Supplementary Data from Sphingosine Kinase 2 in Stromal Fibroblasts Creates a Hospitable Tumor Microenvironment in Breast Cancer

Supplementary Data from Sphingosine Kinase 2 in Stromal Fibroblasts Creates a Hospitable Tumor Microenvironment in Breast Cancer

<p>Supplementary Table 2</p>

محفوظ في:

التفاصيل البيبلوغرافية
المؤلف الرئيسي:	Cynthia Weigel (14963361) (author)
مؤلفون آخرون:	Melissa A. Maczis (14963364) (author), Elisa N.D. Palladino (14963367) (author), Christopher D. Green (14963370) (author), Michael Maceyka (14963373) (author), Chunqing Guo (14963376) (author), Xiang-Yang Wang (14963379) (author), Mikhail G. Dozmorov (9144837) (author), Sheldon Milstien (14963382) (author), Sarah Spiegel (14963385) (author)
منشور في:	2025
الموضوعات:	Cancer Cancer Biology Molecular and Cellular Biology Breast Cancer Cell Signaling Oncogenes & Tumor Suppressors p53
الوسوم:	إضافة وسم لا توجد وسوم, كن أول من يضع وسما على هذه التسجيلة!

مواد مشابهة

Supplementary Data from Sphingosine Kinase 2 in Stromal Fibroblasts Creates a Hospitable Tumor Microenvironment in Breast Cancer
حسب: Cynthia Weigel (14963361)
منشور في: (2025)

Supplementary Data from Sphingosine Kinase 2 in Stromal Fibroblasts Creates a Hospitable Tumor Microenvironment in Breast Cancer
حسب: Cynthia Weigel (14963361)
منشور في: (2025)

Supplementary Data from Sphingosine Kinase 2 in Stromal Fibroblasts Creates a Hospitable Tumor Microenvironment in Breast Cancer
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Supplementary Table 2 from Monounsaturated and Diunsaturated Fatty Acids Sensitize Cervical Cancer to Radiation Therapy
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Supplementary Table 2 from Unique Transcriptional Profiles Underlie Osteosarcomagenesis Driven by Different p53 Mutants
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Supplementary Table 3 from Unique Transcriptional Profiles Underlie Osteosarcomagenesis Driven by Different p53 Mutants
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Supplementary Table 4 from Unique Transcriptional Profiles Underlie Osteosarcomagenesis Driven by Different p53 Mutants
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Supplementary Table 5 from Unique Transcriptional Profiles Underlie Osteosarcomagenesis Driven by Different p53 Mutants
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Figure S2 from BRCA1 Insufficiency Induces a Hypersialylated Acidic Tumor Microenvironment That Promotes Metastasis and Immunotherapy Resistance
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Figure S3 from BRCA1 Insufficiency Induces a Hypersialylated Acidic Tumor Microenvironment That Promotes Metastasis and Immunotherapy Resistance
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Figure S4 from BRCA1 Insufficiency Induces a Hypersialylated Acidic Tumor Microenvironment That Promotes Metastasis and Immunotherapy Resistance
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Figure S5 from BRCA1 Insufficiency Induces a Hypersialylated Acidic Tumor Microenvironment That Promotes Metastasis and Immunotherapy Resistance
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Figure S6 from BRCA1 Insufficiency Induces a Hypersialylated Acidic Tumor Microenvironment That Promotes Metastasis and Immunotherapy Resistance
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Figure S7 from BRCA1 Insufficiency Induces a Hypersialylated Acidic Tumor Microenvironment That Promotes Metastasis and Immunotherapy Resistance
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Table S1-S9 from BRCA1 Insufficiency Induces a Hypersialylated Acidic Tumor Microenvironment That Promotes Metastasis and Immunotherapy Resistance
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Table S3 from An <i>In Vivo</i> CRISPR Screen Identifies That SNRPC Promotes Triple-Negative Breast Cancer Progression
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