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Article: Inflammation, Infiltration, and Evasion-Tumor Promotion in the Aging Breast.

Cruz-Reyes, Nicole / Radisky, Derek C

2023 Volume 15, Issue 6

Abstract: Breast cancer is a significant cause of morbidity and mortality in women, with over two million new cases reported worldwide each year, the majority of which occur in post-menopausal women. Despite advances in early detection and treatment, approximately ...

Abstract	Breast cancer is a significant cause of morbidity and mortality in women, with over two million new cases reported worldwide each year, the majority of which occur in post-menopausal women. Despite advances in early detection and treatment, approximately one-third of patients diagnosed with breast cancer will develop metastatic disease. The pathogenesis and progression of breast cancer are influenced by a variety of biological and social risk factors, including age, ethnicity, pregnancy status, diet, and genomic alterations. Recent advancements in breast cancer research have focused on harnessing the power of the patient's adaptive and innate immune systems for diagnostic and therapeutic purposes. The breast immune microenvironment plays a critical role in regulating tissue homeostasis and resistance to tumorigenesis. In this review, we explore the dynamic changes in the breast immune microenvironment that occur with age, how these changes impact breast cancer development and progression, and how targeted therapeutic interventions that leverage the immune system can be used to improve patient outcomes. Our review emphasizes the importance of understanding the complex interplay between aging, the immune system, and breast cancer, and highlights the potential of immune-based therapies in the fight against this devastating disease.
Language	English
Publishing date	2023-03-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15061836
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Article ; Online: Automated Quantitative Measures of Terminal Duct Lobular Unit Involution and Breast Cancer Risk-Letter.

Degnim, Amy C / Radisky, Derek C / Vachon, Celine M / Sherman, Mark E

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

2021 Volume 30, Issue 4, Page(s) 797

MeSH term(s)	Breast ; Breast Neoplasms/epidemiology ; Female ; Humans ; Mammary Glands, Human ; Risk
Language	English
Publishing date	2021-03-26
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	1153420-5
ISSN	1538-7755 ; 1055-9965
ISSN (online)	1538-7755
ISSN	1055-9965
DOI	10.1158/1055-9965.EPI-20-1694
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Article ; Online: Lower Exome Sequencing Coverage of Ancestrally African Patients in The Cancer Genome Atlas.

Wickland, Daniel P / Sherman, Mark E / Radisky, Derek C / Mansfield, Aaron S / Asmann, Yan W

Journal of the National Cancer Institute

2022 Volume 114, Issue 8, Page(s) 1192–1199

Abstract: Background: In the United States, cancer disproportionately impacts Black and African American individuals. Identifying genetic factors underlying cancer disparities has been an important research focus and requires data that are equitable in both ... ...

Abstract	Background: In the United States, cancer disproportionately impacts Black and African American individuals. Identifying genetic factors underlying cancer disparities has been an important research focus and requires data that are equitable in both quantity and quality across racial groups. It is widely recognized that DNA databases quantitatively underrepresent minorities. However, the differences in data quality between racial groups have not been well studied. Methods: We compared the qualities of germline and tumor exomes between ancestrally African and European patients in The Cancer Genome Atlas of 7 cancers with at least 50 self-reported Black patients in the context of sequencing depth, tumor purity, and qualities of germline variants and somatic mutations. Results: Germline and tumor exomes from ancestrally African patients were sequenced at statistically significantly lower depth in 6 out of the 7 cancers. For 3 cancers, most ancestrally European exomes were sequenced in early sample batches at higher depth, whereas ancestrally African exomes were concentrated in later batches and sequenced at much lower depth. For the other 3 cancers, the reasons of lower sequencing coverage of ancestrally African exomes remain unknown. Furthermore, even when the sequencing depths were comparable, African exomes had disproportionally higher percentages of positions with insufficient coverage, likely because of the known European bias in the human reference genome that impacted exome capture kit design. Conclusions: Overall and positional lower sequencing depths of ancestrally African exomes in The Cancer Genome Atlas led to underdetection and lower quality of variants, highlighting the need to consider epidemiological factors for future genomics studies.
MeSH term(s)	Exome/genetics ; Genome, Human ; Genomics ; Humans ; Neoplasms/genetics ; United States/epidemiology ; Whole Exome Sequencing
Language	English
Publishing date	2022-03-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2992-0
ISSN	1460-2105 ; 0027-8874 ; 0198-0157
ISSN (online)	1460-2105
ISSN	0027-8874 ; 0198-0157
DOI	10.1093/jnci/djac054
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Article ; Online: Response to Mitr and Pollack.

