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Muscle mass and association to quality of life in non-small cell lung cancer patients.

1 min 57 sek siden
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Muscle mass and association to quality of life in non-small cell lung cancer patients.

J Cachexia Sarcopenia Muscle. 2017 May 10;:

Authors: Bye A, Sjøblom B, Wentzel-Larsen T, Grønberg BH, Baracos VE, Hjermstad MJ, Aass N, Bremnes RM, Fløtten Ø, Jordhøy M

Abstract
BACKGROUND: Cancer wasting is characterized by muscle loss and may contribute to fatigue and poor quality of life (QoL). Our aim was to investigate associations between skeletal muscle index (SMI) and skeletal muscle radiodensity (SMD) and selected QoL outcomes in advanced non-small cell lung cancer (NSCLC) at diagnosis.
METHODS: Baseline data from patients with stage IIIB/IV NSCLC and performance status 0-2 enrolled in three randomized trials of first-line chemotherapy (n = 1305) were analysed. Associations between SMI (cm(2) /m(2) ) and SMD (Hounsfield units) based on computed tomography-images at the third lumbar level and self-reported physical function (PF), role function (RF), global QoL, fatigue, and dyspnoea were investigated by linear regression using flexible non-linear modelling.
RESULTS: Complete data were available for 734 patients, mean age 65 years. Mean SMI was 47.7 cm(2) /m(2) in men (n = 420) and 39.6 cm(2) /m(2) in women (n = 314). Low SMI values were non-linearly associated with low PF and RF (men P = 0.016/0.020, women P = 0.004/0.012) and with low global QoL (P = 0.001) in men. Low SMI was significantly associated with high fatigue (P = 0.002) and more pain (P = 0.015), in both genders, but not with dyspnoea. All regression analyses showed poorer physical outcomes below an SMI breakpoint of about 42-45 cm(2) /m(2) for men and 37-40 cm(2) /m(2) for women. In both genders, poor PF and more dyspnoea were significantly associated with low SMD.
CONCLUSIONS: Low muscle mass in NSCLC negatively affects the patients' PF, RF, and global QoL, possibly more so in men than in women. However, muscle mass must be below a threshold value before this effect can be detected.

PMID: 28493418 [PubMed - as supplied by publisher]

Trajectory of sleep disturbances in patients undergoing lung cancer surgery: a prospective study.

fre, 05/12/2017 - 09:30
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Trajectory of sleep disturbances in patients undergoing lung cancer surgery: a prospective study.

Interact Cardiovasc Thorac Surg. 2017 May 08;:

Authors: Halle IH, Westgaard TK, Wahba A, Oksholm T, Rustøen T, Gjeilo KH

Abstract
OBJECTIVES: Patients with lung cancer report sleep difficulties to be frequent and bothersome symptoms. This study describes the trajectory of sleep from before and up to 12 months after surgery for lung cancer. Further, it investigates possible associations between sleep disturbance, demographic and clinical characteristics before surgery.
METHODS: This study is part of a longitudinal multicentre study. Sleep disturbance was measured by The General Sleep Disturbance Scale (GSDS) that investigates frequencies of sleep difficulties (21 items) and a total sum score ≥43 indicates a clinically meaningful level of sleep disturbance (score range 0-147). Linear mixed models were used to study changes in sleep from baseline to 1, 5, 9 and 12 months after surgery.
RESULTS: The percentage of patients ( n  = 264) reporting sleep disturbances was 60.9% at baseline, 68.5% at Month 1, 55.4% at Month 5, 51.3% at Month 9 and 49.7% at Month 12. The increase to and decrease from Month 1 was the only significant alteration in the occurrence of sleep disturbance. The patients reported most problems within the subscales sleep quantity, early awakenings and sleep quality. Factors associated with sleep disturbance were lower age, use of pain medication and psychotropic medication and higher comorbidity score.
CONCLUSIONS: Lung cancer patients sleep poorly, before as well as after surgery. There is a need to address sleeping disturbance routinely in clinical practice and screening for sleeping problems is indicated. Further studies are warranted concerning factors that contribute to sleep disturbance and how they best can be treated.

