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2. AXL Is a Driver of Stemness in Normal Mammary Gland and Breast Cancer

Author

Engelsen, Agnete ST, Wnuk-Lipinska, Katarzyna, Bougnaud, Sebastien, Vatter, Fanny A Pelissier, Tiron, Crina, Villadsen, René, Miyano, Masaru, Lotsberg, Maria L, Madeleine, Noëlly, Panahandeh, Pouda, Dhakal, Sushil, Tan, Tuan Zea, Peters, Stacey D’mello, Grøndal, Sturla, Aziz, Sura M, Nord, Silje, Herfindal, Lars, Stampfer, Martha R, Sørlie, Therese, Brekken, Rolf A, Straume, Oddbjørn, Halberg, Nils, Gausdal, Gro, Thiery, Jean Paul, Akslen, Lars A, Petersen, Ole W, LaBarge, Mark A, and Lorens, James B

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Women's Health, Cancer Genomics, Cancer, Genetics, Stem Cell Research, Human Genome, Breast Cancer, Stem Cell Research - Nonembryonic - Non-Human, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Cell Biology, Stem Cells Research
Abstract

The receptor tyrosine kinase AXL is associated with epithelial plasticity in several solid tumors including breast cancer and AXL-targeting agents are currently in clinical trials. We hypothesized that AXL is a driver of stemness traits in cancer by co-option of a regulatory function normally reserved for stem cells. AXL-expressing cells in human mammary epithelial ducts co-expressed markers associated with multipotency, and AXL inhibition abolished colony formation and self-maintenance activities while promoting terminal differentiation in vitro. Axl-null mice did not exhibit a strong developmental phenotype, but enrichment of Axl + cells was required for mouse mammary gland reconstitution upon transplantation, and Axl-null mice had reduced incidence of Wnt1-driven mammary tumors. An AXL-dependent gene signature is a feature of transcriptomes in basal breast cancers and reduced patient survival irrespective of subtype. Our interpretation is that AXL regulates access to epithelial plasticity programs in MaSCs and, when co-opted, maintains acquired stemness in breast cancer cells.

Published
2020

3. AXL Targeting Abrogates Autophagic Flux and Induces Immunogenic Cell Death in Drug-Resistant Cancer Cells

Author

Lotsberg, Maria L, Wnuk-Lipinska, Katarzyna, Terry, Stéphane, Tan, Tuan Zea, Lu, Ning, Trachsel-Moncho, Laura, Røsland, Gro V, Siraji, Muntequa I, Hellesøy, Monica, Rayford, Austin, Jacobsen, Kirstine, Ditzel, Henrik J, Vintermyr, Olav K, Bivona, Trever G, Minna, John, Brekken, Rolf A, Baguley, Bruce, Micklem, David, Akslen, Lars A, Gausdal, Gro, Simonsen, Anne, Thiery, Jean Paul, Chouaib, Salem, Lorens, James B, and Engelsen, Agnete Svendsen Tenfjord

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Cancer, Genetics, Lung Cancer, Prevention, Lung, 5.1 Pharmaceuticals, 2.1 Biological and endogenous factors, Aetiology, Development of treatments and therapeutic interventions, Autophagy, Cell Line, Tumor, Drug Resistance, Neoplasm, ErbB Receptors, Humans, Immunogenic Cell Death, Lung Neoplasms, Pharmaceutical Preparations, Protein Kinase Inhibitors, NSCLC, AXL receptor tyrosine kinase, Acquired EGFR TKI resistance, Phenotypic plasticity, Tumor immune microenvironment, Autophagic flux, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

