Hormones & Cancer最新文献

{"title":"Platelet ATP, Thyroid Hormone Receptor on Integrin αvβ3 and Cancer Metastasis.","authors":"Paul J Davis,&nbsp;Shaker A Mousa,&nbsp;Geraldine P Schechter,&nbsp;Hung-Yun Lin","doi":"10.1007/s12672-019-00371-4","DOIUrl":"https://doi.org/10.1007/s12672-019-00371-4","url":null,"abstract":"<p><p>Activated platelets may contribute to the metastatic behavior of tumor cells when the cancer cells and platelets interact. The interaction requires cell and platelet surface integrin. Thyroid hormone as L-thyroxine (T4) is the principal ligand for a hormone receptor on integrin αvβ3 on tumor cells and platelets. T4 activates the integrin, promoting platelet aggregation and degranulation (local ATP release) and stimulating tumor cell proliferation. By a variety of molecular mechanisms reviewed here, extracellular ATP promotes tumor cell invasiveness and metastasis and supports a role for T4 as a pro-metastatic factor.</p>","PeriodicalId":13060,"journal":{"name":"Hormones & Cancer","volume":"11 1","pages":"13-16"},"PeriodicalIF":3.0,"publicationDate":"2020-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12672-019-00371-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9847437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Thyroid Hormone Receptor-RUNX2 Axis: A Novel Tumor Suppressive Pathway in Breast Cancer.","authors":"Eric L Bolf,&nbsp;Noelle E Gillis,&nbsp;Michael S Barnum,&nbsp;Caitlin M Beaudet,&nbsp;Grace Y Yu,&nbsp;Jennifer A Tomczak,&nbsp;Janet L Stein,&nbsp;Jane B Lian,&nbsp;Gary S Stein,&nbsp;Frances E Carr","doi":"10.1007/s12672-019-00373-2","DOIUrl":"https://doi.org/10.1007/s12672-019-00373-2","url":null,"abstract":"<p><p>Metastatic breast cancer is refractory to conventional therapies and is an end-stage disease. RUNX2 is a transcription factor that becomes oncogenic when aberrantly expressed in multiple tumor types, including breast cancer, supporting tumor progression and metastases. Our previous work demonstrated that the thyroid hormone receptor beta (TRβ) inhibits RUNX2 expression and tumorigenic characteristics in thyroid cells. As TRβ is a tumor suppressor, we investigated the compelling question whether TRβ also regulates RUNX2 in breast cancer. The Cancer Genome Atlas indicates that TRβ expression is decreased in the most aggressive basal-like subtype of breast cancer. We established that modulated levels of TRβ results in corresponding changes in the high levels of RUNX2 expression in metastatic, basal-like breast cells. The MDA-MB-231 triple-negative breast cancer cell line exhibits low expression of TRβ and high levels of RUNX2. Increased expression of TRβ decreased RUNX2 levels. The thyroid hormone-mediated suppression of RUNX2 is TRβ specific as TRα overexpression failed to alter RUNX2 expression. Consistent with these findings, knockdown of TRβ in non-tumor MCF10A mammary epithelial-like cells results in an increase in RUNX2 and RUNX2 target genes. Mechanistically, TRβ directly interacts with the proximal promoter of RUNX2 through a thyroid hormone response element to reduce promoter activity. The TRβ suppression of the oncogene RUNX2 is a signaling pathway shared by thyroid and breast cancers. Our findings provide a novel mechanism for TRβ-mediated tumor suppression in breast cancers. This pathway may be common to many solid tumors and impact treatment for metastatic cancers.</p>","PeriodicalId":13060,"journal":{"name":"Hormones & Cancer","volume":" ","pages":"34-41"},"PeriodicalIF":3.0,"publicationDate":"2020-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12672-019-00373-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37481206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular and Electrophysiological Analyses of ATP2B4 Gene Variants in Bilateral Adrenal Hyperaldosteronism.","authors":"Namita Ganesh Hattangady,&nbsp;Jessica Foster,&nbsp;Antonio Marcondes Lerario,&nbsp;Daniela Ponce-Balbuena,&nbsp;Juilee Rege,&nbsp;Silvia Monticone,&nbsp;William E Rainey,&nbsp;Paolo Mulatero,&nbsp;Tobias Else","doi":"10.1007/s12672-019-00375-0","DOIUrl":"https://doi.org/10.1007/s12672-019-00375-0","url":null,"abstract":"<p><p>Primary aldosteronism (PA) is the most common cause of secondary hypertension with a high