Separation and Characterization of Plastic Waste Packaging Contaminated with Food Residues.

In this paper, we present the development of a novel processing technology to tackle hard-to-recycle plastic packaging waste contaminated with food residues. The proof-of-concept (POC) technology can effectively separate food residual amounts from plastic waste materials to a level acceptable for further re-use or recycling of the plastic packaging. To assess this technology, we have conducted spectroscopic, thermal, and calorimetric characterizations of the obtained fractions, such as cleaned mixed plastics (CMP), food waste with mixed plastics (FWMP), and a mixture of microplastics (MP). The analyses were carried out with the aid of Fourier-Transform Infrared spectroscopy (FT-IR), Thermo-Gravimetric Analysis (TGA), Microcone Combustion Calorimetry (MCC), and 'bomb' calorimetry. The highest ratio of CMP to FWMP and the lowest amount of MP were obtained utilizing 700 rpm blade rotational speed and 15 s residence time of contaminated plastics in a cutting mill chamber. The plastics were freed from food contamination by 93-97%, which highlights a strong potential of the POC as a solution for 'dry-cleaning' of similar wastes on a larger scale. The main components of the CMP fraction were low-density polyethylene (LDPE), polypropylene (PP), and polyethylene terephthalate (PET), which are recyclable plastics. The knowledge and understanding of thermal degradation behaviours and calorimetric attributes of separated fractions, determined in this study, are essential in informing the industrial players using pyrolysis as a technique for recycling plastics.

The impact of electronic records on patient safety: a qualitative study.

BACKGROUND: Our aim was to explore NHS staff perceptions and experiences of the impact on patient safety of introducing a maternity system. METHODS: Qualitative semi-structured interviews were conducted with 19 members of NHS staff who represented a variety of staff groups (doctors, midwives, health care assistants), staff grades (consultant and midwife grades) and wards within a maternity unit. Participants represented a single maternity unit at a NHS teaching hospital in the North of England. Interviews were conducted during the first 12 months of the system being implemented and were analysed thematically. RESULTS: Participants perceived there to be an elevated risk to patient safety during the system's implementation. The perceived risks were attributed to a range of social and technical factors. For example, poor system design and human error which resulted in an increased potential for missing information and inputting error. CONCLUSIONS: The first 12 months of introducing the maternity system was perceived to and in some cases had already caused actual risk to patient safety. Trusts throughout the NHS are facing increasing pressure to become paperless and should be aware of the  potential adverse impacts on patient safety that can occur when introducing electronic systems. Given the potential for increased risk identified, recommendations for further research and for NHS trusts introducing electronic systems are proposed.

Implementing electronic patient record systems (EPRs) into England's acute, mental health and community care trusts: a mixed methods study.

BACKGROUND: Our aim was to explore the approaches to and the challenges and benefits of implementing Electronic Patient Record systems (EPRs) into NHS acute, mental health and community care hospitals throughout England. METHODS: A mixed methods approach was adopted that comprised an online survey (n = 59) and semi-structured telephone interviews (n = 8) with chief information officers (or heads of EPR projects) at NHS trusts throughout England. Survey analysis was descriptive, whilst the qualitative interviews were analysed thematically. RESULTS: A range of devices and approaches to implementing EPRs were described with 32 % of survey respondents utilising a best of breed approach. Interviewees' perceived and expected benefits of implementing an EPR included efficiency, availability and accessibility of clinical information, and patient safety. Key challenges to EPR implementation were securing clinician involvement, difficulties posed by government and national policy and limited availability of financial and human resources. CONCLUSIONS: There was no single approach regarding the approaches taken to implementing EPRs among participating English NHS trusts, with various benefits and challenges cited. Policymakers and researchers need to provide clearer guidance for trusts at various stages of implementation ensuring intelligence is shared across England's NHS trusts.

A global profile of gene promoter methylation in treatment-naïve urothelial cancer.

