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  1. AU="Blake, Kerrigan"
  2. AU="Oikawa, Shoko"
  3. AU="Ebert, Martin"
  4. AU="Casillas-Suárez, Catalina"
  5. AU="Wildberger, R"
  6. AU="Cao, Zhijun"
  7. AU=Ghosh Asish K
  8. AU="Ouyang, Wenjun"
  9. AU="Drake, Amelia F"
  10. AU="Kötél, Dóra"
  11. AU="Palacios, Florencia"
  12. AU="Cousin, Xavier"
  13. AU="Zhou, Yongfeng"
  14. AU="Nischal, Neeraj"
  15. AU="Reger de Moura, Coralie"
  16. AU="Kazan, Özgür"
  17. AU="Goto, Yoshiyuki"
  18. AU="Gulati, Ajay S"
  19. AU="Dotan, Yaniv"
  20. AU="Anderson, Jessica J"
  21. AU="Cong, Weimin"
  22. AU="Dong, Dianshuai"
  23. AU="Sydenstricker, Agnes V"
  24. AU="Glazer, Peter M"
  25. AU="Zhang, Haocheng"
  26. AU="Low, Tze-Yi"
  27. AU="Ratemi, Haithm W"
  28. AU="Lee, Kristy"
  29. AU="Nénon, Q"
  30. AU="Tang, Yi-Han"
  31. AU="Parodi, Jose F"
  32. AU="Kabata, Yudai"
  33. AU="Butler, Javed"
  34. AU=Du L
  35. AU="Artin, Hewa"
  36. AU="Bardakov, V M"
  37. AU="Sakaguchi, Bungo"
  38. AU="Boo, Irene"
  39. AU="Tam, Victor Wai-Hou"
  40. AU="Pierfrancesco Pagella"
  41. AU=Sanchez Garcia Elisabet
  42. AU=Yasir Kashif Ammar
  43. AU="Gümüş, Funda"
  44. AU=Bhowmik Deep AU=Bhowmik Deep
  45. AU="Eugene, Alexis"
  46. AU="Janesomboon, Sujintana"
  47. AU="Sonkhya, Nishi"
  48. AU="Vaz, André"
  49. AU="Rugo, Hope S"
  50. AU="Gupta, Sonia"
  51. AU="Molday, Robert S"
  52. AU="Yaodong Hu"
  53. AU=Gimenez-Mascarell Paula
  54. AU="Orlandi, D"
  55. AU="Takeishi, Yasuchika"
  56. AU="Kamath, Karthik Shantharam" AU="Kamath, Karthik Shantharam"
  57. AU="Innocente, Alessandra"
  58. AU="Xing, Lei"
  59. AU="Chen, Mingyu"
  60. AU="Riedl, Sophie"
  61. AU="Ding, Haiyan"
  62. AU=Hu Xiumei AU=Hu Xiumei
  63. AU="Simmonds, Peter"
  64. AU="Chaturvedi, Apeksha"
  65. AU="Madden, Wyatt"
  66. AU="Wald, Moshe"
  67. AU="Zalesak, J."
  68. AU="Krach, Florian"
  69. AU="Modak, Manisha A"
  70. AU="Ottolini, Matteo"
  71. AU="Douglas Hanahan"
  72. AU="Bieniaszewska, Maria"
  73. AU="Alovisi, Camilla"
  74. AU="Lijfering, Willem M."
  75. AU="Rademacher, Jessica"
  76. AU="Dartigues, Jean-François"
  77. AU="Denicola, Anthony J"
  78. AU="Zhang, Xuewei"
  79. AU="Li, Yanjiao"
  80. AU="Botelho Meireles de Souza, Guilherme"
  81. AU="Gong, Yu-Qing"
  82. AU="Eisch, J"
  83. AU=De Vito Eduardo L
  84. AU="Lowsky, Robert"
  85. AU="Lindner, M."
  86. AU="Mugnai, Giacomo"
  87. AU="Chollet-Krugler, Marylène"
  88. AU="Firsanov, Denis"
  89. AU="Jo, Dong-Gyu"
  90. AU="Greenland, John R"
  91. AU="J Natale"
  92. AU="Drost, Carolin Christina"
  93. AU="Silvera, Risset"
  94. AU="Zgubič, M"
  95. AU="Russo, Rosita"
  96. AU="Ruiz-Ortega, Marta"
  97. AU="T Talbot"
  98. AU="Emoto, Kasey C"
  99. AU="Moos, W H" AU="Moos, W H"
  100. AU=Singh Sweta AU=Singh Sweta
  101. AU="Pimentel, Mauricio"
  102. AU="Kim, Ji Hee"
  103. AU=Ross Jeffrey S
  104. AU=Malhotra Atul
  105. AU="Tiesler, Carla M T"
  106. AU="Merighi, Adalberto" AU="Merighi, Adalberto"