prevalence among patients with resistant hypertension. Despite the recent discovery of somatic variants in aldosterone-producing adenoma (APA)-associated PA, causes for PA due to bilateral aldosterone production (bilateral hyperaldosteronism; BHA) remain unknown. Herein, we identified rare gene variants in ATP2B4, in a cohort of patients with BHA. ATP2B4 belongs to the same family of Ca-ATPases as ATP2B3, which is involved in the pathogenesis of APA. Endogenous ATP2B4 expression was characterized in adrenal tissue, and the gene variants were functionally analyzed for effects on aldosterone synthase (CYP11B2) expression, steroid production in basal and agonist-stimulated conditions, and for changes in biophysical properties of channel properties. Knockdown of ATP2B4 in HAC15 exhibited reduced angiotensin II stimulation in one of four shRNA clones. Stable HAC15 cell lines with doxycycline (dox) - inducible wild-type and variant forms of ATP2B4 - were generated, and dox-induced upregulation of ATP2B4 mRNA and protein was confirmed. However, ATP2B4 variants did not alter basal or agonist-stimulated CYP11B2 expression. Whole-cell recordings in HAC15 cells indicated robust endogenous ATP2B4 conductance in native cells but reduced conductance with overexpressed WT and variant ATP2B4. The previously defined PA-causing ATP2B3 variant served as a positive control and exhibited elevated CYP11B2 mRNA. In conclusion, while this study did not confirm a pathogenic role for ATP2B4 variants in BHA, we describe the sequencing analysis for familial and sporadic BHA and outline a template for the thorough in vitro characterization of gene variants.</p>","PeriodicalId":13060,"journal":{"name":"Hormones & Cancer","volume":" ","pages":"52-62"},"PeriodicalIF":3.0,"publicationDate":"2020-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12672-019-00375-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37596759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Computational Statistics Approach to Evaluate Blood Biomarkers for Breast Cancer Risk Stratification.","authors":"Kaan Oktay,&nbsp;Ashlie Santaliz-Casiano,&nbsp;Meera Patel,&nbsp;Natascia Marino,&nbsp;Anna Maria V Storniolo,&nbsp;Hamdi Torun,&nbsp;Burak Acar,&nbsp;Zeynep Madak Erdogan","doi":"10.1007/s12672-019-00372-3","DOIUrl":"https://doi.org/10.1007/s12672-019-00372-3","url":null,"abstract":"<p><p>Breast cancer is the second leading cause of cancer mortality among women. Mammography and tumor biopsy followed by histopathological analysis are the current methods to diagnose breast cancer. Mammography does not detect all breast tumor subtypes, especially those that arise in younger women or women with dense breast tissue, and are more aggressive. There is an urgent need to find circulating prognostic molecules and liquid biopsy methods for breast cancer diagnosis and reducing the mortality rate. In this study, we systematically evaluated metabolites and proteins in blood to develop a pipeline to identify potential circulating biomarkers for breast cancer risk. Our aim is to identify a group of molecules to be used in the design of portable and low-cost biomarker detection devices. We obtained plasma samples from women who are cancer free (healthy) and women who were cancer free at the time of blood collection but developed breast cancer later (susceptible). We extracted potential prognostic biomarkers for breast cancer risk from plasma metabolomics and proteomics data using statistical and discriminative power analyses. We pre-processed the data to ensure the quality of subsequent analyses, and used two main feature selection methods to determine the importance of each molecule. After further feature elimination based on pairwise dependencies, we measured the performance of logistic regression classifier on the remaining molecules and compared their biological relevance. We identified six signatures that predicted breast cancer risk with different specificity and selectivity. The best performing signature had 13 factors. We validated the difference in level of one of the biomarkers, SCF/KITLG, in plasma from healthy and susceptible individuals. These biomarkers will be used to develop low-cost liquid biopsy methods toward early identification of breast cancer risk and hence decreased mortality. Our findings provide the knowledge basis needed to proceed in this direction.