Wickland, Daniel P / Sherman, Mark E / Radisky, Derek C / Mansfield, Aaron S / Asmann, Yan W

Journal of the National Cancer Institute

2022 Volume 114, Issue 12, Page(s) 1729–1730

Language	English
Publishing date	2022-06-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2992-0
ISSN	1460-2105 ; 0027-8874 ; 0198-0157
ISSN (online)	1460-2105
ISSN	0027-8874 ; 0198-0157
DOI	10.1093/jnci/djac133
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Article ; Online: miR-200c at the nexus of epithelial-mesenchymal transition, resistance to apoptosis, and the breast cancer stem cell phenotype.

Radisky, Derek C

Breast cancer research : BCR

2011 Volume 13, Issue 3, Page(s) 110

Abstract: Decreased expression of miRNAs of the miR-200 family has been implicated in the growth and metastasis of breast cancer cells. Of this family, miR-200c has garnered particular attention as a consequence of its ability to target ZEB1 and ZEB2, mediators of ...

Abstract	Decreased expression of miRNAs of the miR-200 family has been implicated in the growth and metastasis of breast cancer cells. Of this family, miR-200c has garnered particular attention as a consequence of its ability to target ZEB1 and ZEB2, mediators of epithelial- mesenchymal transition. An article in the previous issue of Breast Cancer Research identifies additional targets of miR-200c that link increased cancer cell invasiveness, resistance to apoptosis, and induction of breast cancer stem cell characteristics.
MeSH term(s)	Anoikis ; Breast Neoplasms/metabolism ; Cell Movement ; Endometrial Neoplasms/metabolism ; Female ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism
Chemical Substances	MicroRNAs
Language	English
Publishing date	2011-06-10
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	2015059-3
ISSN	1465-542X ; 1465-5411
ISSN (online)	1465-542X
ISSN	1465-5411
DOI	10.1186/bcr2885
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Article ; Online: Function following form: functional differentiation of mammary epithelial cells requires laminin-induced polarization of PI3-kinase.

Radisky, Derek C

Cell cycle (Georgetown, Tex.)

2011 Volume 10, Issue 1, Page(s) 15

MeSH term(s)	Animals ; Laminin/pharmacology ; Phosphatidylinositol 3-Kinases/analysis ; STAT5 Transcription Factor/metabolism
Chemical Substances	Laminin ; STAT5 Transcription Factor ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2011-01-01
Publishing country	United States
Document type	News ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.10.1.14218
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Article ; Online: Matrix metalloproteinases as breast cancer drivers and therapeutic targets.

Radisky, Evette S / Radisky, Derek C

Frontiers in bioscience (Landmark edition)

2015 Volume 20, Issue 7, Page(s) 1144–1163

Abstract: Members of the matrix metalloproteinase (MMP) family have been identified as poor prognosis markers for breast cancer patients and as drivers of many facets of the tumor phenotype in experimental models. Early enthusiasm for MMPs as therapeutic targets ... ...

Abstract	Members of the matrix metalloproteinase (MMP) family have been identified as poor prognosis markers for breast cancer patients and as drivers of many facets of the tumor phenotype in experimental models. Early enthusiasm for MMPs as therapeutic targets was tempered following disappointing clinical trials that utilized broad spectrum, small molecule catalytic site inhibitors. However, subsequent research has continued to define key roles for MMPs as breast cancer promoters, to elucidate the complex roles that that these proteins play in breast cancer development and progression, and to identify how these roles are linked to specific and unique biochemical features of individual members of the MMP family. Here, we provide an overview of the structural features of the MMPs, then discuss clinical studies identifying which MMP family members are linked with breast cancer development and new experimental studies that reveal how these specific MMPs may play unique roles in the breast cancer microenvironment. We conclude with a discussion of the most promising avenues for development of therapeutic agents capable of targeting the tumor-promoting properties of MMPs.
MeSH term(s)	Apoptosis ; Biomarkers, Tumor/metabolism ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Proliferation ; Disease Progression ; Female ; Humans ; Matrix Metalloproteinases/chemistry ; Matrix Metalloproteinases/genetics ; Matrix Metalloproteinases/metabolism ; Matrix Metalloproteinases/physiology ; Models, Molecular ; Neoplasm Invasiveness ; Prognosis ; Protein Structure, Tertiary ; Tumor Microenvironment
Chemical Substances	Biomarkers, Tumor ; Matrix Metalloproteinases (EC 3.4.24.-)
Language	English
Publishing date	2015-06-01
Publishing country	Singapore
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2704569-9
ISSN	2768-6698 ; 1093-9946
ISSN (online)	2768-6698
ISSN	1093-9946
DOI	10.2741/4364
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Article ; Online: Engineering of tissue inhibitor of metalloproteinases TIMP-1 for fine discrimination between closely related stromelysins MMP-3 and MMP-10.