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  1. Artikel ; Online: Microglia promote anti-tumour immunity and suppress breast cancer brain metastasis.

    Evans, Katrina T / Blake, Kerrigan / Longworth, Aaron / Coburn, Morgan A / Insua-Rodríguez, Jacob / McMullen, Timothy P / Nguyen, Quy H / Ma, Dennis / Lev, Tatyana / Hernandez, Grace A / Oganyan, Armani K / Orujyan, Davit / Edwards, Robert A / Pridans, Clare / Green, Kim N / Villalta, S Armando / Blurton-Jones, Mathew / Lawson, Devon A

    Nature cell biology

    2023  Band 25, Heft 12, Seite(n) 1848–1859

    Abstract: Breast cancer brain metastasis (BCBM) is a lethal disease with no effective treatments. Prior work has shown that brain cancers and metastases are densely infiltrated with anti-inflammatory, protumourigenic tumour-associated macrophages, but the role of ... ...

    Abstract Breast cancer brain metastasis (BCBM) is a lethal disease with no effective treatments. Prior work has shown that brain cancers and metastases are densely infiltrated with anti-inflammatory, protumourigenic tumour-associated macrophages, but the role of brain-resident microglia remains controversial because they are challenging to discriminate from other tumour-associated macrophages. Using single-cell RNA sequencing, genetic and humanized mouse models, we specifically identify microglia and find that they play a distinct pro-inflammatory and tumour-suppressive role in BCBM. Animals lacking microglia show increased metastasis, decreased survival and reduced natural killer and T cell responses, showing that microglia are critical to promote anti-tumour immunity to suppress BCBM. We find that the pro-inflammatory response is conserved in human microglia, and markers of their response are associated with better prognosis in patients with BCBM. These findings establish an important role for microglia in anti-tumour immunity and highlight them as a potential immunotherapy target for brain metastasis.
    Mesh-Begriff(e) Mice ; Animals ; Humans ; Female ; Microglia ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Brain Neoplasms/pathology ; Brain/pathology ; Treatment Outcome
    Sprache Englisch
    Erscheinungsdatum 2023-11-13
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 1474722-4
    ISSN 1476-4679 ; 1465-7392
    ISSN (online) 1476-4679
    ISSN 1465-7392
    DOI 10.1038/s41556-023-01273-y
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  2. Artikel ; Online: Patient-derived xenograft culture-transplant system for investigation of human breast cancer metastasis.

    Ma, Dennis / Hernandez, Grace A / Lefebvre, Austin E Y T / Alshetaiwi, Hamad / Blake, Kerrigan / Dave, Kushal R / Rauf, Maha / Williams, Justice W / Davis, Ryan T / Evans, Katrina T / Longworth, Aaron / Masoud, Madona Y G / Lee, Regis / Edwards, Robert A / Digman, Michelle A / Kessenbrock, Kai / Lawson, Devon A

    Communications biology

    2021  Band 4, Heft 1, Seite(n) 1268

    Abstract: Metastasis is a fatal disease where research progress has been hindered by a lack of authentic experimental models. Here, we develop a 3D tumor sphere culture-transplant system that facilitates the growth and engineering of patient-derived xenograft (PDX) ...

