The estimation of the probability of informed trading(PIN)model and its extensions poses significant challenges owing to various computational problems.To address these issues,we propose a novel estimation method call...The estimation of the probability of informed trading(PIN)model and its extensions poses significant challenges owing to various computational problems.To address these issues,we propose a novel estimation method called the expectation-conditional-maximization(ECM)algorithm,which can serve as an alternative to the existing methods for estimating PIN models.Our method provides optimal estimates for the original PIN model as well as two of its extensions:the multilayer PIN model and the adjusted PIN model,along with its restricted versions.Our results indicate that estimations using the ECM algorithm are generally faster,more accurate,and more memory-efficient than the standard methods used in the literature,making it a robust alternative.More importantly,the ECM algorithm is not limited to the models discussed and can be easily adapted to estimate future extensions of the PIN model.展开更多
The phosphatase and tensin homolog （PTEN） and the zinc finger homeobox 3 （ZFHX3）/AT-motif binding factor 1 （ATBF1） genes have been established as tumor suppressor genes in prostate cancer by their frequent delet...The phosphatase and tensin homolog （PTEN） and the zinc finger homeobox 3 （ZFHX3）/AT-motif binding factor 1 （ATBF1） genes have been established as tumor suppressor genes in prostate cancer by their frequent deletions and mutations in human prostate cancer and by the formation of mouse prostatic intraepithelial neoplasia （mPIN） or tumor by their deletions in mouse prostates. However, whether ZFHX3/ATBF1 deletion together with PTEN deletion facilitates prostatic tumorigenesis is unknown. In this study, we simultaneously deleted both genes in mouse prostatic epithelia and performed histological and molecular analyses. While deletion of one Pten allele alone caused low-grade （LG） mPIN as previously reported, concurrent deletion of Zfhx3/Atbfl promoted the progression to high-grade （HG） mPIN or early carcinoma. ZJhx3/Atbfl and Pten deletions together increased cell proliferation, disrupted the smooth muscle layer between epithelium and stroma, and increased the number of apoptotic cells. Deletion of both genes also accelerated the activation of Akt and Erkl/2 oncoproteins. These results suggest an additive effect of ZFHX3/ATBF1 and PTEN deletions on the development and progression of prostate neoplasia.展开更多
基金supported by the Scientific and Technological Research Council of Turkey(TUBITAK)[grant no 122K637].
文摘The estimation of the probability of informed trading(PIN)model and its extensions poses significant challenges owing to various computational problems.To address these issues,we propose a novel estimation method called the expectation-conditional-maximization(ECM)algorithm,which can serve as an alternative to the existing methods for estimating PIN models.Our method provides optimal estimates for the original PIN model as well as two of its extensions:the multilayer PIN model and the adjusted PIN model,along with its restricted versions.Our results indicate that estimations using the ECM algorithm are generally faster,more accurate,and more memory-efficient than the standard methods used in the literature,making it a robust alternative.More importantly,the ECM algorithm is not limited to the models discussed and can be easily adapted to estimate future extensions of the PIN model.
基金supported in part by the grants from the National Cancer Institute(NCI)(No.R01CA121459)the National Institutes of Health(NIH)+1 种基金supported in part by the Integrated Cellular Imaging Shared Resource of Winship Cancer Institute of Emory Universitythe NIH/NCI under award number P30CA138292
文摘The phosphatase and tensin homolog （PTEN） and the zinc finger homeobox 3 （ZFHX3）/AT-motif binding factor 1 （ATBF1） genes have been established as tumor suppressor genes in prostate cancer by their frequent deletions and mutations in human prostate cancer and by the formation of mouse prostatic intraepithelial neoplasia （mPIN） or tumor by their deletions in mouse prostates. However, whether ZFHX3/ATBF1 deletion together with PTEN deletion facilitates prostatic tumorigenesis is unknown. In this study, we simultaneously deleted both genes in mouse prostatic epithelia and performed histological and molecular analyses. While deletion of one Pten allele alone caused low-grade （LG） mPIN as previously reported, concurrent deletion of Zfhx3/Atbfl promoted the progression to high-grade （HG） mPIN or early carcinoma. ZJhx3/Atbfl and Pten deletions together increased cell proliferation, disrupted the smooth muscle layer between epithelium and stroma, and increased the number of apoptotic cells. Deletion of both genes also accelerated the activation of Akt and Erkl/2 oncoproteins. These results suggest an additive effect of ZFHX3/ATBF1 and PTEN deletions on the development and progression of prostate neoplasia.