PMID: 28486702 [PubMed - as supplied by publisher]

Transfer Between Hospitals Is a Risk Situation for Patients After Lung Cancer Surgery.

ons, 05/10/2017 - 09:30
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Transfer Between Hospitals Is a Risk Situation for Patients After Lung Cancer Surgery.

Cancer Nurs. 2017 Apr 20;:

Authors: Oksholm T, Rustoen T, Ekstedt M

Abstract
BACKGROUND: Patients with lung cancer often undergo surgery shortly after diagnosis. Despite undergoing extensive operation, many patients are transferred to a local hospital a few days after surgery. Transitions between different levels of care are risky due to common medication and follow-up errors.
OBJECTIVE: The study purpose was to explore patients' experiences of transfer between hospitals after lung cancer surgery. The study aim was to improve the quality of transitional care.
METHODS: In-depth interviews with 14 patients with lung cancer (6 men, 8 women) were conducted in the patients' homes. Interviews were audiotaped, transcribed, and analyzed using the hermeneutic analysis method.
RESULTS: Patients' experience of transfer between hospitals after lung cancer surgery is one of being in a caregiver gap characterized by feeling unprepared and uncertain, feeling unprotected and not being cared for, and suffering because of inadequate organization. Patients are vulnerable and at risk of injury before and during transfer, as well as after arrival at local hospitals.
CONCLUSIONS: Study findings highlight a rarely considered risk of inadequate care before, during, and after hospital transfer of vulnerable patients. Transition between hospitals after lung cancer surgery is a part of patient care for which there are no policies or care plans and a time during which the borders of responsibility between caregivers are unclear.
IMPLICATIONS FOR PRACTICE: It is important to develop guidelines for clearly defined responsibilities during transfer between hospitals. Healthcare providers need to plan transfers with the same rigor as they do hospital care.

PMID: 28426541 [PubMed - as supplied by publisher]

Copy number variation, increased gene expression and molecular mechanisms of Neurofascin in lung cancer.

fre, 04/21/2017 - 08:30

Copy number variation, increased gene expression and molecular mechanisms of Neurofascin in lung cancer.

Mol Carcinog. 2017 Apr 18;:

Authors: Erdem JS, Arnoldussen YJ, Skaug V, Haugen A, Zienolddiny S

Abstract
Metastasis and cell adhesion are key aspects of cancer progression. Neurofascin (NFASC) is a member of the immunoglobulin superfamily of adhesion molecules and, while studies on NFASC are inadequate, other members have been indicated pivotal roles in cancer progression and metastasis. This study aimed at increasing the knowledge on the involvement of adhesion molecules in lung cancer progression by studying the regulation and role of NFASC in non-small cell lung cancer (NSCLC). Here, copy number variations in the NFASC gene were analyzed in tumor and non-tumorous lung tissues of 204 NSCLC patients. Frequent gene amplifications (OR = 4.50, 95% CI: 2.27-8.92, P ≤ 0.001) and increased expression of NFASC (P = 0.034) were identified in tumors of NSCLC patients. Furthermore, molecular mechanisms of NFASC in lung cancer progression were evaluated by investigating the effects of NFASC silencing on cell proliferation, viability, migration and invasion using siRNA technology in four NSCLC cell lines. Silencing of NFASC did not affect cell proliferation or viability but rather decreased NCSLC cell migration (P ≤ 0.001) and led to morphological changes, rearrangements in the actin cytoskeleton and changes in F-actin networks in migrating NSCLC cell lines. This study is the first to report frequent copy number gain and increased expression of NFASC in NCSLC. Moreover, these data suggest that NFASC is a novel regulator of NSCLC cell motility and support a role of NFASC in the regulation of NSCLC progression. This article is protected by copyright. All rights reserved.