    Abstract Metastasis is a fatal disease where research progress has been hindered by a lack of authentic experimental models. Here, we develop a 3D tumor sphere culture-transplant system that facilitates the growth and engineering of patient-derived xenograft (PDX) tumor cells for functional metastasis assays in vivo. Orthotopic transplantation and RNA sequencing (RNA-seq) analyses show that PDX tumor spheres maintain tumorigenic potential, and the molecular marker and global transcriptome signatures of native tumor cells. Tumor spheres display robust capacity for lentiviral engineering and dissemination in spontaneous and experimental metastasis assays in vivo. Inhibition of pathways previously reported to attenuate metastasis also inhibit metastasis after sphere culture, validating our approach for authentic investigations of metastasis. Finally, we demonstrate a new role for the metabolic enzyme NME1 in promoting breast cancer metastasis, providing proof-of-principle that our culture-transplant system can be used for authentic propagation and engineering of patient tumor cells for functional studies of metastasis.
    Mesh-Begriff(e) Animals ; Breast Neoplasms/pathology ; Disease Models, Animal ; Female ; Heterografts ; Mice ; Neoplasm Metastasis ; Neoplasms, Experimental ; Tumor Microenvironment ; Xenograft Model Antitumor Assays
    Sprache Englisch
    Erscheinungsdatum 2021-11-05
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-021-02596-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: A spatially resolved single cell genomic atlas of the adult human breast.

    Kumar, Tapsi / Nee, Kevin / Wei, Runmin / He, Siyuan / Nguyen, Quy H / Bai, Shanshan / Blake, Kerrigan / Gong, Yanwen / Pein, Maren / Sei, Emi / Hu, Min / Casasent, Anna / Thennavan, Aatish / Li, Jianzhuo / Tran, Tuan / Chen, Ken / Nilges, Benedikt / Kashikar, Nachiket / Braubach, Oliver /
    Cheikh, Bassem Ben / Nikulina, Nadya / Chen, Hui / Teshome, Mediget / Menegaz, Brian / Javaid, Huma / Nagi, Chandandeep / Montalvan, Jessica / Tifrea, Delia F / Edwards, Robert / Lin, Erin / Parajuli, Ritesh / Winocour, Sebastian / Thompson, Alastair / Lim, Bora / Lawson, Devon A / Kessenbrock, Kai / Navin, Nicholas

    bioRxiv : the preprint server for biology

    2023  

    Abstract: The adult human breast comprises an intricate network of epithelial ducts and lobules that are embedded in connective and adipose tissue. While previous studies have mainly focused on the breast epithelial system, many of the non-epithelial cell types ... ...

    Abstract The adult human breast comprises an intricate network of epithelial ducts and lobules that are embedded in connective and adipose tissue. While previous studies have mainly focused on the breast epithelial system, many of the non-epithelial cell types remain understudied. Here, we constructed a comprehensive Human Breast Cell Atlas (HBCA) at single-cell and spatial resolution. Our single-cell transcriptomics data profiled 535,941 cells from 62 women, and 120,024 nuclei from 20 women, identifying 11 major cell types and 53 cell states. These data revealed abundant pericyte, endothelial and immune cell populations, and highly diverse luminal epithelial cell states. Our spatial mapping using three technologies revealed an unexpectedly rich ecosystem of tissue-resident immune cells in the ducts and lobules, as well as distinct molecular differences between ductal and lobular regions. Collectively, these data provide an unprecedented reference of adult normal breast tissue for studying mammary biology and disease states such as breast cancer.
    Sprache Englisch
    Erscheinungsdatum 2023-04-25
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.04.22.537946
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Tumor-intrinsic expression of the autophagy gene Atg16l1 suppresses anti-tumor immunity in colorectal cancer.

    Taraborrelli, Lucia / Şenbabaoğlu, Yasin / Wang, Lifen / Lim, Junghyun / Blake, Kerrigan / Kljavin, Noelyn / Gierke, Sarah / Scherl, Alexis / Ziai, James / McNamara, Erin / Owyong, Mark / Rao, Shilpa / Calviello, Aslihan Karabacak / Oreper, Daniel / Jhunjhunwala, Suchit / Argiles, Guillem / Bendell, Johanna / Kim, Tae Won / Ciardiello, Fortunato /
    Wongchenko, Matthew J / de Sauvage, Frederic J / de Sousa E Melo, Felipe / Yan, Yibing / West, Nathaniel R / Murthy, Aditya

    Nature communications

    2023  Band 14, Heft 1, Seite(n) 5945

    Abstract: Microsatellite-stable colorectal cancer (MSS-CRC) is highly refractory to immunotherapy. Understanding tumor-intrinsic determinants of immunotherapy resistance is critical to improve MSS-CRC patient outcomes. Here, we demonstrate that high tumor ... ...