IntroductionAcquired cancer therapy resistance evolves under selection pressure of immune surveillance and favors mechanisms that promote drug resistance through cell survival and immune evasion. AXL receptor tyrosine kinase is a mediator of cancer cell phenotypic plasticity and suppression of tumor immunity, and AXL expression is associated with drug resistance and diminished long-term survival in a wide range of malignancies, including NSCLC.MethodsWe aimed to investigate the mechanisms underlying AXL-mediated acquired resistance to first- and third-generation small molecule EGFR tyrosine kinase inhibitors (EGFRi) in NSCLC.ResultsWe found that EGFRi resistance was mediated by up-regulation of AXL, and targeting AXL reduced reactivation of the MAPK pathway and blocked onset of acquired resistance to long-term EGFRi treatment in vivo. AXL-expressing EGFRi-resistant cells revealed phenotypic and cell signaling heterogeneity incompatible with a simple bypass signaling mechanism, and were characterized by an increased autophagic flux. AXL kinase inhibition by the small molecule inhibitor bemcentinib or siRNA mediated AXL gene silencing was reported to inhibit the autophagic flux in vitro, bemcentinib treatment blocked clonogenicity and induced immunogenic cell death in drug-resistant NSCLC in vitro, and abrogated the transcription of autophagy-associated genes in vivo. Furthermore, we found a positive correlation between AXL expression and autophagy-associated gene signatures in a large cohort of human NSCLC (n = 1018).ConclusionOur results indicate that AXL signaling supports a drug-resistant persister cell phenotype through a novel autophagy-dependent mechanism and reveals a unique immunogenic effect of AXL inhibition on drug-resistant NSCLC cells.

Published
2020

6. AXL targeting restores PD-1 blockade sensitivity of STK11/LKB1 mutant NSCLC through expansion of TCF1+ CD8 T cells

Author

Li, Huiyu, Liu, Zhida, Liu, Longchao, Zhang, Hongyi, Han, Chuanhui, Girard, Luc, Park, Hyunsil, Zhang, Anli, Dong, Chunbo, Ye, Jianfeng, Rayford, Austin, Peyton, Michael, Li, Xiaoguang, Avila, Kimberley, Cao, Xuezhi, Hu, Shuiqing, Alam, Md Maksudul, Akbay, Esra A., Solis, Luisa M., Behrens, Carmen, Hernandez-Ruiz, Sharia, Lu, Wei, Wistuba, Ignacio, Heymach, John V., Chisamore, Michael, Micklem, David, Gabra, Hani, Gausdal, Gro, Lorens, James B., Li, Bo, Fu, Yang-Xin, Minna, John D., and Brekken, Rolf A.

Published
2022
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7. High-Dimensional Phenotyping Identifies Age-Emergent Cells in Human Mammary Epithelia

Author

Vatter, Fanny A Pelissier, Schapiro, Denis, Chang, Hang, Borowsky, Alexander D, Lee, Jonathan K, Parvin, Bahram, Stampfer, Martha R, LaBarge, Mark A, Bodenmiller, Bernd, and Lorens, James B

Subjects
Biological Sciences, Bioengineering, Stem Cell Research, Aging, Women's Health, Cancer, Breast Cancer, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Aetiology, Underpinning research, Adolescent, Adult, Aged, Aged, 80 and over, Female, Humans, Mammary Glands, Human, Middle Aged, aging, breast cancer, heterogeneity, human mammary epithelia, mass cytometry, single-cell analysis, Biochemistry and Cell Biology, Medical Physiology, Biological sciences
Abstract

Aging is associated with tissue-level changes in cellular composition that are correlated with increased susceptibility to disease. Aging human mammary tissue shows skewed progenitor cell potency, resulting in diminished tumor-suppressive cell types and the accumulation of defective epithelial progenitors. Quantitative characterization of these age-emergent human cell subpopulations is lacking, impeding our understanding of the relationship between age and cancer susceptibility. We conducted single-cell resolution proteomic phenotyping of healthy breast epithelia from 57 women, aged 16-91 years, using mass cytometry. Remarkable heterogeneity was quantified within the two mammary epithelial lineages. Population partitioning identified a subset of aberrant basal-like luminal cells that accumulate with age and originate from age-altered progenitors. Quantification of age-emergent phenotypes enabled robust classification of breast tissues by age in healthy women. This high-resolution mapping highlighted specific epithelial subpopulations that change with age in a manner consistent with increased susceptibility to breast cancer.