The epigenetic alteration of aberrant hypermethylation in the promoter CpG island of a gene is associated with repression of transcription. In neoplastic cells, aberrant hypermethylation is well described as a mechanism of allele inactivation of particular genes with a tumor suppressor function. To investigate the role of aberrant hypermethylation in the biology and progression of urothelial cancer, we examined 101 urothelial (transitional cell) carcinomas (UC), broadly representative of the disease at presentation, with no prior immunotherapy, chemotherapy or radiotherapy, by Infinium HM27 containing 14,495 genes. The genome-wide signature of aberrant promoter hypermethylation in UC consisted of 729 genes significant by a Wilcoxon test, hypermethylated in a CpG island within 1 kb of the transcriptional start site and unmethylated in normal urothelium from aged individuals. We examined differences in gene methylation between the two main groups of UC: the 75% that are superficial, which often recur but rarely progress, and the 25% with muscle invasion and poor prognosis. We further examined pairwise comparisons of the pathologic subgroups of high or low grade, invasive or non-invasive (pTa), and high grade superficial or low grade superficial UC. Pathways analysis indicated over-representation of genes involved in cell adhesion or metabolism in muscle-invasive UC. Notably, the TET2 epigenetic regulator was one of only two genes more frequently methylated in superficial tumors and the sole gene in low grade UC. Other chromatin remodeling genes, MLL3 and ACTL6B, also showed aberrant hypermethylation. The Infinium methylation value for representative genes was verified by pyrosequencing. An available mRNA expression data set indicated many of the hypermethylated genes of interest to be downregulated in UC. Unsupervised clustering of the most differentially methylated genes distinguished muscle invasive from superficial UC. After filtering, cluster analysis showed a CpG Island Methylator Phenotype (CIMP)-like pattern of widespread methylation in 11 (11%) tumors. Nine of these 11 tumors had hypermethylation of TET2. Our analysis provides a basis for further studies of hypermethylation in the development and progression of UC.

MicroRNA expression signatures of stage, grade, and progression in clear cell RCC.

Clear cell RCC is the most common, and more likely to metastasize, of the three main histological types of RCC. Pathologic stage is the most important prognostic indicator and nuclear grade can predict outcome within stages of localized RCC. Epithelial tumors are thought to accumulate a series of genetic and epigenetic changes as they progress through well-defined clinical and histopathological changes. MicroRNAs (miRNAs) are involved in the regulation of mRNA expression from many human genes and miRNA expression is dysregulated in cancer. To better understand the contribution of dysregulated miRNA expression to the progression and biology of ccRCC, we examined the differences in expression levels of 723 human miRNAs through a series of analyses by stage, grade, and disease progression status in a large series of 94 ccRCC. We found a consistent signature that included significant upregulation of miR-21-5p, 142-3p, let-7g-5p, let-7i-5p and 424-5p, as well as downregulation of miR-204-5p, to be associated with ccRCC of high stage, or high grade, or progression. Discrete signatures associated with each of stage, grade, or progression were also identified. The let-7 family was significantly downregulated in ccRCC compared with normal renal parenchyma. Expression of the 6 most significantly differentially expressed miRNAs between ccRCC was verified by stem-loop qRT-PCR. Pathways predicted as targets of the most significantly dysregulated miRNAs included signaling, epithelial cancers, metabolism, and epithelial to mesenchymal transition. Our studies help to further elucidate the biology underlying the progression of ccRCC and identify miRNAs for potential translational application.

Genome-wide promoter methylome of small renal masses.

The majority of renal cell carcinoma (RCC) is now incidentally detected and presents as small renal masses (SRMs) defined as ≤ 4 cm in size. SRMs are heterogeneous comprising several histological types of RCC each with different biology and behavior, and benign tumors mainly oncocytoma. The varied prognosis of the different types of renal tumor has implications for management options. A key epigenetic alteration involved in the initiation and progression of cancer is aberrant methylation in the promoter region of a gene. The hypermethylation is associated with transcriptional repression and is an important mechanism of inactivation of tumor suppressor genes in neoplastic cells. We have determined the genome-wide promoter methylation profiles of 47 pT1a and 2 pT1b clear cell, papillary or chromophobe RCC, 25 benign renal oncocytoma ≤ 4 cm and 4 normal renal parenchyma specimens by Infinium HumanMethylation27 beadchip technology. We identify gene promoter hypermethylation signatures that distinguish clear cell and papillary from each other, from chromophobe and oncocytoma, and from normal renal cells. Pairwise comparisons revealed genes aberrantly hypermethylated in a tumor type but unmethylated in normal, and often unmethylated in the other renal tumor types. About 0.4% to 1.7% of genes comprised the promoter methylome in SRMs. The Infinium methylation score for representative genes was verified by gold standard technologies. The genes identified as differentially methylated implicate pathways involved in metabolism, tissue response to injury, epithelial to mesenchymal transition (EMT), signal transduction and G-protein coupled receptors (GPCRs), cancer, and stem cell regulation in the biology of RCC. Our findings contribute towards an improved understanding of the development of RCC, the different biology and behavior of histological types, and discovery of molecular subtypes. The differential methylation signatures may have utility in early detection and particularly differential diagnosis for prognostic stratification as well as identify novel gene and pathway targets for therapeutic intervention.

