Plasma small ncRNA pair panels as novel biomarkers for early-stage lung adenocarcinoma screening.

Background: Lung cancer is a major cause of cancer-related mortality worldwide, and around two-thirds of patients have metastasis at diagnosis. Thus, detecting lung cancer at an early stage could reduce mortality. Aberrant levels of circulating small non-coding RNAs (small ncRNAs) are potential diagnostic or prognostic markers for lung cancer.

Global lipidomics reveals two plasma lipids as novel biomarkers for the detection of squamous cell lung cancer: A pilot study.

Lipids are known to serve important roles in energy storage, membrane structure and signal transduction as well as in human cancers. In the present study, lipidomics was employed in order to identify plasma lipid markers for the early detection of lung cancer. Mass spectrometry was performed to profile 390 individual lipids in 44 plasma samples obtained from a training discovery cohort, which included 22 patients with squamous cell lung carcinoma (SqCC) and 22 high-risk individuals.

Global lipidomics identified plasma lipids as novel biomarkers for early detection of lung cancer.

Purpose: Lipids play roles in membrane structure, energy storage, and signal transduction as well as in human cancers. Here we adopt lipidomics to identify plasma lipid markers for early screening and detection of lung cancer.

Experimental Design: Using mass spectrometry, we profiled 390 individual lipids using training and validation strategy in a total of 346 plasma samples from 199 early NSCLC patients, including 113 adenocacinoma and 86 squamous cell cancers (SqCC), and from 147 healthy controls.

Plasma lipidomics profiling identified lipid biomarkers in distinguishing early-stage breast cancer from benign lesions.

Background: Breast cancer is very common and highly fatal in women. Current non-invasive detection methods like mammograms are unsatisfactory. Lipidomics, a promising detection method, may serve as a novel prognostic approach for breast cancer in high-risk patients.

Evaluation of Plasma miR-21 and miR-152 as Diagnostic Biomarkers for Common Types of Human Cancers.

Stable blood based miRNA species have allowed for the differentiation of patients with various types of cancer. Therefore, specific blood-based miRNA might be considered as a methodology which could be informative of the presence of cancer potentially from multiple distinct organ sites. Recently, miR-21 has been identified as an "oncomir" in various tumors while miR-152 as a tumor suppressor.

Interleukin-17 acts as double-edged sword in anti-tumor immunity and tumorigenesis.

Interleukin-17 (IL-17), a proinflammatory cytokine, mainly produced by Th17 cells, participates in both innate and adaptive immune responses and is involved in various diseases, including infectious diseases, autoimmune disorders and cancer. Emerging evidence indicates that IL-17 not only has an oncogenic role in tumorigenesis by regulating tumor angiogenesis and enhancing tumor immune evasion but also exerts anti-tumor functions by enhancing natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) activation and through the recruitment of neutrophils, NK cells and CD4 and CD8 T cells to tumor tissue. In this review, we provide an overview on the basic biology of IL-17 and recent findings regarding its enigmatic double-edged features in tumorigenesis, with special attention to the roles of IL-17 produced by tumor cells interacting with other factors in the tumor microenvironment.

RNA-Seq and Network Analysis Revealed Interacting Pathways in TGF-β-Treated Lung Cancer Cell Lines.

Whole transcriptome shotgun sequencing (RNA-Seq) is a useful tool for analyzing the transcriptome of a biological sample. With appropriate statistical and bioinformatic processing, this platform is capable of identifying significant differences in gene expression within the transcriptome and permits pathway and network analyses to determine how these genes interact biologically. In this study, we examined gene expression in two lung adenocarcinoma cell lines (H358 and A459) that were treated with transforming growth factor-β (TGF-β) as a model for induction of the epithelial-to-mesenchymal transition (EMT), commonly associated with disease progression.

Vitamin D directly regulates Mdm2 gene expression in osteoblasts.

While Mdm2 is an important negative regulator of the p53 tumor suppressor, it also possesses p53-independent functions in cellular differentiation processes. Mdm2 expression is alternatively regulated by two P1 and P2 promoters. In this study we show that the P2-intiated transcription of Mdm2 gene is activated by 1,25-dihydroxy vitamin D3 in MC3T3 cells.

p53 and MDM2 are involved in the regulation of osteocalcin gene expression.