    Abstract Microsatellite-stable colorectal cancer (MSS-CRC) is highly refractory to immunotherapy. Understanding tumor-intrinsic determinants of immunotherapy resistance is critical to improve MSS-CRC patient outcomes. Here, we demonstrate that high tumor expression of the core autophagy gene ATG16L1 is associated with poor clinical response to anti-PD-L1 therapy in KRAS-mutant tumors from IMblaze370 (NCT02788279), a large phase III clinical trial of atezolizumab (anti-PD-L1) in advanced metastatic MSS-CRC. Deletion of Atg16l1 in engineered murine colon cancer organoids inhibits tumor growth in primary (colon) and metastatic (liver and lung) niches in syngeneic female hosts, primarily due to increased sensitivity to IFN-γ-mediated immune pressure. ATG16L1 deficiency enhances programmed cell death of colon cancer organoids induced by IFN-γ and TNF, thus increasing their sensitivity to host immunity. In parallel, ATG16L1 deficiency reduces tumor stem-like populations in vivo independently of adaptive immune pressure. This work reveals autophagy as a clinically relevant mechanism of immune evasion and tumor fitness in MSS-CRC and provides a rationale for autophagy inhibition to boost immunotherapy responses in the clinic.
    Mesh-Begriff(e) Animals ; Female ; Humans ; Mice ; Autophagy/genetics ; Autophagy-Related Proteins/genetics ; Colonic Neoplasms ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Genes, Regulator ; Liver ; Clinical Trials, Phase III as Topic
    Chemische Substanzen Atg16l1 protein, mouse ; Autophagy-Related Proteins
    Sprache Englisch
    Erscheinungsdatum 2023-09-23
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-41618-7
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Small-molecule inhibition of glycogen synthase 1 for the treatment of Pompe disease and other glycogen storage disorders.

    Ullman, Julie C / Mellem, Kevin T / Xi, Yannan / Ramanan, Vyas / Merritt, Hanne / Choy, Rebeca / Gujral, Tarunmeet / Young, Lyndsay E A / Blake, Kerrigan / Tep, Samnang / Homburger, Julian R / O'Regan, Adam / Ganesh, Sandya / Wong, Perryn / Satterfield, Terrence F / Lin, Baiwei / Situ, Eva / Yu, Cecile / Espanol, Bryan /
    Sarwaikar, Richa / Fastman, Nathan / Tzitzilonis, Christos / Lee, Patrick / Reiton, Daniel / Morton, Vivian / Santiago, Pam / Won, Walter / Powers, Hannah / Cummings, Beryl B / Hoek, Maarten / Graham, Robert R / Chandriani, Sanjay J / Bainer, Russell / DePaoli-Roach, Anna A / Roach, Peter J / Hurley, Thomas D / Sun, Ramon C / Gentry, Matthew S / Sinz, Christopher / Dick, Ryan A / Noonberg, Sarah B / Beattie, David T / Morgans, David J / Green, Eric M

    Science translational medicine

    2024  Band 16, Heft 730, Seite(n) eadf1691

    Abstract: Glycogen synthase 1 (GYS1), the rate-limiting enzyme in muscle glycogen synthesis, plays a central role in energy homeostasis and has been proposed as a therapeutic target in multiple glycogen storage diseases. Despite decades of investigation, there are ...