PMID: 28418179 [PubMed - as supplied by publisher]

High number of kinome-mutations in non-small cell lung cancer is associated with reduced immune response and poor relapse-free survival.

ons, 04/19/2017 - 09:30
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High number of kinome-mutations in non-small cell lung cancer is associated with reduced immune response and poor relapse-free survival.

Int J Cancer. 2017 Apr 07;:

Authors: Helland Å, Brustugun OT, Nakken S, Halvorsen AR, Dønnem T, Bremnes R, Busund LT, Sun J, Lorenz S, Solberg SK, Jørgensen LH, Vodak D, Myklebost O, Hovig E, Meza-Zepeda LA

Abstract
Lung cancer is the leading cause of cancer related death, and the past years' improved insight into underlying molecular events has significantly improved outcome for specific subsets of patients. In particular, several new therapies that target protein kinases have been implemented, and many more are becoming available. We have investigated lung cancer specimens for somatic mutations in a targeted panel of 612 human genes, the majority being protein kinases. The somatic mutation profiles were correlated to profiles of immune cell infiltration as well as relapse-free survival. Targeted deep sequencing was performed on 117 tumour/normal pairs using the SureSelect Human Kinome kit (Agilent Technologies), with capture probes targeting 3.2 Mb of the human genome, including exons and UTRs of all known kinases, kinase receptors and selected cancer-related genes (612 genes in total). CD8 staining was determined by using Ventana Benchmark. Survival analyses were performed using SPSS. The number of mutations per sample ranged from 0 to 50 (within the 612 genes tested), with a median of nine. The prognosis was worse for patients with more than the median number of mutations. A significant correlation was found between mutations in one of selected DNA-repair genes and the total number of mutations in that tumour (P<0.001). There was a significant inverse correlation between the number of infiltrating stromal CD8+ lymphocytes and the presence of EGFR mutations. This article is protected by copyright. All rights reserved.

PMID: 28387924 [PubMed - as supplied by publisher]

Real-world data on nivolumab treatment of non-small cell lung cancer.

ons, 04/19/2017 - 09:30
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Real-world data on nivolumab treatment of non-small cell lung cancer.

Acta Oncol. 2017 Mar;56(3):438-440

Authors: Brustugun OT, Sprauten M, Helland Å

Abstract
BACKGROUND: Checkpoint inhibitors have proven effectiveness in clinical trials for non-small cell lung cancer (NSCLC) patients, but if this is congruent with routine patient care is discussed. We present real-world experience with the PD1-inhibitor nivolumab in NSCLC.
PATIENTS AND METHODS: Patients with NSCLC were considered eligible for nivolumab treatment after one or more lines of chemotherapy, and when in reasonable performance status (PS) [Eastern Cooperative Oncology Group (ECOG) < 3]. Treatment was given according to guidelines in the two phase III studies, CA209017 and CA209057. Response evaluation was done according to Recist 1.1, and treatment given until unequivocal progression or intolerable toxicity.
RESULTS: Fifty-eight patients (30 females) commenced therapy in the period June-August 2015. Median age was 64.6 years (range 32.3-88.2). Twenty-four patients had squamous cell carcinoma and 32 adenocarcinoma, 38 had received two or more prior lines of therapy. Fourteen cases (24%) were in ECOG PS 2. After a medium observation time of 14.3 months, 13 (22%) are still in treatment. Median time to treatment failure (TTF) was 4.0 months, 34% were off treatment during the first two months. Median overall survival (OS) is 11.7 months. There was no difference in TTF or OS among patients with squamous versus non-squamous histology or between 1 versus >1 prior line of therapy. Four patients (7%) were off treatment due to toxicity, none were grade 4 or 5.
CONCLUSION: Nivolumab treatment outside clinical trials seems to perform as expected.

PMID: 27892773 [PubMed - indexed for MEDLINE]

Epithelial-mesenchymal transition and FOXA genes during tobacco smoke carcinogen induced transformation of human bronchial epithelial cells.

lør, 04/08/2017 - 09:30
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Epithelial-mesenchymal transition and FOXA genes during tobacco smoke carcinogen induced transformation of human bronchial epithelial cells.