Osteocalcin (OC) is a major noncollagenous bone matrix protein and an osteoblast marker whose expression is limited to mature osteoblasts during the late differentiation stage. In previous studies we have shown osteosarcomas to lose p53 function with a corresponding loss of osteocalcin gene expression. Introduction of wild type p53 resulted in re expression of the osteocalcin gene.

Osteocalcin gene expression is regulated by wild-type p53.

The tumor-suppressor p53 is a transcription factor that regulates a number of genes in the process of cell-cycle inhibition, apoptosis, and DNA damage. Recent studies have revealed a crucial role for p53 in bone remodeling. In our previous studies we have shown that p53 is an important regulator of osteoblast differentiation.

Effects of griseofulvin on apoptosis through caspase-3- and caspase-9-dependent pathways in K562 leukemia cells: An in vitro study.

Background: Griseofulvin, an oral nontoxic antifungal drug, has been reported to possess anticancer effect in human cancer cells, while the mechanisms are not completely understood.

Objective: The aim of this study was to investigate the cytotoxic effect of griseofulvin on K562 cells and to understand its underlying molecular pathways.

Methods: K562 cells were treated with griseofulvin at different concentrations for 24 hours, and the inhibition effect of griseofulvin on K562 cell proliferation was assessed by tetrazolium salt colorimetric assay.

Replication of prostate cancer risk loci on 8q24, 11q13, 17q12, 19q33, and Xp11 in African Americans.

Background: Prostate cancer (Pca) is a common malignancy that disproportionately affects African American men (AA). Recently there have been several genome-wide association studies (GWAS) implicating new prostate cancer risk loci along chromosomes 2, 3, 6, 7, 8, 10, 11, 12, 17, 19, and X in populations of European ancestry. Given the higher incidence and mortality for AAs, and differences in allele frequencies and haplotype structures between African and European descent populations, it is important to assess the impact of these candidate risk loci in AAs.

Adverse prognostic significance of KIT mutations in adult acute myeloid leukemia with inv(16) and t(8;21): a Cancer and Leukemia Group B Study.

Purpose: To analyze the prognostic impact of mutated KIT (mutKIT) in core-binding factor acute myeloid leukemia (AML) with inv(16)(p13q22) and t(8;21)(q22;q22).

Patients And Methods: Sixty-one adults with inv(16) and 49 adults with t(8;21), assigned to postremission therapy with repetitive cycles of higher dose cytarabine were analyzed for mutKIT in exon 17 (mutKIT17) and 8 (mutKIT8) by denaturing high-performance liquid chromatography and direct sequencing at diagnosis. The median follow-up was 5.

ICAM gene cluster SNPs and prostate cancer risk in African Americans.

Intercellular adhesion molecules (ICAMs) are known to be involved in various human cancers. An ICAM gene cluster lying within a 26 kb region on chromosome 19p13.2, and containing ICAM1, ICAM4, and ICAM5 has recently been identified as harboring a breast and prostate cancer susceptibility locus in two populations of European ancestry from Germany and Australia.

A functional variant in the transcriptional regulatory region of gene LOC344967 cosegregates with disease phenotype in familial nasopharyngeal carcinoma.

Nasopharyngeal carcinoma is a common malignancy in Southeast Asian countries, and genetic background is a well-known component of the complexity underlying its tumorigenic process. We have mapped a nasopharyngeal carcinoma susceptibility locus to chromosome 4p15.1-q12 in a previous linkage study on nasopharyngeal carcinoma pedigrees.

Adenoviral expression of a truncated S1 subunit of SARS-CoV spike protein results in specific humoral immune responses against SARS-CoV in rats.

The causative agent of severe acute respiratory syndrome (SARS) has been identified as SARS-associated coronavirus (SARS-CoV), but the prophylactic treatment of SARS-CoV is still under investigation. We constructed a recombinant adenovirus containing a truncated N-terminal fragment of the SARS-CoV Spike (S) gene (from--45 to 1469, designated Ad-S(N)), which encoded a truncated S protein (490 amino-acid residues, a part of 672 amino-acid S1 subunit), and investigated whether this construct could induce effective immunity against SARS-CoV in Wistar rats. Rats were immunized either subcutaneously or intranasally with Ad-S(N) once a week for three consecutive weeks.