</p>","PeriodicalId":13060,"journal":{"name":"Hormones & Cancer","volume":"11 1","pages":"17-33"},"PeriodicalIF":3.0,"publicationDate":"2020-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12672-019-00372-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9847438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of miR-196-5p Induced by Hypoxia Drives Tumorigenesis and Metastasis in Hepatocellular Carcinoma.","authors":"Hao Zheng, Feng-Rui Bi, Yuan Yang, Yong-Gang Hong, Jun-Sheng Ni, Long Ma, Ming-Hua Liu, Li-Qiang Hao, Wei-Ping Zhou, Li-Hua Song, Hong-Li Yan","doi":"10.1007/s12672-019-00370-5","DOIUrl":"10.1007/s12672-019-00370-5","url":null,"abstract":"<p><p>In hepatocellular carcinoma (HCC), the hypoxic tumor microenvironment can drive enhance tumor malignancy and recurrence. The microRNA (miRNA) miR-196-5p has been shown to modulate the progression of several cancer types, but its roles in HCC remain uncertain. In the present report we observed significant miR-196-5p downregulation in HCC tissues and cells, and we found that the expression of this miRNA significantly impaired the proliferation and metastatic potential of HCC in vitro and in vivo. We identified high-mobility group AT-hook 2 (HMGA2) as a miR-196-5p target gene that was associated with the ability of miR-196-5p to modulate the progression of HCC. Expression of miR-196-5p and HMGA2 were correlated with the clinical characteristics and poor outcomes in patients with HCC. Finally, we found that hypoxic conditions were linked with reduced miR-196-5p expression in the context of HCC. Together these results highlight the role for miR-196-5p as an inhibitor of the proliferation and metastasis of HCC via the targeting of HMGA2, with this novel hypoxia/miR-196-5p/HMGA2 pathway serving as a potential target for future therapeutic intervention.</p>","PeriodicalId":13060,"journal":{"name":"Hormones & Cancer","volume":"10 4-6","pages":"177-189"},"PeriodicalIF":3.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10355717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9901726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Collagen and PAPP-A in the Etiology of Postpartum Breast Cancer.","authors":"Elizabeth Slocum,&nbsp;Doris Germain","doi":"10.1007/s12672-019-00368-z","DOIUrl":"https://doi.org/10.1007/s12672-019-00368-z","url":null,"abstract":"<p><p>Pregnancy has a dual effect on the risk of breast cancer. On one hand, pregnancy at a young age is known to be protective. However, pregnancy is also associated with a transient increased risk of breast cancer. For women that have children after the age of 30, the risk remains higher than women who never had children for decades. Involution of the breast has been identified as a window of mammary development associated with the adverse effect of pregnancy. In this review, we summarize the current understanding of the role of involution and describe the role of collagen in this setting. We also discuss the role of a collagen-dependent protease, pappalysin-1, in postpartum breast cancer and its role in activating both insulin-like growth factor signaling and discoidin domain collagen receptor 2, DDR2. Together, these novel advances in our understanding of postpartum breast cancer open the way to targeted therapies against this aggressive breast cancer sub-type.</p>","PeriodicalId":13060,"journal":{"name":"Hormones & Cancer","volume":"10 4-6","pages":"137-144"},"PeriodicalIF":3.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12672-019-00368-z","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10205119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-4500 Regulates PLXNC1 and Inhibits Papillary Thyroid Cancer Progression.","authors":"Rui Li,&nbsp;Xin Teng,&nbsp;Haicheng Zhu,&nbsp;Tongliang Han,&nbsp;Qingwei Liu","doi":"10.1007/s12672-019-00366-1","DOIUrl":"https://doi.org/10.1007/s12672-019-00366-1","url":null,"abstract":"<p><p>Although most patients with papillary thyroid cancer (PTC) are curable, there are still a few patients showing poor outcomes and increased risk of secondary cancers after therapies. In this study, we aimed to investigate the correlation between miR-4500 and PTC and to explore its molecular functions. A total of 50 patients were included, and sonography and histological examinations were used for diagnosis. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied for detection of mRNA levels while Western blotting was used for measuring protein expression. Cell proliferation was tested using CCK-8 and colony formation assays. Caspase-3 activity and nucleosomal fragmentation assays were employed to test cell apoptosis. Cell invasive ability was measured using transwell assay. MiR-4500 target was identified using luciferase assay and RNA pull-down assay. MiR-4500 expression was significantly decreased in five PTC cell lines compared with Nthy-ori 3-1 cells and in PTC tissues compared with adjacent normal thyroid tissues, respectively. Decreased expression of miR-4500 showed lower survival rate, higher cancer stage, and lymphatic metastasis. Therefore, our results implied that miR-4500 could serve as a potential biomarker for PTC prognosis. Overexpression of miR-4500 repressed colony formation, proliferation, and invasiveness of PTC cells whereas increased cell apoptosis. We identified that PLXNC1 was a direct target of miR-4500. PLXNC1 knockdown showed similar effects on cell viability, colony formation, and cell apoptosis as overexpression of miR-4500 in PTC cells. In conclusion, miR-4500 inhibits the malignant transformation of PTC cells by directly targeting and repressing PLXNC1.</p>","PeriodicalId":13060,"journal":{"name":"Hormones & Cancer","volume":"10 4-6","pages":"150-160"},"PeriodicalIF":3.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12672-019-00366-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9901721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the Effect of Vitamin D Replacement on Basal Cell Carcinoma Occurrence and Recurrence Rates in Patients with Vitamin D Deficiency.","authors":"Bilsev Ince,&nbsp;Mehmet Emin Cem Yildirim,&nbsp;Mehmet Dadaci","doi":"10.1007/s12672-019-00365-2","DOIUrl":"https://doi.org/10.1007/s12672-019-00365-2","url":null,"abstract":"<p><p>The study aimed to determine whether 25-OH vitamin D₃ deficiency is present in patients with diagnosed BCC, and the effect of vitamin D replacement on the rates of BCC recurrence in patients with 25-OH vitamin D₃ deficiency. In this prospective study, between 2012 and 2017, in the first stage, 25-OH vitamin D₃ levels of all patients diagnosed with BCC between 2012 and 2013 were evaluated. In the second stage between 2014 and 2015, we evaluated the 25-OH vitamin D₃ level of patients who had 25-OH vitamin D₃ level < 25 ng/mL. All the patients included in the second stage had BCC recurrence. In the third stage, the patients who were diagnosed 25-OH vitamin D₃ deficiency with BCC, between 2015 and 2017, were studied. The mean 25-OH vitamin D₃ level of the patients in the second stage was 10.12 ng/mL. Recurrence was observed in 9.64% of the patients in the second stage. The mean level of serum 25-OH vitamin D₃ in the third stage was 40.1 ng/mL, and 3.49% of these patients presented with recurrence. In all the patients as the initial diagnosis and following the 25-OH vitamin D₃ level in all the patients with BCC recurrence, maintaining 25-OH vitamin D₃ levels above 25 ng/mL can significantly reduce the recurrence rate.</p>","PeriodicalId":13060,"journal":{"name":"Hormones & Cancer","volume":"10 4-6","pages":"145-149"},"PeriodicalIF":3.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12672-019-00365-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10205111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Long-Term Dynamics in Circulating Testosterone with Serum PSA in Prostate Cancer-Free Men with Initial-PSA < 4 ng/mL.","authors":"Kai Wang,&nbsp;Xinguang Chen,&nbsp;Ting-Yuan David Cheng,&nbsp;Peihua Qiu,&nbsp;Victoria Y Bird,&nbsp;Mattia Prosperi","doi":"10.1007/s12672-019-00369-y","DOIUrl":"https://doi.org/10.1007/s12672-019-00369-y","url":null,"abstract":"<p><p>We previously reported that an accelerated decline in circulating testosterone level is associated with a higher risk of prostate cancer (PCa). This study is to examine whether testosterone change rate is