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Article ; Online: Novel insights into molecular and immune subtypes of biliary tract cancers.

Bramel, Emily R / Sia, Daniela

2022 Volume 156, Page(s) 167–199

Abstract: Biliary tract cancers (BTCs), which include cholangiocarcinoma (CCA) and gallbladder cancer (GBC), are heterogenous malignancies characterized by distinct molecular features often associated with specific clinical traits and/or outcomes. Such complex ... ...

Abstract	Biliary tract cancers (BTCs), which include cholangiocarcinoma (CCA) and gallbladder cancer (GBC), are heterogenous malignancies characterized by distinct molecular features often associated with specific clinical traits and/or outcomes. Such complex molecular heterogeneity, both within each BTC subtype and between distinct subtypes, poses a great challenge to personalized medicine. Recent technological advances have allowed the integration of multiple -omics derived from large cohorts of patients with distinct solid cancers to ultimately design stratification algorithms for prognostic prediction or more efficient treatment allocation. In this regard, although BTCs lag behind other tumors when it comes to our understanding of their molecular complexity, over the past decade, tremendous efforts have been made to generate supervised or unsupervised molecular classifications. As a result, CCAs and GBCs can be assigned to distinct molecular and/or prognostic classes. Notably, the discovery of biologically relevant subgroups of tumors harboring frequent targetable alterations (i.e., mutations in IDH1, FGFR2 fusion proteins) holds important therapeutic implications for BTCs, particularly iCCA. Furthermore, the recent application of single cell-based technologies or more conservative (and less precise) "virtual microdissection" algorithms to isolate signals derived from the immune and stromal cells has identified the first microenvironment-based classes. In this chapter, we will review the molecular and immune classes of BTCs, with a particular focus on their clinical implications.
MeSH term(s)	Bile Duct Neoplasms/pathology ; Bile Ducts, Intrahepatic/pathology ; Biliary Tract Neoplasms/drug therapy ; Biliary Tract Neoplasms/genetics ; Biliary Tract Neoplasms/pathology ; Cholangiocarcinoma/genetics ; Cholangiocarcinoma/pathology ; Humans ; Prognosis ; Tumor Microenvironment
Language	English
Publishing date	2022-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	127-2
ISSN	2162-5557 ; 0065-230X
ISSN (online)	2162-5557
ISSN	0065-230X
DOI	10.1016/bs.acr.2022.01.008
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Article ; Online: The Molecular Pathogenesis and Targeted Therapies for Cholangiocarcinoma.

Param, Nesteene Joy / Bramel, Emily R / Sia, Daniela

Surgical pathology clinics

2022 Volume 15, Issue 3, Page(s) 529–539

Abstract: Cholangiocarcinoma (CCA) is a group of malignancies of the bile ducts with high mortality rates and limited treatment options. In the past decades, remarkable efforts have been dedicated toward elucidating the specific molecular signaling pathways and ... ...

Abstract	Cholangiocarcinoma (CCA) is a group of malignancies of the bile ducts with high mortality rates and limited treatment options. In the past decades, remarkable efforts have been dedicated toward elucidating the specific molecular signaling pathways and oncogenic loops driving cholangiocarcinogenesis to ultimately develop more effective therapies. Despite some recent advances, an extensive intra- and inter-tumor heterogeneity together with a poorly understood immunosuppressive microenvironment significantly compromises the efficacy of available treatments. Here, we provide a concise review of the latest advances and current knowledge of the molecular pathogenesis of CCA focusing on clinically relevant aberrations as well as future research avenues.
MeSH term(s)	Bile Duct Neoplasms/drug therapy ; Bile Duct Neoplasms/genetics ; Bile Ducts, Intrahepatic/metabolism ; Bile Ducts, Intrahepatic/pathology ; Cholangiocarcinoma/drug therapy ; Cholangiocarcinoma/genetics ; Humans ; Molecular Targeted Therapy ; Tumor Microenvironment
Language	English
Publishing date	2022-08-02
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1875-9157
ISSN (online)	1875-9157
DOI	10.1016/j.path.2022.05.006
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Article ; Online: Translating cancer genomics for precision oncology in biliary tract cancers.

Haber, Philipp K / Sia, Daniela

Discovery medicine

2020 Volume 28, Issue 155, Page(s) 255–265

Abstract: Biliary tract cancers (BTC), which include cholangiocarcinoma (both intra- and extrahepatic) and gallbladder, represent a heterogeneous group of malignancies with relatively low-incidence and poor prognosis. Therapeutic options for BTC patients at ... ...