Raeeszadeh-Sarmazdeh, Maryam / Coban, Mathew / Mahajan, Shivansh / Hockla, Alexandra / Sankaran, Banumathi / Downey, Gregory P / Radisky, Derek C / Radisky, Evette S

The Journal of biological chemistry

2022 Volume 298, Issue 3, Page(s) 101654

Abstract: Matrix metalloproteinases (MMPs) have long been known as key drivers in the development and progression of diseases, including cancer and neurodegenerative, cardiovascular, and many other inflammatory and degenerative diseases, making them attractive ... ...

Abstract	Matrix metalloproteinases (MMPs) have long been known as key drivers in the development and progression of diseases, including cancer and neurodegenerative, cardiovascular, and many other inflammatory and degenerative diseases, making them attractive potential drug targets. Engineering selective inhibitors based upon tissue inhibitors of metalloproteinases (TIMPs), endogenous human proteins that tightly yet nonspecifically bind to the family of MMPs, represents a promising new avenue for therapeutic development. Here, we used a counter-selective screening strategy for directed evolution of yeast-displayed human TIMP-1 to obtain TIMP-1 variants highly selective for the inhibition of MMP-3 in preference over MMP-10. As MMP-3 and MMP-10 are the most similar MMPs in sequence, structure, and function, our results thus clearly demonstrate the capability for engineering full-length TIMP proteins to be highly selective MMP inhibitors. We show using protein crystal structures and models of MMP-3-selective TIMP-1 variants bound to MMP-3 and counter-target MMP-10 how structural alterations within the N-terminal and C-terminal TIMP-1 domains create new favorable and selective interactions with MMP-3 and disrupt unique interactions with MMP-10. While our MMP-3-selective inhibitors may be of interest for future investigation in diseases where this enzyme drives pathology, our platform and screening strategy can be employed for developing selective inhibitors of additional MMPs implicated as therapeutic targets in disease.
MeSH term(s)	Humans ; Matrix Metalloproteinase 10/chemistry ; Matrix Metalloproteinase 10/genetics ; Matrix Metalloproteinase 10/metabolism ; Matrix Metalloproteinase 3/chemistry ; Matrix Metalloproteinase 3/genetics ; Matrix Metalloproteinase 3/metabolism ; Protein Engineering ; Tissue Inhibitor of Metalloproteinase-1/chemistry ; Tissue Inhibitor of Metalloproteinase-1/genetics ; Tissue Inhibitor of Metalloproteinase-1/metabolism
Chemical Substances	TIMP1 protein, human ; Tissue Inhibitor of Metalloproteinase-1 ; MMP3 protein, human (EC 3.4.24.17) ; Matrix Metalloproteinase 3 (EC 3.4.24.17) ; MMP10 protein, human (EC 3.4.24.22) ; Matrix Metalloproteinase 10 (EC 3.4.24.22)
Language	English
Publishing date	2022-01-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2022.101654
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Article ; Online: Activity-based protein profiling reveals active serine proteases that drive malignancy of human ovarian clear cell carcinoma.

Mehner, Christine / Hockla, Alexandra / Coban, Mathew / Madden, Benjamin / Estrada, Rosendo / Radisky, Derek C / Radisky, Evette S

The Journal of biological chemistry

2022 Volume 298, Issue 8, Page(s) 102146

Abstract: Ovarian clear cell carcinoma (OCCC) is an understudied poor prognosis subtype of ovarian cancer lacking in effective targeted therapies. Efforts to define molecular drivers of OCCC malignancy may lead to new therapeutic targets and approaches. Among ... ...