Aberrant promoter hypermethylation of PBRM1, BAP1, SETD2, KDM6A and other chromatin-modifying genes is absent or rare in clear cell RCC.

Recent sequencing studies of clear cell (conventional) renal cell carcinoma (ccRCC) have identified inactivating point mutations in the chromatin-modifying genes PBRM1, KDM6A/UTX, KDM5C/JARID1C, SETD2, MLL2 and BAP1. To investigate whether aberrant hypermethylation is a mechanism of inactivation of these tumor suppressor genes in ccRCC, we sequenced the promoter region within a bona fide CpG island of PBRM1, KDM6A, SETD2 and BAP1 in bisulfite-modified DNA of a representative series of 50 primary ccRCC, 4 normal renal parenchyma specimens and 5 RCC cell lines. We also interrogated the promoter methylation status of KDM5C and ARID1A in the Cancer Genome Atlas (TCGA) ccRCC Infinium data set. PBRM1, KDM6A, SETD2 and BAP1 were unmethylated in all tumor and normal specimens. KDM5C and ARID1A were unmethylated in the TCGA 219 ccRCC and 119 adjacent normal specimens. Aberrant promoter hypermethylation of PBRM1, BAP1 and the other chromatin-modifying genes examined here is therefore absent or rare in ccRCC.

ALDH1A1 is a novel EZH2 target gene in epithelial ovarian cancer identified by genome-wide approaches.

Epithelial ovarian cancer (EOC) remains the most lethal gynecologic malignancy in the United States. EZH2 silences gene expression through trimethylating lysine 27 on histone H3 (H3K27Me3). EZH2 is often overexpressed in EOC and has been suggested as a target for EOC intervention. However, EZH2 target genes in EOC remain poorly understood. Here, we mapped the genomic loci occupied by EZH2/H3K27Me3 using chromatin immunoprecipitation followed by next-generation sequencing (ChIP-seq) and globally profiled gene expression in EZH2-knockdown EOC cells. Cross-examination of gene expression and ChIP-seq revealed a list of 60 EZH2 direct target genes whose expression was upregulated more than 1.5-fold upon EZH2 knockdown. For three selected genes (ALDH1A1, SSTR1, and DACT3), we validated their upregulation upon EZH2 knockdown and confirmed the binding of EZH2/H3K27Me3 to their genomic loci. Furthermore, the presence of H3K27Me3 at the genomic loci of these EZH2 target genes was dependent upon EZH2. Interestingly, expression of ALDH1A1, a putative marker for EOC stem cells, was significantly downregulated in high-grade serous EOC (n = 53) compared with ovarian surface epithelial cells (n = 10, P < 0.001). Notably, expression of ALDH1A1 negatively correlated with expression of EZH2 (n = 63, Spearman r = -0.41, P < 0.001). Thus, we identified a list of 60 EZH2 target genes and established that ALDH1A1 is a novel EZH2 target gene in EOC cells. Our results suggest a role for EZH2 in regulating EOC stem cell equilibrium via regulation of ALDH1A1 expression.

Epigenetics of kidney cancer and bladder cancer.

This article focuses on the epigenetic alterations of aberrant promoter hypermethylation of genes, and histone modifications or RNA interference in cancer cells. Current knowledge of the hypermethylation of allele(s) in classical tumor suppressor genes in inherited and sporadic cancer, candidate tumor suppressor and other cancer genes is summarized gene by gene. Global and array-based studies of tumor cell hypermethylation are discussed. The importance of standardization of scoring of the methylation status of a gene is highlighted. The histone marks associated with hypermethylated genes, and the miRNAs with dysregulated expression, in kidney or bladder tumor cells are also discussed. Kidney cancer has the highest mortality rate of the genito-urinary cancers. There are management issues associated with the high recurrence rate of superficial bladder cancer, while muscle-invasive bladder cancer has a poor prognosis. These clinical problems are the basis for the translational application of gene hypermethylation in the diagnosis and prognosis of kidney and bladder cancer.