A rare polymorphism of the COX7B2 gene in a Cantonese family with nasopharyngeal carcinoma.

Nasopharyngeal carcinoma (NPC) is the most common head and neck cancer in southern China, and the genetic susceptibility is believed to play an important role in the aetiology of this malignancy. In our previous studies, one candidate susceptibility locus has been mapped to chromosome 4p11-p14 in a subset of NPC families. In the present study, we screened the cytochrome oxidase VIIb2 (COX7B2) gene which resides in this region and investigated the relationship of single nucleotide polymorphisms (SNPs) of this gene with these familial NPC patients.

Transcriptional gene expression profile of human nasopharynx.

Inflammation in the nasopharynx is very common worldwide and nasopharyngeal carcinoma (NPC) results in significant morbidity and mortality in southeast Asia and north Africa. To facilitate the understanding of pathogenesis of these diseases as well as normal nasopharynx biology, transcriptional gene expression profile of normal human nasopharynx, from undissected biopsies, was established in this study by generating a large amount of ESTs, followed by bioinformatics analysis. A total of 27,209 ESTs generated from human nasopharynx cDNA library were integrated into 8,420 non-redundant clusters, of which, 6,070 (72.

Genetic polymorphisms of CYP2A13 and its relationship to nasopharyngeal carcinoma in the Cantonese population.

Nasopharyngeal carcinoma (NPC) is characterized by a high prevalence in Southern China, especially among Cantonese individuals of the Guangdong Province. Epidemiological studies have suggested that frequent exposure to high levels of nitrosamine from preserved foods such as salted fish could be a risk factor for NPC. Cytochrome P450 encompasses a family of enzymes that metabolize carcinogens and CYP2A13, a member of this family, is expressed predominantly in the respiratory tract with the highest levels in the nasal mucosa.

[Mutation and amplification of RIT1 gene in hepatocellular carcinoma].

Objective: To explore the mutation and amplification of RIT1 gene and their correlation with carcinogenesis of hepatocellular carcinoma (HCC).

Methods: The polymerase chain reactioindirect sequencing method was used for detecting the mutations in the sequence of all 6 exons in the RIT1 gene of 50 HCC tissues and paratumor tissues. And the amplification of RIT1 gene was examined by fluorescence quantitative polymerase chain reaction method.

[Amplification of RIT1 in hepatocellular carcinoma and its clinical significance].

Background & Objective: Previous study has demonstrated that high frequent gain of 1q was detected in hepatocellular carcinoma (HCC), 1q21-22 was identified as the minimum overlapping amplified region and might contain the candidate oncogenes involved in HCC. RIT1 gene is located in 1q21.3 region and is a member of Ras subfamily.

Alterations of BLU, a candidate tumor suppressor gene on chromosome 3p21.3, in human nasopharyngeal carcinoma.

Nonrandom allelic loss on chromosome 3p is a common event in nasopharyngeal carcinoma (NPC) with the implication that certain tumor suppressor gene(s) in this region are involved in the pathogenesis of these tumors. The BLU gene, located at 3p21.3, has recently been identified as a candidate tumor suppressor gene due to the occurrence of missense mutations and loss of its expression in lung cancer.

[Mutation and expression of SEMA3B and SEMA3F gene in nasopharyngeal carcinoma].

Background & Objective: Though the molecular etiology of nasopharyngeal carcinoma(NPC) is currently unknown, evidence from both loss of heterozygosity analysis and functional studies suggested that there are NPC-associated tumor suppressor genes(TSGs) residing in chromosome 3p21.3. Recently, two members of semaphorin family, SEMA3B and SEMA3F gene, located at 3p21.

[Mutation analysis of KLF6 gene in human nasopharyngeal carcinomas].

Background & Objective: Nasopharyngeal carcinoma (NPC) is one of the most common cancers in South China and Southeast Asia. The etiological factor is believed to be the interaction between genetic susceptibility, EBV infection and environmental factors, involved in the multi-step process of carcinogenesis and development of NPC. However, the molecular pathology of NPC is unclear yet.