siemianowicz, Krzysztof; Gmiński, Jan; Stajszczyk, Marcin; Wojakowski, Wojtek; Goss, M; Machalski, M; Telega, Aleksandra; Bruliński, Krzysztof; Magiera-Molendowska, H

doi:10.3892/ijmm.6.3.307

Cited by 27 publications

(24 citation statements)

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“…That association has also been seen in case-control studies of lung cancer [7][8][9], however those studies were based on relatively small numbers of cases and compared mean levels of HDLcholesterol in cases and controls without always adjusting for age or smoking status. The most comprehensive of those studies [10], examined association of lipoproteins (LDL-cholesterol, HDL-cholesterol, triglycerides) and multiple cancer types.…”

Section: Discussionmentioning

confidence: 83%

“…This association was found to be independent of type and stage of lung cancer [7], but not all adjusted for smoking or other confounders. Furthermore, levels of plasma HDL-cholesterol may change as a consequence of lung cancer, and prospective studies are needed to better understand the temporal relationship between low plasma HDL-cholesterol levels and cancer incidence.…”

Section: Introductionmentioning

confidence: 72%

“…Case-control studies of newly diagnosed lung cancer have shown that HDL-cholesterol levels are reduced in lung cancer cases relative to levels observed in the control groups [7][8][9][10]. This association was found to be independent of type and stage of lung cancer [7], but not all adjusted for smoking or other confounders.…”

Section: Introductionmentioning

confidence: 90%

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HDL-cholesterol and the incidence of lung cancer in the Atherosclerosis Risk in Communities (ARIC) study

et al. 2008

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This study examined prospectively the association of baseline plasma HDL-cholesterol levels with incidence of lung cancer in 14,547 members of the Atherosclerosis Risk in Communities (ARIC) cohort. There were 259 cases of incident lung cancer identified during follow-up from 1987 through 2000. Results of this study indicated a relatively weak inverse association of HDL-cholesterol with lung cancer that was dependent on smoking status. The hazard ratio of lung cancer incidence in relation to low HDL-cholesterol, adjusted for race, gender, exercise, alcohol consumption, body mass index, triglycerides, age, and cigarette pack-years of smoking, was 1.45 (95% confidence interval 1.10, 1.92). This association was observed among former smokers (hazard ratio: 1.77, 95% confidence interval 1.05, 2.97), but not current smokers. The number of cases among never smokers in this study was too small (n=13) for meaningful interpretation of effect estimates. Excluding cases occurring within 5 years of baseline did not appreciably change the point estimates, suggesting lack of reverse causality. The modest association of low plasma HDL-cholesterol with greater incident lung cancer observed in this study is in agreement with existing case-control studies.

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Section: Discussionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 72%

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HDL-cholesterol and the incidence of lung cancer in the Atherosclerosis Risk in Communities (ARIC) study

et al. 2008

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“…SCLC grows rapidly and is extremely aggressive, and if the disease is not treated effectively in time, the patient will succumb within a few months (12). SCLC has the features of a high growth score and short doubling time, often with distant metastases at the diagnosis of the disease.…”

Section: Discussionmentioning

confidence: 99%

Cryptotanshinone inhibits lung tumor growth by increasing CD4+ T cell cytotoxicity through activation of the JAK2/STAT4 pathway

et al. 2016

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Abstract. Cryptotanshinone is one of the fat-soluble phenanthrene quinone components. In vitro studies have shown that tanshinone compounds can inhibit the proliferation of various tumor cells and affect cell cycle distribution. The aim of the present study was to better understand the effect of cryptotanshinone on the inhibition of small cell lung cancer by cytotoxic cluster of differentiation (CD)4 + T cells through activation of the Janus kinase 2/signal transducer and activator of transcription 4 (JAK2/STAT4) pathway. The Cell Counting kit-8 assay and the lactate dehydrogenase assay were used to analyze the cell proliferation of H446 and CD4 + T cells, and the cell cytotoxicity of CD4 + and CD8 + T cells, respectively. JAK2 and STAT4 protein expression was measured by western blot analysis. Cryptotanshinone effectively inhibited the tumor growth of the H446 cells and the cell proliferation of the CD4 + T cells. Treatment with cryptotanshinone increased the cytotoxicity of the CD4 + T cells, but could not affect the cytotoxicity of the CD8 + T cells. Meanwhile, cryptotanshinone induced phosphorylated (p)-JAK2 and p-STAT4 protein expression in the CD4 + T cells. These results suggest that cryptotanshinone inhibits the cell growth of lung tumors by increasing CD4 + T cell toxicity through activation of the JAK2/STAT4 pathway.

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“…A number of cancers have been associated with faulty cholesterol metabolism, including prostate [35] , breast [36] , pancreatic [37] , squamous cell and small cell lung [38] , acute myelogenous leukemia (AML) [39] and colorectal cancers [40] . Cholesterol levels affect cell signaling, survival and differentiation, processes that are all critical to the development and progression of cancer [41] .…”

Section: Cancer Development and Chemotherapy Resistancementioning

confidence: 99%

ABCA2 as a therapeutic target in cancer and nervous system disorders

Mack

Brown

Tew

2008

Expert Opinion on Therapeutic Targets

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Serum HDL cholesterol concentration in patients with squamous cell and small cell lung cancer.

Cited by 27 publications

References 0 publications

HDL-cholesterol and the incidence of lung cancer in the Atherosclerosis Risk in Communities (ARIC) study

HDL-cholesterol and the incidence of lung cancer in the Atherosclerosis Risk in Communities (ARIC) study

Cryptotanshinone inhibits lung tumor growth by increasing CD4+ T cell cytotoxicity through activation of the JAK2/STAT4 pathway

ABCA2 as a therapeutic target in cancer and nervous system disorders

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