related to serum prostate-specific antigen (PSA) concentration among PCa-free men. Longitudinal data were derived from electronic medical records at a tertiary hospital in the Southeastern USA. PCa-free men with initial-PSA < 4 ng/mL and ≥ 2 testosterone measurements were included (n = 632). Three PSA measures (peak, the most recent, and average PSA) during the study period (from first testosterone measurement to the most recent hospital visit) were examined using multivariable-adjusted geometric means and were compared across quintiles of testosterone change rate (ng/dL/month) and current testosterone level (cross-sectional). Mean (standard deviation, SD) age at baseline was 59.3 (10.5) years; mean study period was 93.0 (55.3) months. After adjusting for covariates including baseline testosterone, the three PSA measures all significantly increased across quintile of testosterone change rate from increase to decline (peak PSA: quint 1 = 1.09, quint 5 = 1.41; the most recent PSA: quint 1 = 0.85, quint 5 = 1.00; average PSA: quint 1 = 0.89, quint 5 = 1.02; all P_trend < 0.001). But current testosterone level was not associated with PSA levels. Stratified analyses indicated men with higher adiposity (body mass index > 24.1 kg/m²) or lower baseline testosterone (≤ 296 ng/dL) were more sensitive to testosterone change in regard to PSA. Among PCa-free men, accelerated testosterone decline might correlate with higher serum PSA concentration. It will help to elucidate the mechanisms relating aging-accompanying testosterone dynamics to prostate carcinogenesis.</p>","PeriodicalId":13060,"journal":{"name":"Hormones & Cancer","volume":"10 4-6","pages":"168-176"},"PeriodicalIF":3.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12672-019-00369-y","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10205118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metastatic Adrenocortical Carcinoma: a Single Institutional Experience.","authors":"Dwight H Owen,&nbsp;Sandipkumar Patel,&nbsp;Lai Wei,&nbsp;John E Phay,&nbsp;Lawrence A Shirley,&nbsp;Lawrence S Kirschner,&nbsp;Carl Schmidt,&nbsp;Sherif Abdel-Misih,&nbsp;Pamela Brock,&nbsp;Manisha H Shah,&nbsp;Bhavana Konda","doi":"10.1007/s12672-019-00367-0","DOIUrl":"https://doi.org/10.1007/s12672-019-00367-0","url":null,"abstract":"<p><p>Adrenocortical carcinoma (ACC) is a rare malignancy with limited data to guide the management of metastatic disease. The optimal treatment strategies and outcomes of patients with metastatic ACC remain areas of active interest. We retrospectively reviewed patients with ACC who were treated with systemic therapy between January 1997 and October 2016 at The Ohio State University Comprehensive Cancer Center. Kaplan-Meier and Cox proportional hazards regression models were used for survival analysis. We identified 65 patients diagnosed with ACC during the given time period, and 36 patients received systemic therapy for distant metastatic disease. Median age at diagnosis was 50 (range 28-87). Median overall survival (OS) from time of diagnosis of ACC was 27 months (95% CI 19.6-39.3), and median OS from time of systemic treatment for metastatic disease was 18.7 months (95% CI 9.3-26.0). Clinical characteristics at time of initiation of systemic therapy were assessed, and presence of bone metastases (p = 0.66), ascites (p = 0.19), lung metastases (p = 0.12), liver metastases (p = 0.47), as well as hormonal activity of tumor (p = 0.19), were not prognostic for survival. Six patients with liver metastases treated with systemic therapy who received liver-directed therapy with either transarterial chemoembolization (TACE) or selective internal radiation therapy (SIRT) had longer survival than those who did not (p = 0.011). Our data expands the knowledge of clinical characteristics and outcomes of patients with ACC and suggests a possible role for incorporating liver-directed therapies for patients with hepatic metastases.</p>","PeriodicalId":13060,"journal":{"name":"Hormones & Cancer","volume":"10 4-6","pages":"161-167"},"PeriodicalIF":3.0,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s12672-019-00367-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10223771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}