Published
2018

8. High-Dimensional Phenotyping Identifies Age-Emergent Cells in Human Mammary Epithelia.

Author

Pelissier Vatter, Fanny A, Schapiro, Denis, Chang, Hang, Borowsky, Alexander D, Lee, Jonathan K, Parvin, Bahram, Stampfer, Martha R, LaBarge, Mark A, Bodenmiller, Bernd, and Lorens, James B

Subjects
Mammary Glands, Human, Humans, Aging, Adolescent, Adult, Aged, Aged, 80 and over, Middle Aged, Female, aging, breast cancer, heterogeneity, human mammary epithelia, mass cytometry, single-cell analysis, Mammary Glands, Human, and over, Breast Cancer, Cancer, Stem Cell Research, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Biochemistry and Cell Biology, Medical Physiology
Abstract

Aging is associated with tissue-level changes in cellular composition that are correlated with increased susceptibility to disease. Aging human mammary tissue shows skewed progenitor cell potency, resulting in diminished tumor-suppressive cell types and the accumulation of defective epithelial progenitors. Quantitative characterization of these age-emergent human cell subpopulations is lacking, impeding our understanding of the relationship between age and cancer susceptibility. We conducted single-cell resolution proteomic phenotyping of healthy breast epithelia from 57 women, aged 16-91 years, using mass cytometry. Remarkable heterogeneity was quantified within the two mammary epithelial lineages. Population partitioning identified a subset of aberrant basal-like luminal cells that accumulate with age and originate from age-altered progenitors. Quantification of age-emergent phenotypes enabled robust classification of breast tissues by age in healthy women. This high-resolution mapping highlighted specific epithelial subpopulations that change with age in a manner consistent with increased susceptibility to breast cancer.

Published
2018

9. Microenvironment-Induced Non-sporadic Expression of the AXL and cKIT Receptors Are Related to Epithelial Plasticity and Drug Resistance.

Author

Jokela, Tiina A, Engelsen, Agnete ST, Rybicka, Agata, Pelissier Vatter, Fanny A, Garbe, James C, Miyano, Masaru, Tiron, Crina, Ferariu, Dan, Akslen, Lars A, Stampfer, Martha R, Lorens, James B, and LaBarge, Mark A

Subjects
AXL, MEMA, breast cancer, cKIT, drug resistance, epithelial plasticity, microenvironment, Stem Cell Research - Nonembryonic - Human, Breast Cancer, Stem Cell Research, Genetics, Cancer, 2.1 Biological and endogenous factors
Abstract

The existence of rare cancer cells that sporadically acquire drug-tolerance through epigenetic mechanisms is proposed as one mechanism that drives cancer therapy failure. Here we provide evidence that specific microenvironments impose non-sporadic expression of proteins related to epithelial plasticity and drug resistance. Microarrays of robotically printed combinatorial microenvironments of known composition were used to make cell-based functional associations between microenvironments, which were design-inspired by normal and tumor-burdened breast tissues, and cell phenotypes. We hypothesized that specific combinations of microenvironment constituents non-sporadically impose the induction of the AXL and cKIT receptor tyrosine kinase proteins, which are known to be involved in epithelial plasticity and drug-tolerance, in an isogenic human mammary epithelial cell (HMEC) malignant progression series. Dimension reduction analysis reveals type I collagen as a dominant feature, inducing expression of both markers in pre-stasis finite lifespan HMECs, and transformed non-malignant and malignant immortal cell lines. Basement membrane-associated matrix proteins, laminin-111 and type IV collagen, suppress AXL and cKIT expression in pre-stasis and non-malignant cells. However, AXL and cKIT are not suppressed by laminin-111 in malignant cells. General linear models identified key factors, osteopontin, IL-8, and type VIα3 collagen, which significantly upregulated AXL and cKIT, as well as a plasticity-related gene expression program that is often observed in stem cells and in epithelial-to-mesenchymal-transition. These factors are co-located with AXL-expressing cells in situ in normal and breast cancer tissues, and associated with resistance to paclitaxel. A greater diversity of microenvironments induced AXL and cKIT expression consistent with plasticity and drug-tolerant phenotypes in tumorigenic cells compared to normal or immortal cells, suggesting a reduced perception of microenvironment specificity in malignant cells. Microenvironment-imposed reprogramming could explain why resistant cells are seemingly persistent and rapidly adaptable to multiple classes of drugs. These results support the notion that specific microenvironments drive drug-tolerant cellular phenotypes and suggest a novel interventional avenue for preventing acquired therapy resistance.