Wnt5a suppresses epithelial ovarian cancer by promoting cellular senescence.

Epithelial ovarian cancer (EOC) remains the most lethal gynecologic malignancy in the United States. Thus, there is an urgent need to develop novel therapeutics for this disease. Cellular senescence is an important tumor suppression mechanism that has recently been suggested as a novel mechanism to target for developing cancer therapeutics. Wnt5a is a noncanonical Wnt ligand that plays a context-dependent role in human cancers. Here, we investigate the role of Wnt5a in regulating senescence of EOC cells. We show that Wnt5a is expressed at significantly lower levels in human EOC cell lines and in primary human EOCs (n = 130) compared with either normal ovarian surface epithelium (n = 31; P = 0.039) or fallopian tube epithelium (n = 28; P < 0.001). Notably, a lower level of Wnt5a expression correlates with tumor stage (P = 0.003) and predicts shorter overall survival in EOC patients (P = 0.003). Significantly, restoration of Wnt5a expression inhibits the proliferation of human EOC cells both in vitro and in vivo in an orthotopic EOC mouse model. Mechanistically, Wnt5a antagonizes canonical Wnt/ß-catenin signaling and induces cellular senescence by activating the histone repressor A/promyelocytic leukemia senescence pathway. In summary, we show that loss of Wnt5a predicts poor outcome in EOC patients and Wnt5a suppresses the growth of EOC cells by triggering cellular senescence. We suggest that strategies to drive senescence in EOC cells by reconstituting Wnt5a signaling may offer an effective new strategy for EOC therapy.

Assays for hypermethylation of the BRCA1 gene promoter in tumor cells to predict sensitivity to PARP-inhibitor therapy.

The breast cancer 1 and 2, early onset (BRCA1 and BRCA2) genes are important for double-strand break repair by homologous recombination. Cells with inactivating mutations of the BRCA1 or BRCA2 tumor suppressor genes show increased sensitivity to Poly-ADP ribose polymerase (PARP)-inhibitors in vitro. Sporadic breast tumors with BRCA1 promoter hypermethylation show a similar phenotype to familial BRCA1 patient tumors termed "BRCAness." Sporadic ovarian tumors with functional inactivation of BRCA1 by hypermethylation will also have the BRCA-deficiency phenocopy. The loss of BRCA1 expression associated with promoter hypermethylation will disrupt BRCA-associated DNA repair and may sensitize tumors to BRCA-directed therapies. Thus, the determination of methylation status of BRCA1 may be an important predictive classifier of response to PARP-inhibitor therapy. The methylation, and thereby functional, status of other genes implicated in the wider BRCA/homologous recombination (HR) pathway may also be relevant to the prediction of response to PARP-inhibitor therapy. Here, we describe the four optimal technologies for assaying the promoter methylation status of BRCA1 and/or other genes.

Translational application of epigenetic alterations: ovarian cancer as a model.

Cancer is a disease initiated and driven by the accumulation and interplay of genetic and epigenetic mutations of genes involved in the regulation of cell growth and signaling. Dysregulation of these genes and pathways in a cell leads to a growth advantage and clonal expansion. The epigenetic alterations involved in the initiation and progression of cancer are DNA methylation and histone modifications which interact to remodel chromatin, as well as RNA interference. These alterations can be used as candidate targets in molecular tests for risk, early detection, prognosis, prediction of response to therapy, and monitoring, as well as new therapeutic targets in cancer. In this review, we discuss the rationale, studies to date, and issues in the translational application of epigenetics using epithelial ovarian cancer as a specific example of all types of cancer.

Signaling pathways in renal cell carcinoma.

Renal cell carcinoma (RCC), the most lethal type of genitourinary cancer, is generally resistant to chemotherapy and radiation therapy. Surgical excision of the tumor at a localized stage remains the mainstay for curative therapy. A number of drugs developed in recent years have shown limited to significant efficacy in treating RCC. These drugs act by blocking critical signaling pathways associated with RCC tumor growth and survival, and angiogenesis. Beyond well-validated signaling targets such as VHL, VEGFR and mTOR, additional pathways including HGF/c-MET and Wnt/ß-catenin have emerged as important to RCC pathogenesis. Mutations in one or more components of these signaling networks may affect tumor response to therapy. This review summarizes the state of knowledge about signaling pathways in RCC and discusses the known genetic and epigenetic alterations that underlie dysregulation of these pathways.