Toxicol In Vitro. 2016 Sep;35:55-65

Authors: Bersaas A, Arnoldussen YJ, Sjøberg M, Haugen A, Mollerup S

Abstract
Lung cancer is largely an environmentally caused disease with poor prognosis. An in vitro transformation model of human bronchial epithelial cells (HBEC) was used to study long-term effects of tobacco smoke carcinogens on epithelial-mesenchymal transition (EMT) and the forkhead box transcription factors FOXA1 and FOXA2. CDK4 and hTERT immortalized HBEC2 and HBEC12 cell lines were exposed weekly to either cigarette smoke condensate (CSC), benzo[a]pyrene, or methylnitrosourea. Transformed cell lines were established from soft-agar colonies after 12weeks of exposure. HBEC12 was transformed by all exposures while HBEC2 was only transformed by CSC. Untransformed HBEC2 showed little invasive capacity, whereas transformed cell lines completely closed the gap in a matrigel scratch wound assay. CDH1 was down-regulated in all of the transformed cell lines. In contrast, CDH2 was up-regulated in both HBEC2 and one of the HBEC12 transformed cell lines. Furthermore, transformed cells showed activation of EMT markers including SNAI1, ZEB1, VIM, and MMP2. All transformed cell lines had significant down-regulation of FOXA1 and FOXA2, indicating a possible role in cell transformation and EMT. ChIP analysis showed increased binding of Histone-H3 and macroH2A in FOXA1 and FOXA2 in the transformed HBEC2 cell lines, indicating a compact chromatin. In conclusion, long-term carcinogen exposure lead to down-regulation of FOXA1 and FOXA2 concomitantly with the occurrence of EMT and in vitro transformation in HBEC cells.

PMID: 27221058 [PubMed - indexed for MEDLINE]

Genetic Risk Can Be Decreased: Quitting Smoking Decreases and Delays Lung Cancer for Smokers With High and Low CHRNA5 Risk Genotypes - A Meta-Analysis.

ons, 04/05/2017 - 09:30
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Genetic Risk Can Be Decreased: Quitting Smoking Decreases and Delays Lung Cancer for Smokers With High and Low CHRNA5 Risk Genotypes - A Meta-Analysis.

EBioMedicine. 2016 Sep;11:219-226

Authors: Chen LS, Baker T, Hung RJ, Horton A, Culverhouse R, Hartz S, Saccone N, Cheng I, Deng B, Han Y, Hansen HM, Horsman J, Kim C, Rosenberger A, Aben KK, Andrew AS, Chang SC, Saum KU, Dienemann H, Hatsukami DK, Johnson EO, Pande M, Wrensch MR, McLaughlin J, Skaug V, van der Heijden EH, Wampfler J, Wenzlaff A, Woll P, Zienolddiny S, Bickeböller H, Brenner H, Duell EJ, Haugen A, Brüske I, Kiemeney LA, Lazarus P, Le Marchand L, Liu G, Mayordomo J, Risch A, Schwartz AG, Teare MD, Wu X, Wiencke JK, Yang P, Zhang ZF, Spitz MR, Amos CI, Bierut LJ