Published
2018

10. Data from AXL/WRNIP1 Mediates Replication Stress Response and Promotes Therapy Resistance and Metachronous Metastasis in HER2+ Breast Cancer

Author

Marquez-Palencia, Mauricio, primary, Reza Herrera, Luis, primary, Parida, Pravat Kumar, primary, Ghosh, Suvranil, primary, Kim, Kangsan, primary, Das, Nikitha M., primary, Gonzalez-Ericsson, Paula I., primary, Sanders, Melinda E., primary, Mobley, Bret C., primary, Diegeler, Sebastian, primary, Aguilera, Todd A., primary, Peng, Yan, primary, Lewis, Cheryl M., primary, Arteaga, Carlos L., primary, Hanker, Ariella B., primary, Whitehurst, Angelique W., primary, Lorens, James B., primary, Brekken, Rolf A., primary, Davis, Anthony J., primary, and Malladi, Srinivas, primary

Published
2024
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11. Supplementary Figure 5 from AXL/WRNIP1 Mediates Replication Stress Response and Promotes Therapy Resistance and Metachronous Metastasis in HER2+ Breast Cancer

Author

Marquez-Palencia, Mauricio, primary, Reza Herrera, Luis, primary, Parida, Pravat Kumar, primary, Ghosh, Suvranil, primary, Kim, Kangsan, primary, Das, Nikitha M., primary, Gonzalez-Ericsson, Paula I., primary, Sanders, Melinda E., primary, Mobley, Bret C., primary, Diegeler, Sebastian, primary, Aguilera, Todd A., primary, Peng, Yan, primary, Lewis, Cheryl M., primary, Arteaga, Carlos L., primary, Hanker, Ariella B., primary, Whitehurst, Angelique W., primary, Lorens, James B., primary, Brekken, Rolf A., primary, Davis, Anthony J., primary, and Malladi, Srinivas, primary

Published
2024
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12. Supplementary tables from AXL/WRNIP1 Mediates Replication Stress Response and Promotes Therapy Resistance and Metachronous Metastasis in HER2+ Breast Cancer

Author

Marquez-Palencia, Mauricio, primary, Reza Herrera, Luis, primary, Parida, Pravat Kumar, primary, Ghosh, Suvranil, primary, Kim, Kangsan, primary, Das, Nikitha M., primary, Gonzalez-Ericsson, Paula I., primary, Sanders, Melinda E., primary, Mobley, Bret C., primary, Diegeler, Sebastian, primary, Aguilera, Todd A., primary, Peng, Yan, primary, Lewis, Cheryl M., primary, Arteaga, Carlos L., primary, Hanker, Ariella B., primary, Whitehurst, Angelique W., primary, Lorens, James B., primary, Brekken, Rolf A., primary, Davis, Anthony J., primary, and Malladi, Srinivas, primary

Published
2024
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13. Supplementary Figure 2 from AXL/WRNIP1 Mediates Replication Stress Response and Promotes Therapy Resistance and Metachronous Metastasis in HER2+ Breast Cancer

Author

Marquez-Palencia, Mauricio, primary, Reza Herrera, Luis, primary, Parida, Pravat Kumar, primary, Ghosh, Suvranil, primary, Kim, Kangsan, primary, Das, Nikitha M., primary, Gonzalez-Ericsson, Paula I., primary, Sanders, Melinda E., primary, Mobley, Bret C., primary, Diegeler, Sebastian, primary, Aguilera, Todd A., primary, Peng, Yan, primary, Lewis, Cheryl M., primary, Arteaga, Carlos L., primary, Hanker, Ariella B., primary, Whitehurst, Angelique W., primary, Lorens, James B., primary, Brekken, Rolf A., primary, Davis, Anthony J., primary, and Malladi, Srinivas, primary

Published
2024
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14. Supplementary Figure 4 from AXL/WRNIP1 Mediates Replication Stress Response and Promotes Therapy Resistance and Metachronous Metastasis in HER2+ Breast Cancer

Author

Marquez-Palencia, Mauricio, primary, Reza Herrera, Luis, primary, Parida, Pravat Kumar, primary, Ghosh, Suvranil, primary, Kim, Kangsan, primary, Das, Nikitha M., primary, Gonzalez-Ericsson, Paula I., primary, Sanders, Melinda E., primary, Mobley, Bret C., primary, Diegeler, Sebastian, primary, Aguilera, Todd A., primary, Peng, Yan, primary, Lewis, Cheryl M., primary, Arteaga, Carlos L., primary, Hanker, Ariella B., primary, Whitehurst, Angelique W., primary, Lorens, James B., primary, Brekken, Rolf A., primary, Davis, Anthony J., primary, and Malladi, Srinivas, primary