Global reactivation of epigenetically silenced genes in prostate cancer.

Transcriptional silencing associated with aberrant promoter hypermethylation is a common mechanism of inactivation of tumor suppressor genes in cancer cells. To globally profile the genes silenced by hypermethylation in prostate cancer, we screened a whole genome expression microarray for genes reactivated in the LNCaP, DU-145, PC-3, and MDA2b prostate tumor cell lines after treatment with the demethylating drug 5-aza-2-deoxycytidine and the histone deacetylation-inhibiting drug trichostatin A. A total of 2,997 genes showed at least 2-fold upregulation of expression after drug treatment in at least one prostate tumor cell line. For validation, we examined the first 45 genes, ranked by upregulation of expression, which had a typical CpG island and were known to be expressed in the normal cell counterpart. Two important findings were, first, that several genes known to be frequently hypermethylated in prostate cancer were apparent, and, second, that validation studies revealed eight novel genes hypermethylated in the prostate tumor cell lines, four of which were unmethylated in normal prostate cells and hypermethylated in primary prostate tumors (SLC15A3, 66%; KRT7, 54%; TACSTD2, 17%; GADD45b, 3%). Thus, we established the utility of our screen for genes hypermethylated in prostate cancer cells. One of the novel genes was TACSTD2/TROP2, a marker of human prostate basal cells with stem cell characteristics. TACSTD2 was unmethylated in prostatic intraepithelial neoplasia and may have utility in emerging methylation-based prostate cancer tests. Further study of the hypermethylome will provide insight into the biology of the disease and facilitate translational studies in prostate cancer.

DNA methylation in pre-diagnostic serum samples of breast cancer cases: results of a nested case-control study.

BACKGROUND: Promoter methylation of tumor suppressor genes is a frequent and early event in breast carcinogenesis. Paired tumor tissue and serum samples from women with breast cancer show that promoter methylation is detectable in both sample types, with good concordance. This suggests the potential for these serum markers to be used for breast cancer detection. METHODS: The current study was a case-control study nested within the prospective New York University Women's Health Study cohort aimed to assess the ability of promoter methylation in serum to detect pre-clinical disease. Cases were women with blood samples collected within the 6 months preceding breast cancer diagnosis (n=50). Each case was matched to 2 healthy cancer-free controls and 1 cancer-free control with a history of benign breast disease (BBD). RESULTS: Promoter methylation analysis of four cancer-related genes: -RASSF1A, GSTP1, APC and RARß2, - was conducted using quantitative methylation-specific PCR. Results showed that the frequency of methylation was lower than expected among cases and higher than expected among controls. Methylation was detected in the promoter region of: RASSF1A in 22.0%, 22.9% and 17.2% of cases, BBD controls and healthy controls respectively; GSTP1 in 4%, 10.4% and 7.1% respectively; APC in 2.0%, 4.4% and 4.2% respectively and RARß2 in 6.7%, 2.3% and 1.1% respectively. CONCLUSION: Methylation status of the four genes included in this study was unable to distinguish between cases and either control group. This study highlights some methodological issues to be addressed in planning prospective studies to evaluate methylation markers as diagnostic biomarkers.

Renal cell carcinoma.

Renal Cell Carcinoma (RCC) has the highest mortality rate of the genitourinary cancers and the incidence of RCC has risen steadily. If detected early, RCC is curable by surgery although a minority are at risk of recurrence. Increasing incidental detection and an ageing population has led to active surveillance as an option for patients with small renal masses. RCC is heterogeneous and comprises several histological cell types with different genetics, biology and behavior. The identification of the genes predisposing to inherited syndromes with RCC has provided much of our knowledge of the molecular basis of early sporadic RCC. Many of the oncogenes and tumor suppressor genes that are mutated leading to pathway dysregulation in RCC remain to be elucidated. Global studies of copy number, gene sequencing, gene expression, miRNA expression and gene methylation in primary RCC will lead towards this goal. The natural history of RCC indicated by candidate precursor lesions, multifocal or bilateral disease, growth rate of small renal masses under surveillance, and high risk populations provide insight into the behavior of this disease. The use of molecular markers for early detection and prognosis merits more attention with ongoing advances in omics technologies. This review focuses on early RCC, that is disease confined within the renal capsule.