Abstract	Biliary tract cancers (BTC), which include cholangiocarcinoma (both intra- and extrahepatic) and gallbladder, represent a heterogeneous group of malignancies with relatively low-incidence and poor prognosis. Therapeutic options for BTC patients at advanced stage are severely limited and palliative chemotherapy remains the maintreatment option. In the past decade, genome profiling via next-generation sequencing of large international cohorts has paved the way for precision oncology in BTC, identifying unique molecular subtypes, recurrent mutations, and genomic rearrangements. Targeted therapies directed against some of these aberrations are currently under investigation in phase 3 clinical studies and hold great promise to improve the prognosis of this disease. Thus, in the near term, the individual molecular alterations of the disease rather than the anatomic location will likely drive the design of clinical trials. In this review, we summarize recent molecular discoveries in BTC with a special emphasis on the most promising therapeutic targets, ultimately providing an update on current and future directions in the management of this disease.
MeSH term(s)	Biliary Tract Neoplasms/classification ; Biliary Tract Neoplasms/epidemiology ; Biliary Tract Neoplasms/genetics ; Biliary Tract Neoplasms/therapy ; Genomics ; Humans ; Molecular Targeted Therapy ; Mutation/genetics ; Precision Medicine ; Translational Medical Research
Language	English
Publishing date	2020-02-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1944-7930
ISSN (online)	1944-7930
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Article ; Online: Friend or foe? The elusive role of hepatic stellate cells in liver cancer.

Cogliati, Bruno / Yashaswini, Chittampalli N / Wang, Shuang / Sia, Daniela / Friedman, Scott L

Nature reviews. Gastroenterology & hepatology

2023 Volume 20, Issue 10, Page(s) 647–661

Abstract: Liver fibrosis is a substantial risk factor for the development and progression of liver cancer, which includes hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA). Studies utilizing cell fate mapping and single-cell transcriptomics ...

Abstract	Liver fibrosis is a substantial risk factor for the development and progression of liver cancer, which includes hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA). Studies utilizing cell fate mapping and single-cell transcriptomics techniques have identified quiescent perisinusoidal hepatic stellate cells (HSCs) as the primary source of activated collagen-producing HSCs and liver cancer-associated fibroblasts (CAFs) in HCC and liver metastasis, complemented in iCCA by contributions from portal fibroblasts. At the same time, integrative computational analysis of single-cell, single-nucleus and spatial RNA sequencing data have revealed marked heterogeneity among HSCs and CAFs, with distinct subpopulations displaying unique gene expression signatures and functions. Some of these subpopulations have divergent roles in promoting or inhibiting liver fibrogenesis and carcinogenesis. In this Review, we discuss the dual roles of HSC subpopulations in liver fibrogenesis and their contribution to liver cancer promotion, progression and metastasis. We review the transcriptomic and functional similarities between HSC and CAF subpopulations, highlighting the pathways that either promote or prevent fibrosis and cancer, and the immunological landscape from which these pathways emerge. Insights from ongoing studies will yield novel strategies for developing biomarkers, assessing prognosis and generating new therapies for both HCC and iCCA prevention and treatment.
MeSH term(s)	Humans ; Liver Neoplasms/metabolism ; Carcinoma, Hepatocellular/metabolism ; Hepatic Stellate Cells/metabolism ; Liver Cirrhosis/pathology
Language	English
Publishing date	2023-08-07
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2493722-8
ISSN	1759-5053 ; 1759-5045
ISSN (online)	1759-5053
ISSN	1759-5045
DOI	10.1038/s41575-023-00821-z
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Article ; Online: Cell of origin in biliary tract cancers and clinical implications.

Moeini, Agrin / Haber, Philipp K / Sia, Daniela

JHEP reports : innovation in hepatology

2021 Volume 3, Issue 2, Page(s) 100226

Abstract: Biliary tract cancers (BTCs) are aggressive epithelial malignancies that can arise at any point of the biliary tree. Albeit rare, their incidence and mortality rates have been rising steadily over the past 40 years, highlighting the need to improve ... ...

Abstract	Biliary tract cancers (BTCs) are aggressive epithelial malignancies that can arise at any point of the biliary tree. Albeit rare, their incidence and mortality rates have been rising steadily over the past 40 years, highlighting the need to improve current diagnostic and therapeutic strategies. BTCs show high inter- and intra-tumour heterogeneity both at the morphological and molecular level. Such complex heterogeneity poses a substantial obstacle to effective interventions. It is widely accepted that the observed heterogeneity may be the result of a complex interplay of different elements, including risk factors, distinct molecular alterations and multiple potential cells of origin. The use of genetic lineage tracing systems in experimental models has identified cholangiocytes, hepatocytes and/or progenitor-like cells as the cells of origin of BTCs. Genomic evidence in support of the distinct cell of origin hypotheses is growing. In this review, we focus on recent advances in the histopathological subtyping of BTCs, discuss current genomic evidence and outline lineage tracing studies that have contributed to the current knowledge surrounding the cell of origin of these tumours.
Language	English
Publishing date	2021-01-19
Publishing country	Netherlands
Document type	Journal Article ; Review
ISSN	2589-5559
ISSN (online)	2589-5559
DOI	10.1016/j.jhepr.2021.100226
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Article ; Online: Liver cancer: Translating '-omics' results into precision medicine for hepatocellular carcinoma.