Published
2024
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15. Supplementary Figure 3 from AXL/WRNIP1 Mediates Replication Stress Response and Promotes Therapy Resistance and Metachronous Metastasis in HER2+ Breast Cancer

Author

Marquez-Palencia, Mauricio, primary, Reza Herrera, Luis, primary, Parida, Pravat Kumar, primary, Ghosh, Suvranil, primary, Kim, Kangsan, primary, Das, Nikitha M., primary, Gonzalez-Ericsson, Paula I., primary, Sanders, Melinda E., primary, Mobley, Bret C., primary, Diegeler, Sebastian, primary, Aguilera, Todd A., primary, Peng, Yan, primary, Lewis, Cheryl M., primary, Arteaga, Carlos L., primary, Hanker, Ariella B., primary, Whitehurst, Angelique W., primary, Lorens, James B., primary, Brekken, Rolf A., primary, Davis, Anthony J., primary, and Malladi, Srinivas, primary

Published
2024
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16. Supplementary Figure 1 from AXL/WRNIP1 Mediates Replication Stress Response and Promotes Therapy Resistance and Metachronous Metastasis in HER2+ Breast Cancer

Author

Marquez-Palencia, Mauricio, primary, Reza Herrera, Luis, primary, Parida, Pravat Kumar, primary, Ghosh, Suvranil, primary, Kim, Kangsan, primary, Das, Nikitha M., primary, Gonzalez-Ericsson, Paula I., primary, Sanders, Melinda E., primary, Mobley, Bret C., primary, Diegeler, Sebastian, primary, Aguilera, Todd A., primary, Peng, Yan, primary, Lewis, Cheryl M., primary, Arteaga, Carlos L., primary, Hanker, Ariella B., primary, Whitehurst, Angelique W., primary, Lorens, James B., primary, Brekken, Rolf A., primary, Davis, Anthony J., primary, and Malladi, Srinivas, primary

Published
2024
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17. AXL/WRNIP1 Mediates Replication Stress Response and Promotes Therapy Resistance and Metachronous Metastasis in HER2+ Breast Cancer

Author

Marquez-Palencia, Mauricio, primary, Reza Herrera, Luis, additional, Parida, Pravat Kumar, additional, Ghosh, Suvranil, additional, Kim, Kangsan, additional, Das, Nikitha M., additional, Gonzalez-Ericsson, Paula I., additional, Sanders, Melinda E., additional, Mobley, Bret C., additional, Diegeler, Sebastian, additional, Aguilera, Todd A., additional, Peng, Yan, additional, Lewis, Cheryl M., additional, Arteaga, Carlos L., additional, Hanker, Ariella B., additional, Whitehurst, Angelique W., additional, Lorens, James B., additional, Brekken, Rolf A., additional, Davis, Anthony J., additional, and Malladi, Srinivas, additional

Published
2024
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20. Age-related dysfunction in mechanotransduction impairs differentiation of human mammary epithelial progenitors.

Author

Pelissier, Fanny A, Garbe, James C, Ananthanarayanan, Badriprasad, Miyano, Masaru, Lin, ChunHan, Jokela, Tiina, Kumar, Sanjay, Stampfer, Martha R, Lorens, James B, and LaBarge, Mark A

Subjects
Mammary Glands, Human, Epithelial Cells, Stem Cells, Humans, Adaptor Proteins, Signal Transducing, Phosphoproteins, Transcription Factors, Age Factors, Mechanotransduction, Cellular, Cell Differentiation, Adult, Middle Aged, Female, Mammary Glands, Human, Adaptor Proteins, Signal Transducing, Mechanotransduction, Cellular, Stem Cell Research - Nonembryonic - Non-Human, Stem Cell Research, Stem Cell Research - Nonembryonic - Human, Aging, 1.1 Normal biological development and functioning, Biochemistry and Cell Biology, Medical Physiology
Abstract

Dysfunctional progenitor and luminal cells with acquired basal cell properties accumulate during human mammary epithelial aging for reasons not understood. Multipotent progenitors from women aged 55 years is unaffected by physiological stiffness changes. Efficient activation of Hippo pathway transducers YAP and TAZ is required for the modulus-dependent myoepithelial/basal bias in younger progenitors. In older progenitors, YAP and TAZ are activated only when stressed with extraphysiologically stiff matrices, which bias differentiation towards luminal-like phenotypes. In vivo YAP is primarily active in myoepithelia of younger breasts, but localization and activity increases in luminal cells with age. Thus, aging phenotypes of mammary epithelia may arise partly because alterations in Hippo pathway activation impair microenvironment-directed differentiation and lineage specificity.

