{"title":"Increased PAFAH1B3 was associated with poor prognosis and T-cell exhaustion microenvironment in hepatocellular carcinoma","authors":"Genhao Zhang","doi":"10.1007/s12672-023-00845-6","DOIUrl":"https://doi.org/10.1007/s12672-023-00845-6","url":null,"abstract":"<p>The link between T-cell exhaustion (TEX) and PAFAH1B3 in hepatocellular carcinoma (HCC) remains unknown, even though both of them are related to overall survival. PAFAH1B3 expression was investigated in TCGA and ICGC data, and 50 paired clinical tissue section samples were used for qRT-PCR and immunohistochemistry (IHC) confirmation. The Immunocell Abundance Identifier (ImmuCellAI) was used to precisely calculate the abundance of TEX, and its accuracy was verified by single-cell RNA-seq and labeling of CD8 + T cells in clinical tissue sections. The IMVigor 210 cohort was used to demonstrate the predictive value of PAFAH1B3 for immunotherapy efficacy. Increased PAFAH1B3 is a standalone effector of poor prognosis in HCC patients. Patients who had greater PAFAH1B3 levels had more TEX infiltration. PAFAH1B3 expression was increased in TEX in the single-cell RNA-seq data. Patients with high PAFAH1B3 expression were more likely to respond favorably to PD1/PD-L1 treatment. In conclusion, PAFAH1B3 is closely related to TEX in the tumor microenvironment (TME) and can be a useful indicator for PD1/PD-L1 therapy.</p>","PeriodicalId":13170,"journal":{"name":"Hormones and Cancer","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138563503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Infection with COVID-19 promotes the progression of pancreatic cancer through the PI3K-AKT signaling pathway","authors":"Xusheng Zhang, Bendong Chen, Kejun Liu, Yongxin Ma, Yimin Liu, Hongcai Zhou, Peng Wei","doi":"10.1007/s12672-023-00842-9","DOIUrl":"https://doi.org/10.1007/s12672-023-00842-9","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Objective</h3><p>To investigate the effect of COVID-19 infection on pancreatic cancer.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>Based on the mRNA-Seq data of COVID-19 patients and pancreatic cancer (PC) patients in the GEO database, we used a support vector machine (SVM), LASSO-Cox regression analysis and random forest tree (RF) to screen the common signature genes of the two diseases and further investigate their effects and functional characteristics on PC, respectively. The above procedures were performed in R software.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>The proteins COL10A1/FAP/FN1 were found to be common signature genes for COVID-19 and PC, were significantly up-regulated in both diseases and showed good diagnostic efficacy for PC. The risk model based on COL10A1/FAP/FN1 showed good PC risk prediction ability and clinical application potential. Tumor typing based on COL10A1/FAP/FN1 expression levels effectively classified PC into different subtypes and showed significant differences between the two subtypes in terms of survival prognosis, immune levels, immune checkpoint expression levels, mutation status of common tumor mutation sites, and drug sensitivity analysis. While pathway analysis also revealed that FN1 as an extracellular matrix component may be involved in the biological process of PC by regulating the PI3K-AKT signaling axis.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>The upregulated expression of COL10A1/FAP/FN1, the characteristic genes of COVID-19, are potential diagnostic targets for PC, and the upregulated expression of FN1 may promote the progression of PC by activating the PI3K-AKT signaling pathway. The COL10A1/FAP/FN1-based typing provides a new typing approach for PC, and also provides a good reference and idea for the refinement of PC treatment and subsequent clinical research.</p>","PeriodicalId":13170,"journal":{"name":"Hormones and Cancer","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138563237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jessica L. Christenson, Kiel T. Butterfield, Nicole S. Spoelstra, J. Norris, J. Josan, Julie A. Pollock, D. McDonnell, B. Katzenellenbogen, J. Katzenellenbogen, J. Richer
{"title":"MMTV-PyMT and Derived Met-1 Mouse Mammary Tumor Cells as Models for Studying the Role of the Androgen Receptor in Triple-Negative Breast Cancer Progression","authors":"Jessica L. Christenson, Kiel T. Butterfield, Nicole S. Spoelstra, J. Norris, J. Josan, Julie A. Pollock, D. McDonnell, B. Katzenellenbogen, J. Katzenellenbogen, J. Richer","doi":"10.1007/s12672-017-0285-6","DOIUrl":"https://doi.org/10.1007/s12672-017-0285-6","url":null,"abstract":"","PeriodicalId":13170,"journal":{"name":"Hormones and Cancer","volume":"86 1 1","pages":"69-77"},"PeriodicalIF":0.0,"publicationDate":"2017-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87678485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Contribution of Cholesterol and Its Metabolites to the Pathophysiology of Breast Cancer","authors":"A. Baek, E. Nelson","doi":"10.1007/s12672-016-0262-5","DOIUrl":"https://doi.org/10.1007/s12672-016-0262-5","url":null,"abstract":"","PeriodicalId":13170,"journal":{"name":"Hormones and Cancer","volume":"60 1","pages":"219-228"},"PeriodicalIF":0.0,"publicationDate":"2016-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84703095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R. Chatterton, Richard E. Heinz, A. Fought, D. Ivancic, C. Shappell, Subhashini Allu, S. Gapstur, D. Scholtens, P. Gann, S. Khan