    Abstract Glycogen synthase 1 (GYS1), the rate-limiting enzyme in muscle glycogen synthesis, plays a central role in energy homeostasis and has been proposed as a therapeutic target in multiple glycogen storage diseases. Despite decades of investigation, there are no known potent, selective small-molecule inhibitors of this enzyme. Here, we report the preclinical characterization of MZ-101, a small molecule that potently inhibits GYS1 in vitro and in vivo without inhibiting GYS2, a related isoform essential for synthesizing liver glycogen. Chronic treatment with MZ-101 depleted muscle glycogen and was well tolerated in mice. Pompe disease, a glycogen storage disease caused by mutations in acid α glucosidase (GAA), results in pathological accumulation of glycogen and consequent autophagolysosomal abnormalities, metabolic dysregulation, and muscle atrophy. Enzyme replacement therapy (ERT) with recombinant GAA is the only approved treatment for Pompe disease, but it requires frequent infusions, and efficacy is limited by suboptimal skeletal muscle distribution. In a mouse model of Pompe disease, chronic oral administration of MZ-101 alone reduced glycogen buildup in skeletal muscle with comparable efficacy to ERT. In addition, treatment with MZ-101 in combination with ERT had an additive effect and could normalize muscle glycogen concentrations. Biochemical, metabolomic, and transcriptomic analyses of muscle tissue demonstrated that lowering of glycogen concentrations with MZ-101, alone or in combination with ERT, corrected the cellular pathology in this mouse model. These data suggest that substrate reduction therapy with GYS1 inhibition may be a promising therapeutic approach for Pompe disease and other glycogen storage diseases.
    Mesh-Begriff(e) Mice ; Animals ; Glycogen Storage Disease Type II/drug therapy ; Glycogen Synthase/metabolism ; Glycogen Synthase/pharmacology ; Mice, Knockout ; Glycogen/metabolism ; Muscle, Skeletal/metabolism ; Enzyme Replacement Therapy/methods
    Chemische Substanzen Glycogen Synthase (EC 2.4.1.11) ; Glycogen (9005-79-2)
    Sprache Englisch
    Erscheinungsdatum 2024-01-17
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.adf1691
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Transcriptional diversity and bioenergetic shift in human breast cancer metastasis revealed by single-cell RNA sequencing.

    Davis, Ryan T / Blake, Kerrigan / Ma, Dennis / Gabra, Mari B Ishak / Hernandez, Grace A / Phung, Anh T / Yang, Ying / Maurer, Dustin / Lefebvre, Austin E Y T / Alshetaiwi, Hamad / Xiao, Zhengtao / Liu, Juan / Locasale, Jason W / Digman, Michelle A / Mjolsness, Eric / Kong, Mei / Werb, Zena / Lawson, Devon A

    Nature cell biology

    2020  Band 22, Heft 3, Seite(n) 310–320

    Abstract: Although metastasis remains the cause of most cancer-related mortality, mechanisms governing seeding in distal tissues are poorly understood. Here, we establish a robust method for the identification of global transcriptomic changes in rare metastatic ... ...

    Abstract Although metastasis remains the cause of most cancer-related mortality, mechanisms governing seeding in distal tissues are poorly understood. Here, we establish a robust method for the identification of global transcriptomic changes in rare metastatic cells during seeding using single-cell RNA sequencing and patient-derived-xenograft models of breast cancer. We find that both primary tumours and micrometastases display transcriptional heterogeneity but micrometastases harbour a distinct transcriptome program conserved across patient-derived-xenograft models that is highly predictive of poor survival of patients. Pathway analysis revealed mitochondrial oxidative phosphorylation as the top pathway upregulated in micrometastases, in contrast to higher levels of glycolytic enzymes in primary tumour cells, which we corroborated by flow cytometric and metabolomic analyses. Pharmacological inhibition of oxidative phosphorylation dramatically attenuated metastatic seeding in the lungs, which demonstrates the functional importance of oxidative phosphorylation in metastasis and highlights its potential as a therapeutic target to prevent metastatic spread in patients with breast cancer.
    Mesh-Begriff(e) Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Energy Metabolism ; Female ; Humans ; Mice, Inbred NOD ; Mice, SCID ; Mitochondria/metabolism ; Neoplasm Metastasis ; Oxidative Phosphorylation ; Sequence Analysis, RNA ; Single-Cell Analysis ; Transcription, Genetic ; Transcriptome
    Sprache Englisch
    Erscheinungsdatum 2020-03-06
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1474722-4
    ISSN 1476-4679 ; 1465-7392
    ISSN (online) 1476-4679
    ISSN 1465-7392
    DOI 10.1038/s41556-020-0477-0
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: A spatially resolved single-cell genomic atlas of the adult human breast.