Abstract
BACKGROUND: Recent meta-analyses show that individuals with high risk variants in CHRNA5 on chromosome 15q25 are likely to develop lung cancer earlier than those with low-risk genotypes. The same high-risk genetic variants also predict nicotine dependence and delayed smoking cessation. It is unclear whether smoking cessation confers the same benefits in terms of lung cancer risk reduction for those who possess CHRNA5 risk variants versus those who do not.
METHODS: Meta-analyses examined the association between smoking cessation and lung cancer risk in 15 studies of individuals with European ancestry who possessed varying rs16969968 genotypes (N=12,690 ever smokers, including 6988 cases of lung cancer and 5702 controls) in the International Lung Cancer Consortium.
RESULTS: Smoking cessation (former vs. current smokers) was associated with a lower likelihood of lung cancer (OR=0.48, 95%CI=0.30-0.75, p=0.0015). Among lung cancer patients, smoking cessation was associated with a 7-year delay in median age of lung cancer diagnosis (HR=0.68, 95%CI=0.61-0.77, p=4.9∗10(-10)). The CHRNA5 rs16969968 risk genotype (AA) was associated with increased risk and earlier diagnosis for lung cancer, but the beneficial effects of smoking cessation were very similar in those with and without the risk genotype.
CONCLUSION: We demonstrate that quitting smoking is highly beneficial in reducing lung cancer risks for smokers regardless of their CHRNA5 rs16969968 genetic risk status. Smokers with high-risk CHRNA5 genotypes, on average, can largely eliminate their elevated genetic risk for lung cancer by quitting smoking- cutting their risk of lung cancer in half and delaying its onset by 7years for those who develop it. These results: 1) underscore the potential value of smoking cessation for all smokers, 2) suggest that CHRNA5 rs16969968 genotype affects lung cancer diagnosis through its effects on smoking, and 3) have potential value for framing preventive interventions for those who smoke.

PMID: 27543155 [PubMed - indexed for MEDLINE]

Detection of disseminated tumor cells in lymph nodes from patients with early stage non-small cell lung cancer.

ons, 02/15/2017 - 10:30
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Detection of disseminated tumor cells in lymph nodes from patients with early stage non-small cell lung cancer.

Diagn Pathol. 2016 Jun 17;11(1):50

Authors: Rud AK, Boye K, Fodstad Ø, Juell S, Jørgensen LH, Solberg S, Helland Å, Brustugun OT, Mælandsmo GM

Abstract
BACKGROUND: The regional lymph node involvement is a major prognostic factor in patients with non-small cell lung cancer (NSCLC) undergoing surgical resection. Disease relapse is common, suggesting that early disseminated disease is already present in the regional lymph nodes at the time of surgery, and that the current nodal staging classification might be suboptimal. Early detection of disseminated tumor cells (DTCs) in lymph nodes could potentially enable identification of subcategories of patients with high risk of disease relapse.
METHOD: Lymph node samples were collected from 128 NSCLC patients at the time of surgery and the presence of DTCs determined by immunomagnetic selection (IMS) using the MOC31 antibody recognizing EpCAM. Results obtained with IMS were compared to the pathological staging obtained by histopathology. Associations between the presence of DTCs and clinicopathological variables and patient outcome were investigated.
RESULTS: DTCs were detected in 40 % of the lymph node samples by IMS. Their presence was significantly associated with pN status as assessed by histopathology, and samples from 83 % of the patients with lymph node metastases (pN1-2) had detectable DTCs. In the group of patients who were negative for lymph node metastases by standard histopathology (pN0) DTCs were detected in 32 %. The presence of DTCs was not associated with any other clinicopathological variables. Patients with IMS-positive samples showed decreased relapse free survival compared to patients with IMS-negative samples, but the difference was not statistically significant. The pN status was significantly associated with both relapse free and overall survival, but the presence of DTCs had no prognostic impact in the subcategory of patients with pN0 status.
CONCLUSION: Our findings do not support further development of lymph node DTC detection for clinical use in early stage NSCLC.

PMID: 27316334 [PubMed - indexed for MEDLINE]

Randomized phase II trial comparing twice daily hyperfractionated with once daily hypofractionated thoracic radiotherapy in limited disease small cell lung cancer.

søn, 02/12/2017 - 10:30
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Randomized phase II trial comparing twice daily hyperfractionated with once daily hypofractionated thoracic radiotherapy in limited disease small cell lung cancer.

