Abstract: Cancer specific DNA methylation regions have been studied to find cancer specific DNA methylation markers for most common cancers. Differentially methylated regions for individual cancer types were identified and those were further filtered against data from normal tissues to obtain marker regions with cancer specific methylation, resulting in total of 1,250 hypermethylated and 584 hypomethylated marker CpGs. Optimal sets of six markers for each TCGA cancer type that could identify most tumors with high specificity and sensitivity (AUC 0.969-1.00) were chosen from hypermethylated markers and a universal 12 marker set that can detect tumors of all 33 TCGA cancer types (AUC>0.84) was also chosen from hypermethylated markers.

Abstract: Cancer specific DNA methylation regions have been studied to find cancer specific DNA methylation markers for most common cancers. Differentially methylated regions for individual cancer types were identified and those were further filtered against data from normal tissues to obtain marker regions with cancer specific methylation, resulting in total of 1,250 hypermethylated and 584 hypomethylated marker CpGs. Optimal sets of six markers for each TCGA cancer type that could identify most tumors with high specificity and sensitivity (AUC 0.969-1.00) were chosen from hypermethylated markers and a universal 12 marker set that can detect tumors of all 33 TCGA cancer types (AUC>0.84) was also chosen from hypermethylated markers.

Abstract: Cancer is the second most common cause of death worldwide, identification of cancer-specific DNA methylation events released by tumors into blood can be used for cost-effective, minimally invasive diagnostics and monitoring of cancer. The present invention clinically tested a set of ten DNA methylation specific qPCR amplicons, designed to detect most common human carcinoma types, in cell free DNA extracted from plasma fraction of blood samples from healthy controls and non-small cell lung cancer (NSCLC) cases. The DNA methylation biomarkers distinguish lung cancer cases from controls with high sensitivity and specificity (AUC=0.956), and furthermore, the signal from the markers depends on the tumor size and decreases after surgical resection of lung tumors. These observations indicate clinical value of these DNA methylation biomarkers for minimally invasive diagnostics and monitoring of NSCLC. It is predicted that these DNA methylation biomarkers will detect additional carcinoma types as well.

Abstract: Aspects of the present disclosure include RNAs that confer a mortal phenotype and nucleic acids encoding same. Liposomes, recombinant cells, and pharmaceutical compositions that include the RNAs or nucleic acids encoding same are also provided. Further provided are methods involving quantifying MORT RNAs and/or determining the methylation status of the MORT promoter, as well as methods that employ the RNAs or nucleic acids encoding same.

Abstract: Cancer specific DNA methylation regions have been studied to find cancer specific DNA methylation markers for most common cancers. Differentially methylated regions for individual cancer types were identified and those were further filtered against data from normal tissues to obtain marker regions with cancer specific methylation, resulting in total of 1,250 hypermethylated and 584 hypomethylated marker CpGs. Optimal sets of six markers for each TCGA cancer type that could identify most tumors with high specificity and sensitivity (AUC 0.969-1.00) were chosen from hypermethylated markers and a universal 12 marker set that can detect tumors of all 33 TCGA cancer types (AUC >0.84) was also chosen from hypermethylated markers.

Abstract: Aspects of the present disclosure include RNAs that confer a mortal phenotype and nucleic acids encoding same. Liposomes, recombinant cells, and pharmaceutical compositions that include the RNAs or nucleic acids encoding same are also provided. Further provided are methods involving quantifying MORT RNAs and/or determining the methylation status of the MORT promoter, as well as methods that employ the RNAs or nucleic acids encoding same.

Abstract: Methods for inducing non-clonal immortalization of normal epithelial cells by directly targeting the two main senescence barriers encountered by cultured epithelial cells. In finite lifespan pre-stasis human mammary epithelial cells (HMEC), the stress-associated stasis barrier was bypassed, and in post-stasis HMEC, the replicative senescence barrier, a consequence of critically shortened telomeres, was bypassed. Early passage non-clonal immortalized lines exhibited normal karyotypes. Methods of efficient HMEC immortalization, in the absence of “passenger” genomic errors, should facilitate examination of telomerase regulation and immortalization during human carcinoma progression, methods for screening for toxic and environmental effect on progression, and the development of therapeutics targeting the process of immortalization.

Abstract: Methods for inducing non-clonal immortalization of normal epithelial cells by directly targeting the two main senescence barriers encountered by cultured epithelial cells. In human mammary epithelial cells (HMEC), the stress-associated stasis barrier was bypassed and the replicative senescence barrier, a consequence of critically shortened telomeres, was bypassed in post-stasis HMEC. Early passage non-clonal immortalized lines exhibited normal karyotypes. Methods of efficient HMEC immortalization, in the absence of “passenger” genomic errors, should facilitate examination of telomerase regulation, immortalization during human carcinoma progression, and methods for screening for toxic and environmental effect on progression.