Sia, Daniela / Llovet, Josep M

Nature reviews. Gastroenterology & hepatology

2017 Volume 14, Issue 10, Page(s) 571–572

MeSH term(s)	Adult ; Carcinoma, Hepatocellular/genetics ; Genome ; Genomics ; Humans ; Liver Neoplasms/genetics ; Precision Medicine
Language	English
Publishing date	2017-08-02
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	2493722-8
ISSN	1759-5053 ; 1759-5045
ISSN (online)	1759-5053
ISSN	1759-5045
DOI	10.1038/nrgastro.2017.103
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Article ; Online: Stellate cell-specific adhesion molecule protocadherin 7 regulates sinusoidal contraction.

Carter, James K / Tsai, Ming-Chao / Venturini, Nicholas / Hu, Jiangting / Lemasters, John J / Torres Martin, Miguel / Sia, Daniela / Wang, Shuang / Lee, Youngmin A / Friedman, Scott L

Hepatology (Baltimore, Md.)

2024

Abstract: Background and aims: Sustained inflammation and hepatocyte injury in chronic liver disease activate HSCs to transdifferentiate into fibrogenic, contractile myofibroblasts. We investigated the role of protocadherin 7 (PCDH7), a cadherin family member not ...

Abstract	Background and aims: Sustained inflammation and hepatocyte injury in chronic liver disease activate HSCs to transdifferentiate into fibrogenic, contractile myofibroblasts. We investigated the role of protocadherin 7 (PCDH7), a cadherin family member not previously characterized in the liver, whose expression is restricted to HSCs. Approach and results: We created a PCDH7 fl/fl mouse line, which was crossed to lecithin retinol acyltransferase-Cre mice to generate HSC-specific PCDH7 knockout animals. HSC contraction in vivo was tested in response to the HSC-selective vasoconstrictor endothelin-1 using intravital multiphoton microscopy. To establish a PCDH7 null HSC line, cells were isolated from PCDH7 fl/fl mice and infected with adenovirus-expressing Cre. Hepatic expression of PCDH7 was strictly restricted to HSCs. Knockout of PCDH7 in vivo abrogated HSC-mediated sinusoidal contraction in response to endothelin-1. In cultured HSCs, loss of PCDH7 markedly attenuated contractility within collagen gels and led to altered gene expression in pathways governing adhesion and vasoregulation. Loss of contractility in PCDH7 knockout cells was impaired Rho-GTPase signaling, as demonstrated by altered gene expression, reduced assembly of F-actin fibers, and loss of focal adhesions. Conclusions: The stellate cell-specific cadherin, PCDH7, is a novel regulator of HSC contractility whose loss leads to cytoskeletal remodeling and sinusoidal relaxation.
Language	English
Publishing date	2024-02-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1097/HEP.0000000000000782
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Article ; Online: Immune Exclusion-Wnt/CTNNB1 Class Predicts Resistance to Immunotherapies in HCC.

Pinyol, Roser / Sia, Daniela / Llovet, Josep M

Clinical cancer research : an official journal of the American Association for Cancer Research

2019 Volume 25, Issue 7, Page(s) 2021–2023

Abstract: Next-generation sequencing has provided information on actionable targets and biomarkers of response in oncology. In hepatocellular carcinoma (HCC), Wnt/CTNNB1 mutations characterize the immune-excluded class (cold tumors) and might represent the ... ...

Abstract	Next-generation sequencing has provided information on actionable targets and biomarkers of response in oncology. In hepatocellular carcinoma (HCC), Wnt/CTNNB1 mutations characterize the immune-excluded class (cold tumors) and might represent the biomarkers predicting resistance to immune checkpoint inhibitors. Large-scale validation of these data is needed to customize immunotherapy in advanced HCC.
MeSH term(s)	Adult ; Carcinoma, Hepatocellular/genetics ; Humans ; Immunotherapy ; Liver Neoplasms/genetics ; beta Catenin
Chemical Substances	CTNNB1 protein, human ; beta Catenin
Language	English
Publishing date	2019-01-07
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-18-3778
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Article ; Online: Transcriptomic profiling of a multiethnic pediatric NAFLD cohort reveals genes and pathways associated with disease.