Abstract	Ovarian clear cell carcinoma (OCCC) is an understudied poor prognosis subtype of ovarian cancer lacking in effective targeted therapies. Efforts to define molecular drivers of OCCC malignancy may lead to new therapeutic targets and approaches. Among potential targets are secreted proteases, enzymes which in many cancers serve as key drivers of malignant progression. Here, we found that inhibitors of trypsin-like serine proteases suppressed malignant phenotypes of OCCC cell lines. To identify the proteases responsible for malignancy in OCCC, we employed activity-based protein profiling to directly analyze enzyme activity. We developed an activity-based probe featuring an arginine diphenylphosphonate warhead to detect active serine proteases of trypsin-like specificity and a biotin handle to facilitate affinity purification of labeled proteases. Using this probe, we identified active trypsin-like serine proteases within the complex proteomes secreted by OCCC cell lines, including two proteases in common, tissue plasminogen activator and urokinase-type plasminogen activator. Further interrogation of these proteases showed that both were involved in cancer cell invasion and proliferation of OCCC cells and were also detected in in vivo models of OCCC. We conclude the detection of tissue plasminogen activator and urokinase-type plasminogen activator as catalytically active proteases and significant drivers of the malignant phenotype may point to these enzymes as targets for new therapeutic strategies in OCCC. Our activity-based probe and profiling methodology will also serve as a valuable tool for detection of active trypsin-like serine proteases in models of other cancers and other diseases.
MeSH term(s)	Adenocarcinoma, Clear Cell/enzymology ; Adenocarcinoma, Clear Cell/pathology ; Female ; Humans ; Ovarian Neoplasms/enzymology ; Ovarian Neoplasms/pathology ; Serine Proteases/metabolism ; Tissue Plasminogen Activator/metabolism ; Trypsin ; Urokinase-Type Plasminogen Activator/metabolism
Chemical Substances	Serine Proteases (EC 3.4.-) ; Trypsin (EC 3.4.21.4) ; Tissue Plasminogen Activator (EC 3.4.21.68) ; Urokinase-Type Plasminogen Activator (EC 3.4.21.73)
Language	English
Publishing date	2022-06-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2022.102146
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Article ; Online: Defining a role for the homeoprotein Six1 in EMT and mammary tumorigenesis.

Radisky, Derek C

The Journal of clinical investigation

2009 Volume 119, Issue 9, Page(s) 2528–2531

Abstract: Homeobox (Hox) genes encode transcription factors that act as critical regulators of growth and differentiation during embryogenesis. While many studies have identified increased expression of Hox genes in tumors, much less is known about the mechanistic ...

Abstract	Homeobox (Hox) genes encode transcription factors that act as critical regulators of growth and differentiation during embryogenesis. While many studies have identified increased expression of Hox genes in tumors, much less is known about the mechanistic basis by which Hox genes facilitate tumor development. In this issue of the JCI, McCoy and colleagues show that transgenic mice that express the homeoprotein Six1 in mammary epithelial cells show increases in stem/progenitor cell populations and subsequent tumor development, while in a separate study Micalizzi and colleagues show that overexpression of Six1 facilitates breast cancer cell metastasis by inducing epithelial-mesenchymal transition (EMT) (see the related articles beginning on pages 2663 and 2678, respectively). Their findings implicate Six1 as a central mediator of breast cancer development.
MeSH term(s)	Animals ; Breast Neoplasms/etiology ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Breast Neoplasms/physiopathology ; Epithelium/pathology ; Female ; Genes, Homeobox ; Homeodomain Proteins/genetics ; Homeodomain Proteins/physiology ; Humans ; Mammary Neoplasms, Experimental/etiology ; Mammary Neoplasms, Experimental/genetics ; Mammary Neoplasms, Experimental/pathology ; Mammary Neoplasms, Experimental/physiopathology ; Mesoderm/pathology ; Mice ; Mice, Transgenic ; Neoplastic Stem Cells/pathology
Chemical Substances	Homeodomain Proteins ; SIX1 protein, human ; Six1 protein, mouse
Language	English
Publishing date	2009-08-24
Publishing country	United States
Document type	Comment ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI40555
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