Acta Oncol. 2016 May;55(5):591-7

Authors: Grønberg BH, Halvorsen TO, Fløtten Ø, Brustugun OT, Brunsvig PF, Aasebø U, Bremnes RM, Tollåli T, Hornslien K, Aksnessæther BY, Liaaen ED, Sundstrøm S, Norwegian Lung Cancer Study Group

Abstract
BACKGROUND: Concurrent chemotherapy and thoracic radiotherapy (TRT) is recommended for limited disease small cell lung cancer (LD SCLC). Twice daily TRT is well documented, but not universally implemented - probably mainly due to inconvenience and concerns about toxicity. A schedule of three-week hypofractionated TRT is a commonly used alternative. This is the first randomized trial comparing twice daily and hypofractionated TRT in LD SCLC.
MATERIAL AND METHODS: Patients received four courses of cisplatin/etoposide (PE) and were randomized to TRT of 42 Gy in 15 fractions (once daily, OD) or 45 Gy in 30 fractions (twice daily, BID) between the second and third PE course. Good responders received prophylactic cranial irradiation of 30 Gy in 15 fractions.
RESULTS: 157 patients were enrolled between May 2005 and January 2011 (OD: n = 84, BID: n = 73). Median age was 63 years, 52% were men, 84% had performance status 0-1, 72% had stage III disease and 11% non-malignant pleural effusion. The treatment arms were well balanced. The response rates were similar (OD: 92%, BID: 88%; p = 0.41), but more BID patients achieved a complete response (OD: 13%, BID: 33%; p = 0.003). There was no difference in one-year progression-free survival (PFS) (OD: 45%, BID: 49%; p = 0.61) or median PFS (OD: 10.2 months, BID: 11.4 months; p = 0.93). The median overall survival in the BID arm was 6.3 months longer (OD: 18.8 months, BID: 25.1 months; p = 0.61). There were no differences in grade 3-4 esophagitis (OD: 31%, BID: 33%, p = 0.80) or pneumonitis (OD: 2%, BID: 3%, p = 1.0). Patients on the BID arm reported slightly more dysphagia at the end of the TRT.
CONCLUSION: There was no difference in severe toxicity between the two TRT schedules. The twice daily schedule resulted in significantly more complete responses and a numerically longer median overall survival, but no firm conclusions about efficacy could be drawn from this phase II trial.

PMID: 26494411 [PubMed - indexed for MEDLINE]

Estrogen receptor expression and gene promoter methylation in non-small cell lung cancer - a short report.

tor, 02/09/2017 - 10:30
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Estrogen receptor expression and gene promoter methylation in non-small cell lung cancer - a short report.

Cell Oncol (Dordr). 2016 Dec;39(6):583-589

Authors: Tekpli X, Skaug V, Bæra R, Phillips DH, Haugen A, Mollerup S

Abstract
PURPOSE: In the past, anomalous estrogen receptor (ER) regulation has been associated with various lung pathologies, but so far its involvement in lung cancer initiation and/or progression has remained unclear. Here, we aimed at assessing in vivo and in vitro ER expression and its possible epigenetic regulation in non-small cell lung cancer (NSCLC) samples and their corresponding normal tissues and cells.
METHODS: ERα and ERβ gene expression levels were assessed using real time quantitative PCR (RT-qPCR), whereas ERα and ERβ gene promoter methylation levels were assessed using DNA bisulfite conversion followed by pyrosequencing. We included NSCLC (n = 87) and adjacent histologically normal lung tissue samples from lung cancer patients (n = 184), primary normal bronchial epithelial-derived cell cultures (n = 11), immortalized bronchial epithelial-derived cell lines (n = 3) and NSCLC derived cell lines (n = 9).
RESULTS: Using RT-qPCR we found significantly lower ERα and ERβ expression levels in the NSCLC tissue samples compared to their normal adjacent tissue samples. These lower ER expression levels were confirmed in vitro using primary normal bronchial epithelial-derived cell cultures, immortalized bronchial epithelial-derived cell lines and NSCLC-derived cell lines. By using this latter panel of cells, we found that ER gene promoter hypermethylation was associated with decreased ER expression. In addition we found that in tumor and normal lung tissues, smoking was associated with decreased ER expression and that normal lung tissues with a low ERβ expression level exhibited increased smoking-related DNA adducts.
CONCLUSIONS: Taken together, our results indicate that decreased ER expression mediated by DNA methylation may play a role in NSCLC development.

PMID: 27572263 [PubMed - indexed for MEDLINE]