Published
2014

22. Contributors

Author

Adami, Pascale, primary, Adotévi, Olivier, additional, Apetoh, Lionel, additional, Garcia, Alvaro Baeza, additional, Baguley, Bruce, additional, Berchem, Guy, additional, Bonavida, Benjamin, additional, Boschetti, Gilles, additional, Cavalli, Giulio, additional, Cenci, Simone, additional, Chen, Sandy, additional, Chouaib, Salem, additional, Ciechomska, I.A., additional, Cyranowski, S., additional, Czystowska, Malgorzata, additional, Delage-Mourroux, Régis, additional, Dhakal, Sushil, additional, Duhem, Caroline, additional, Engelsen, Agnete S.T., additional, Faure, Mathias, additional, Fonderflick, Leïla, additional, Guittaut, Michaël, additional, Hasmim, Meriem, additional, Jacquin, Elise, additional, Janji, Bassam, additional, Kaminska, B., additional, Lorens, James B., additional, Lotsberg, Maria Lie, additional, Nancey, Stephane, additional, Noman, Muhammad Zaeem, additional, Rozières, Aurore, additional, Thiery, Jerome, additional, Viret, Christophe, additional, Viry, Elodie, additional, Whiteside, Theresa L., additional, Wiersma, Valerie R., additional, and Xiao, Malina, additional

Published
2020
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24. Supplementary Table S2 from AXL Targeting Overcomes Human Lung Cancer Cell Resistance to NK- and CTL-Mediated Cytotoxicity

Author

Terry, Stéphane, primary, Abdou, Abderemane, primary, Engelsen, Agnete S.T., primary, Buart, Stéphanie, primary, Dessen, Philippe, primary, Corgnac, Stéphanie, primary, Collares, Davi, primary, Meurice, Guillaume, primary, Gausdal, Gro, primary, Baud, Véronique, primary, Saintigny, Pierre, primary, Lorens, James B., primary, Thiery, Jean-Paul, primary, Mami-Chouaib, Fathia, primary, and Chouaib, Salem, primary

Published
2023
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25. Data from AXL Targeting Overcomes Human Lung Cancer Cell Resistance to NK- and CTL-Mediated Cytotoxicity

Author

Terry, Stéphane, primary, Abdou, Abderemane, primary, Engelsen, Agnete S.T., primary, Buart, Stéphanie, primary, Dessen, Philippe, primary, Corgnac, Stéphanie, primary, Collares, Davi, primary, Meurice, Guillaume, primary, Gausdal, Gro, primary, Baud, Véronique, primary, Saintigny, Pierre, primary, Lorens, James B., primary, Thiery, Jean-Paul, primary, Mami-Chouaib, Fathia, primary, and Chouaib, Salem, primary

Published
2023
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26. Supplementary Data from AXL Targeting Overcomes Human Lung Cancer Cell Resistance to NK- and CTL-Mediated Cytotoxicity

Author

Terry, Stéphane, primary, Abdou, Abderemane, primary, Engelsen, Agnete S.T., primary, Buart, Stéphanie, primary, Dessen, Philippe, primary, Corgnac, Stéphanie, primary, Collares, Davi, primary, Meurice, Guillaume, primary, Gausdal, Gro, primary, Baud, Véronique, primary, Saintigny, Pierre, primary, Lorens, James B., primary, Thiery, Jean-Paul, primary, Mami-Chouaib, Fathia, primary, and Chouaib, Salem, primary

Published
2023
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29. Data from Small-Molecule Inhibition of Axl Targets Tumor Immune Suppression and Enhances Chemotherapy in Pancreatic Cancer

Author

Ludwig, Kathleen F., primary, Du, Wenting, primary, Sorrelle, Noah B., primary, Wnuk-Lipinska, Katarzyna, primary, Topalovski, Mary, primary, Toombs, Jason E., primary, Cruz, Victoria H., primary, Yabuuchi, Shinichi, primary, Rajeshkumar, N.V., primary, Maitra, Anirban, primary, Lorens, James B., primary, and Brekken, Rolf A., primary