{"title":"Nipple Aspirate Fluid Hormone Concentrations and Breast Cancer Risk","authors":"R. Chatterton, Richard E. Heinz, A. Fought, D. Ivancic, C. Shappell, Subhashini Allu, S. Gapstur, D. Scholtens, P. Gann, S. Khan","doi":"10.1007/s12672-016-0252-7","DOIUrl":"https://doi.org/10.1007/s12672-016-0252-7","url":null,"abstract":"","PeriodicalId":13170,"journal":{"name":"Hormones and Cancer","volume":"1 1","pages":"127-136"},"PeriodicalIF":0.0,"publicationDate":"2016-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84151951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hormones and CancerPub Date : 2016-02-01Epub Date: 2016-01-04DOI: 10.1007/s12672-015-0237-y
Cher M Dallal, James V Lacey, Ruth M Pfeiffer, Douglas C Bauer, Roni T Falk, Diana S M Buist, Jane A Cauley, Trisha F Hue, Andrea Z LaCroix, Jeffrey A Tice, Timothy D Veenstra, Xia Xu, Louise A Brinton
{"title":"Estrogen Metabolism and Risk of Postmenopausal Endometrial and Ovarian Cancer: the B ∼ FIT Cohort.","authors":"Cher M Dallal, James V Lacey, Ruth M Pfeiffer, Douglas C Bauer, Roni T Falk, Diana S M Buist, Jane A Cauley, Trisha F Hue, Andrea Z LaCroix, Jeffrey A Tice, Timothy D Veenstra, Xia Xu, Louise A Brinton","doi":"10.1007/s12672-015-0237-y","DOIUrl":"10.1007/s12672-015-0237-y","url":null,"abstract":"<p><p>Estrogen metabolites may have different genotoxic and mitogenic properties yet their relationship with endometrial and ovarian cancer risk remains unclear. Within the Breast and Bone Follow-up to the Fracture Intervention Trial (B ∼ FIT, n = 15,595), we conducted a case-cohort study to evaluate 15 pre-diagnostic serum estrogens and estrogen metabolites with risk of incident endometrial and ovarian cancer among postmenopausal women not on hormone therapy. Participants included 66 endometrial and 67 ovarian cancer cases diagnosed during follow-up (∼ 10 years) and subcohorts of 346 and 416 women, respectively, after relevant exclusions. Serum concentrations were measured by liquid chromatography-tandem mass spectrometry. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazard regression. Exposures were categorized in tertiles (T) and analyzed individually, as metabolic pathways (C-2, -4, or -16) and as ratios to parent estrogens (estradiol, estrone). Estradiol was significantly associated with increased endometrial cancer risk (BMI-adjusted HRT3vsT1 = 4.09, 95% CI 1.70, 9.85; p trend = 0.003). 2-Hydroxyestrone and 16α-hydroxyestrone were not associated with endometrial risk after estradiol adjustment (2-OHE1:HRT3vsT1 = 1.97, 95% CI 0.78, 4.94; 16-OHE1:HRT3vsT1 = 1.50, 95% CI 0.65, 3.46; p trend = 0.16 and 0.36, respectively). Ratios of 2- and 4-pathway catechol-to-methylated estrogens remained positively associated with endometrial cancer after BMI or estradiol adjustment (2-pathway catechols-to-methylated: HRT3vsT1 = 4.02, 95% CI 1.60, 10.1; 4-pathway catechols-to-methylated: HRT3vsT1 = 4.59, 95% CI 1.64, 12.9; p trend = 0.002 for both). Estrogens and estrogen metabolites were not associated with ovarian cancer risk; however, larger studies are needed to better evaluate these relationships. Estrogen metabolism may be important in endometrial carcinogenesis, particularly with less extensive methylation of 2- or 4-pathway catechols associated with elevated endometrial cancer risk.</p>","PeriodicalId":13170,"journal":{"name":"Hormones and Cancer","volume":"7 1","pages":"49-64"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8900527/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81456039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ailin Zhang, Jiawei Zhang, S. Plymate, E. Mostaghel
{"title":"Classical and Non-Classical Roles for Pre-Receptor Control of DHT Metabolism in Prostate Cancer Progression","authors":"Ailin Zhang, Jiawei Zhang, S. Plymate, E. Mostaghel","doi":"10.1007/s12672-016-0250-9","DOIUrl":"https://doi.org/10.1007/s12672-016-0250-9","url":null,"abstract":"","PeriodicalId":13170,"journal":{"name":"Hormones and Cancer","volume":"51 1","pages":"104-113"},"PeriodicalIF":0.0,"publicationDate":"2016-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86155255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Wierman, R. Auchus, D. Haisenleder, J. Hall, David Handelsman, S. Hankinson, W. Rosner, Ravinder J Singh, P. Sluss, F. Stanczyk
{"title":"The New Instructions to Authors for the Reporting of Steroid Hormone Measurements","authors":"M. Wierman, R. Auchus, D. Haisenleder, J. Hall, David Handelsman, S. Hankinson, W. Rosner, Ravinder J Singh, P. Sluss, F. Stanczyk","doi":"10.1007/s12672-014-0202-1","DOIUrl":"https://doi.org/10.1007/s12672-014-0202-1","url":null,"abstract":"","PeriodicalId":13170,"journal":{"name":"Hormones and Cancer","volume":"23 3 1","pages":"357"},"PeriodicalIF":0.0,"publicationDate":"2014-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83579246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hormones and Cancer is Alive and Well at ICE/ENDO 2014","authors":"C. Lange","doi":"10.1007/s12672-014-0178-x","DOIUrl":"https://doi.org/10.1007/s12672-014-0178-x","url":null,"abstract":"","PeriodicalId":13170,"journal":{"name":"Hormones and Cancer","volume":"54 1","pages":"125-126"},"PeriodicalIF":0.0,"publicationDate":"2014-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73056189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}