Promoter methylation and the detection of breast cancer.

Mammographic screening has been shown to reduce breast cancer mortality in women over the age of 50 years, and to a lesser extent in younger women. The sensitivity of mammography, however, is reduced in some groups of women. There remains a need for a minimally invasive, cost-effective procedure that could be used along side mammography to improve screening sensitivity. Silencing of tumor suppressor genes through promoter hypermethylation is known to be a frequent and early event in carcinogenesis. Further, changes in methylation patterns observed in tumors are also detectable in the circulation of women with breast cancer. This makes these alterations candidate markers for early tumor detection. In this paper, we review the current literature on promoter hypermethylation changes and breast cancer and discuss issues that remain to be addressed in order for the potential of these markers to augment the sensitivity of screening mammography. In general, studies in well-defined populations, including appropriate controls and larger numbers are needed. Further, focus on the optimization of methods of methylation detection in small amounts of DNA is needed.

5'-azacytidine expression arrays.

Epigenetic silencing of a gene can be reversed, resulting in reactivation of expression, by drugs such as the DNA methylation inhibitor 5-Aza-2'-deoxycytidine (5Aza-dC, azacytidine). This drug is added to cell culture media and is incorporated into the new strand during DNA replication in the cell. 5Aza-dC forms a covalent complex with the active sites of the DNA methyltransferase, depleting methyltransferase activity, which results in generalized demethylation. Until recently, global analyses of gene methylation in cancer cells were largely restricted to array or gel-based comparisons of the methylation status of CpG islands between normal and tumor cell DNA. An expression microarray-based screen has the advantage of a more genome-wide analysis with a better gene annotation and, coupled with a reactivation strategy, has the further advantage that it should preferentially identify reexpression of epigenetically silenced genes over methylated CpG islands that do not influence transcription. However, the direct reactivation of methylated genes, as well as secondary effects of azacytidine treatment, can lead to a cascade of deregulation in downstream unmethylated gene expression. A validation strategy is therefore the key for efficient identification of genes methylated in the wild-type cultured tumor cells. An azacytidine-based reactivation approach can only be used on cell lines so validation should include analysis of primary tumors. The potential of this approach for the identification of new hypermethylated genes and pathways has been demonstrated in bladder, colorectal, esophageal, and most other cancer types.

VILIP-1 downregulation in non-small cell lung carcinomas: mechanisms and prediction of survival.

VILIP-1, a member of the neuronal Ca++ sensor protein family, acts as a tumor suppressor gene in an experimental animal model by inhibiting cell proliferation, adhesion and invasiveness of squamous cell carcinoma cells. Western Blot analysis of human tumor cells showed that VILIP-1 expression was undetectable in several types of human tumor cells, including 11 out of 12 non-small cell lung carcinoma (NSCLC) cell lines. The down-regulation of VILIP-1 was due to loss of VILIP-1 mRNA transcripts. Rearrangements, large gene deletions or mutations were not found. Hypermethylation of the VILIP-1 promoter played an important role in gene silencing. In most VILIP-1-silent cells the VILIP-1 promoter was methylated. In vitro methylation of the VILIP-1 promoter reduced its activity in a promoter-reporter assay. Transcriptional activity of endogenous VILIP-1 promoter was recovered by treatment with 5'-aza-2'-deoxycytidine (5'-Aza-dC). Trichostatin A (TSA), a histone deacetylase inhibitor, potently induced VILIP-1 expression, indicating that histone deacetylation is an additional mechanism of VILIP-1 silencing. TSA increased histone H3 and H4 acetylation in the region of the VILIP-1 promoter. Furthermore, statistical analysis of expression and promoter methylation (n = 150 primary NSCLC samples) showed a significant relationship between promoter methylation and protein expression downregulation as well as between survival and decreased or absent VILIP-1 expression in lung cancer tissues (p<0.0001). VILIP-1 expression is silenced by promoter hypermethylation and histone deacetylation in aggressive NSCLC cell lines and primary tumors and its clinical evaluation could have a role as a predictor of short-term survival in lung cancer patients.