Yao, Kangning / Tarabra, Elena / Sia, Daniela / Morotti, Raffaella / Fawaz, Rima / Valentino, Pamela / Santoro, Nicola / Caprio, Sonia / Liu, Silvia / Yimlamai, Dean

Hepatology communications

2022 Volume 6, Issue 7, Page(s) 1598–1610

Abstract: Nonalcoholic fatty liver disease (NAFLD) is the most common type of chronic liver disease in children. The mechanisms that drive NAFLD disease progression in this specific patient population remain poorly defined. In this study, we obtained liver biopsy ... ...

Abstract	Nonalcoholic fatty liver disease (NAFLD) is the most common type of chronic liver disease in children. The mechanisms that drive NAFLD disease progression in this specific patient population remain poorly defined. In this study, we obtained liver biopsy samples from a multiethnic cohort of pediatric patients with NAFLD (n = 52, mean age = 13.6 years) and healthy liver controls (n = 5). We analyzed transcriptomic changes associated with NAFLD stages using high-throughput RNA sequencing. Unsupervised clustering as well as pairwise transcriptome comparison distinguished NAFLD from healthy livers. We identified perturbations in pathways including calcium and insulin/glucose signaling occurring early in NAFLD disease, before the presence of histopathologic evidence of advanced disease. Transcriptomic comparisons identified a 25-gene signature associated with the degree of liver fibrosis. We also identified expression of the insulin-like growth factor binding protein (IGFBP) gene family (1/2/3/7) as correlating with disease stages, and it has the potential to be used as a peripheral biomarker in NAFLD. Comparing our data set with publicly available adult and adolescent transcriptomic data, we identified similarities and differences in pathway enrichment and gene-expression profiles between adult and pediatric patients with NAFLD. Regulation of genes including interleukin-32, IGFBP1, IGFBP2, and IGFBP7 was consistently found in both NAFLD populations, whereas IGFBP3 was specific to pediatric NAFLD. Conclusion: This paper expands our knowledge on the molecular mechanisms underlying pediatric NAFLD. It identifies potential biomarkers and directs us toward new therapies in this population.
MeSH term(s)	Adolescent ; Adult ; Biomarkers ; Child ; Gene Expression Profiling ; Humans ; Insulin/genetics ; Liver Cirrhosis/genetics ; Non-alcoholic Fatty Liver Disease/genetics ; Transcriptome/genetics
Chemical Substances	Biomarkers ; Insulin
Language	English
Publishing date	2022-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2471-254X
ISSN (online)	2471-254X
DOI	10.1002/hep4.1940
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Article ; Online: Age alters the oncogenic trajectory toward luminal mammary tumors that activate unfolded proteins responses.

Jenkins, Edmund Charles / Chattopadhyay, Mrittika / Gomez, Maria / Torre, Denis / Ma'ayan, Avi / Torres-Martin, Miguel / Sia, Daniela / Germain, Doris

Aging cell

2022 Volume 21, Issue 10, Page(s) e13665

Abstract: A major limitation in the use of mouse models in breast cancer research is that most mice develop estrogen receptor-alpha (ERα)-negative mammary tumors, while in humans, the majority of breast cancers are ERα-positive. Therefore, developing mouse models ... ...

Abstract	A major limitation in the use of mouse models in breast cancer research is that most mice develop estrogen receptor-alpha (ERα)-negative mammary tumors, while in humans, the majority of breast cancers are ERα-positive. Therefore, developing mouse models that best mimic the disease in humans is of fundamental need. Here, using an inducible MMTV-rtTA/TetO-NeuNT mouse model, we show that despite being driven by the same oncogene, mammary tumors in young mice are ERα-negative, while they are ERα-positive in aged mice. To further elucidate the mechanisms for this observation, we performed RNAseq analysis and identified genes that are uniquely expressed in aged female-derived mammary tumors. We found these genes to be involved in the activation of the ERα axis of the mitochondrial UPR and the ERα-mediated regulation of XBP-1s, a gene involved in the endoplasmic reticulum UPR. Collectively, our results indicate that aging alters the oncogenic trajectory towards the ERα-positive subtype of breast cancers, and that mammary tumors in aged mice are characterized by the upregulation of multiple UPR stress responses regulated by the ERα.
MeSH term(s)	Aged ; Animals ; Carcinogenesis/genetics ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Female ; Humans ; Mice ; Oncogenes ; Receptors, Estrogen/metabolism ; Unfolded Protein Response/genetics
Chemical Substances	Estrogen Receptor alpha ; Receptors, Estrogen
Language	English
Publishing date	2022-09-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13665
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