Published
2023
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30. Supplementary Methods from Small-Molecule Inhibition of Axl Targets Tumor Immune Suppression and Enhances Chemotherapy in Pancreatic Cancer

Author

Ludwig, Kathleen F., primary, Du, Wenting, primary, Sorrelle, Noah B., primary, Wnuk-Lipinska, Katarzyna, primary, Topalovski, Mary, primary, Toombs, Jason E., primary, Cruz, Victoria H., primary, Yabuuchi, Shinichi, primary, Rajeshkumar, N.V., primary, Maitra, Anirban, primary, Lorens, James B., primary, and Brekken, Rolf A., primary

Published
2023
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31. Supplementary Data from Association of AXL and PD-L1 Expression with Clinical Outcomes in Patients with Advanced Renal Cell Carcinoma Treated with PD-1 Blockade

Author

Terry, Stéphane, primary, Dalban, Cécile, primary, Rioux-Leclercq, Nathalie, primary, Adam, Julien, primary, Meylan, Maxime, primary, Buart, Stéphanie, primary, Bougoüin, Antoine, primary, Lespagnol, Alexandra, primary, Dugay, Frédéric, primary, Moreno, Irelka Colina, primary, Lacroix, Guillaume, primary, Lorens, James B., primary, Gausdal, Gro, primary, Fridman, Wolf H., primary, Mami-Chouaib, Fathia, primary, Chaput, Nathalie, primary, Beuselinck, Benoit, primary, Chabaud, Sylvie, primary, Barros-Monteiro, Janice, primary, Vano, Yann, primary, Escudier, Bernard, primary, Sautès-Fridman, Catherine, primary, Albiges, Laurence, primary, and Chouaib, Salem, primary

Published
2023
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32. Supplementary Figures from Small-Molecule Inhibition of Axl Targets Tumor Immune Suppression and Enhances Chemotherapy in Pancreatic Cancer

Author

Ludwig, Kathleen F., primary, Du, Wenting, primary, Sorrelle, Noah B., primary, Wnuk-Lipinska, Katarzyna, primary, Topalovski, Mary, primary, Toombs, Jason E., primary, Cruz, Victoria H., primary, Yabuuchi, Shinichi, primary, Rajeshkumar, N.V., primary, Maitra, Anirban, primary, Lorens, James B., primary, and Brekken, Rolf A., primary

Published
2023
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33. Data from Multiple Roles for the Receptor Tyrosine Kinase Axl in Tumor Formation

Author

Holland, Sacha J., primary, Powell, Mark J., primary, Franci, Christian, primary, Chan, Emily W., primary, Friera, Annabelle M., primary, Atchison, Robert E., primary, McLaughlin, John, primary, Swift, Susan E., primary, Pali, Erlina S., primary, Yam, George, primary, Wong, Stephen, primary, Lasaga, Joe, primary, Shen, Mary R., primary, Yu, Simon, primary, Xu, Weiduan, primary, Hitoshi, Yasumichi, primary, Bogenberger, Jakob, primary, Nör, Jacques E., primary, Payan, Donald G., primary, and Lorens, James B., primary

Published
2023
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34. Supplementary Methods and References from Warfarin Blocks Gas6-Mediated Axl Activation Required for Pancreatic Cancer Epithelial Plasticity and Metastasis

Author

Kirane, Amanda, primary, Ludwig, Kathleen F., primary, Sorrelle, Noah, primary, Haaland, Gry, primary, Sandal, Tone, primary, Ranaweera, Renate, primary, Toombs, Jason E., primary, Wang, Miao, primary, Dineen, Sean P., primary, Micklem, David, primary, Dellinger, Michael T., primary, Lorens, James B., primary, and Brekken, Rolf A., primary

Published
2023
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36. Data from Vimentin–ERK Signaling Uncouples Slug Gene Regulatory Function

Author

Virtakoivu, Reetta, primary, Mai, Anja, primary, Mattila, Elina, primary, De Franceschi, Nicola, primary, Imanishi, Susumu Y., primary, Corthals, Garry, primary, Kaukonen, Riina, primary, Saari, Markku, primary, Cheng, Fang, primary, Torvaldson, Elin, primary, Kosma, Veli-Matti, primary, Mannermaa, Arto, primary, Muharram, Ghaffar, primary, Gilles, Christine, primary, Eriksson, John, primary, Soini, Ylermi, primary, Lorens, James B., primary, and Ivaska, Johanna, primary