    Kumar, Tapsi / Nee, Kevin / Wei, Runmin / He, Siyuan / Nguyen, Quy H / Bai, Shanshan / Blake, Kerrigan / Pein, Maren / Gong, Yanwen / Sei, Emi / Hu, Min / Casasent, Anna K / Thennavan, Aatish / Li, Jianzhuo / Tran, Tuan / Chen, Ken / Nilges, Benedikt / Kashikar, Nachiket / Braubach, Oliver /
    Ben Cheikh, Bassem / Nikulina, Nadya / Chen, Hui / Teshome, Mediget / Menegaz, Brian / Javaid, Huma / Nagi, Chandandeep / Montalvan, Jessica / Lev, Tatyana / Mallya, Sharmila / Tifrea, Delia F / Edwards, Robert / Lin, Erin / Parajuli, Ritesh / Hanson, Summer / Winocour, Sebastian / Thompson, Alastair / Lim, Bora / Lawson, Devon A / Kessenbrock, Kai / Navin, Nicholas

    Nature

    2023  Band 620, Heft 7972, Seite(n) 181–191

    Abstract: The adult human breast is comprised of an intricate network of epithelial ducts and lobules that are embedded in connective and adipose ... ...

    Abstract The adult human breast is comprised of an intricate network of epithelial ducts and lobules that are embedded in connective and adipose tissue
    Mesh-Begriff(e) Adult ; Female ; Humans ; Breast/cytology ; Breast/immunology ; Breast/metabolism ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Endothelial Cells/classification ; Endothelial Cells/metabolism ; Epithelial Cells/classification ; Epithelial Cells/metabolism ; Gene Expression Profiling ; Genomics ; Single-Cell Analysis ; Immunity
    Sprache Englisch
    Erscheinungsdatum 2023-06-28
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-023-06252-9
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Profiling human breast epithelial cells using single cell RNA sequencing identifies cell diversity.

    Nguyen, Quy H / Pervolarakis, Nicholas / Blake, Kerrigan / Ma, Dennis / Davis, Ryan Tevia / James, Nathan / Phung, Anh T / Willey, Elizabeth / Kumar, Raj / Jabart, Eric / Driver, Ian / Rock, Jason / Goga, Andrei / Khan, Seema A / Lawson, Devon A / Werb, Zena / Kessenbrock, Kai

    Nature communications

    2018  Band 9, Heft 1, Seite(n) 2028

    Abstract: Breast cancer arises from breast epithelial cells that acquire genetic alterations leading to subsequent loss of tissue homeostasis. Several distinct epithelial subpopulations have been proposed, but complete understanding of the spectrum of ... ...

    Abstract Breast cancer arises from breast epithelial cells that acquire genetic alterations leading to subsequent loss of tissue homeostasis. Several distinct epithelial subpopulations have been proposed, but complete understanding of the spectrum of heterogeneity and differentiation hierarchy in the human breast remains elusive. Here, we use single-cell mRNA sequencing (scRNAseq) to profile the transcriptomes of 25,790 primary human breast epithelial cells isolated from reduction mammoplasties of seven individuals. Unbiased clustering analysis reveals the existence of three distinct epithelial cell populations, one basal and two luminal cell types, which we identify as secretory L1- and hormone-responsive L2-type cells. Pseudotemporal reconstruction of differentiation trajectories produces one continuous lineage hierarchy that closely connects the basal lineage to the two differentiated luminal branches. Our comprehensive cell atlas provides insights into the cellular blueprint of the human breast epithelium and will form the foundation to understand how the system goes awry during breast cancer.
    Mesh-Begriff(e) Adult ; Biomarkers, Tumor/genetics ; Breast/cytology ; Breast/pathology ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Differentiation/genetics ; Cell Lineage/genetics ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/pathology ; Cluster Analysis ; Epithelial Cells/physiology ; Female ; Gene Expression Profiling/methods ; Humans ; Sequence Analysis, RNA/methods ; Single-Cell Analysis/methods ; Transcriptome/genetics
    Chemische Substanzen Biomarkers, Tumor
    Sprache Englisch
    Erscheinungsdatum 2018-05-23
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-018-04334-1
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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