Published
2023
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38. Supplementary figures S1-5, materials and methods from Vimentin–ERK Signaling Uncouples Slug Gene Regulatory Function

Author

Virtakoivu, Reetta, primary, Mai, Anja, primary, Mattila, Elina, primary, De Franceschi, Nicola, primary, Imanishi, Susumu Y., primary, Corthals, Garry, primary, Kaukonen, Riina, primary, Saari, Markku, primary, Cheng, Fang, primary, Torvaldson, Elin, primary, Kosma, Veli-Matti, primary, Mannermaa, Arto, primary, Muharram, Ghaffar, primary, Gilles, Christine, primary, Eriksson, John, primary, Soini, Ylermi, primary, Lorens, James B., primary, and Ivaska, Johanna, primary

Published
2023
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39. Supplementary Tables S1-S2 from Warfarin Blocks Gas6-Mediated Axl Activation Required for Pancreatic Cancer Epithelial Plasticity and Metastasis

Author

Kirane, Amanda, primary, Ludwig, Kathleen F., primary, Sorrelle, Noah, primary, Haaland, Gry, primary, Sandal, Tone, primary, Ranaweera, Renate, primary, Toombs, Jason E., primary, Wang, Miao, primary, Dineen, Sean P., primary, Micklem, David, primary, Dellinger, Michael T., primary, Lorens, James B., primary, and Brekken, Rolf A., primary

Published
2023
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43. Supplementary Figures 1-4, Table 1 from Multiple Roles for the Receptor Tyrosine Kinase Axl in Tumor Formation

Author

Holland, Sacha J., primary, Powell, Mark J., primary, Franci, Christian, primary, Chan, Emily W., primary, Friera, Annabelle M., primary, Atchison, Robert E., primary, McLaughlin, John, primary, Swift, Susan E., primary, Pali, Erlina S., primary, Yam, George, primary, Wong, Stephen, primary, Lasaga, Joe, primary, Shen, Mary R., primary, Yu, Simon, primary, Xu, Weiduan, primary, Hitoshi, Yasumichi, primary, Bogenberger, Jakob, primary, Nör, Jacques E., primary, Payan, Donald G., primary, and Lorens, James B., primary

Published
2023
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44. Data from Warfarin Blocks Gas6-Mediated Axl Activation Required for Pancreatic Cancer Epithelial Plasticity and Metastasis

Author

Kirane, Amanda, primary, Ludwig, Kathleen F., primary, Sorrelle, Noah, primary, Haaland, Gry, primary, Sandal, Tone, primary, Ranaweera, Renate, primary, Toombs, Jason E., primary, Wang, Miao, primary, Dineen, Sean P., primary, Micklem, David, primary, Dellinger, Michael T., primary, Lorens, James B., primary, and Brekken, Rolf A., primary

Published
2023
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46. Supplementary Figures S1-S6 from Warfarin Blocks Gas6-Mediated Axl Activation Required for Pancreatic Cancer Epithelial Plasticity and Metastasis

Author

Kirane, Amanda, primary, Ludwig, Kathleen F., primary, Sorrelle, Noah, primary, Haaland, Gry, primary, Sandal, Tone, primary, Ranaweera, Renate, primary, Toombs, Jason E., primary, Wang, Miao, primary, Dineen, Sean P., primary, Micklem, David, primary, Dellinger, Michael T., primary, Lorens, James B., primary, and Brekken, Rolf A., primary

Published
2023
Full Text
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50. Supplementary Figure and Table Legends from Multiple Roles for the Receptor Tyrosine Kinase Axl in Tumor Formation

Author

Holland, Sacha J., primary, Powell, Mark J., primary, Franci, Christian, primary, Chan, Emily W., primary, Friera, Annabelle M., primary, Atchison, Robert E., primary, McLaughlin, John, primary, Swift, Susan E., primary, Pali, Erlina S., primary, Yam, George, primary, Wong, Stephen, primary, Lasaga, Joe, primary, Shen, Mary R., primary, Yu, Simon, primary, Xu, Weiduan, primary, Hitoshi, Yasumichi, primary, Bogenberger, Jakob, primary, Nör, Jacques E., primary, Payan, Donald G., primary, and Lorens, James B., primary

Published
2023
Full Text
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