Solimando, A. G., Da Via, M. C., Bolli, N. & Steinbrunn, T. The route of the malignant plasma cell in its survival niche: exploring “multiple myelomas”. Cancers 14, 3271 (2022).
Kumar, S. K. et al. Improved survival in multiple myeloma and the impact of novel therapies. Blood 111, 2516–2520 (2008).
Google Scholar
Hoy, S. M. Pomalidomide: a review in relapsed and refractory multiple myeloma. Drugs 77, 1897–1908 (2017).
Google Scholar
Laubach, J. P., Richardson, P. G. & Anderson, K. C. The evolution and impact of therapy in multiple myeloma. Med Oncol. 27(Suppl 1), S1–S6 (2010).
Google Scholar
Sanderson, R. D. & Borset, M. Syndecan-1 in B lymphoid malignancies. Ann. Hematol. 81, 125–135 (2002).
Google Scholar
Ren, Z., Spaargaren, M. & Pals, S. T. Syndecan-1 and stromal heparan sulfate proteoglycans: key moderators of plasma cell biology and myeloma pathogenesis. Blood 137, 1713–1718 (2021).
Google Scholar
Lovell, R. et al. Soluble syndecan-1 level at diagnosis is an independent prognostic factor in multiple myeloma and the extent of fall from diagnosis to plateau predicts for overall survival. Br. J. Haematol. 130, 542–548 (2005).
Google Scholar
Purushothaman, A. et al. Heparanase-enhanced shedding of syndecan-1 by myeloma cells promotes endothelial invasion and angiogenesis. Blood 115, 2449–2457 (2010).
Google Scholar
Rangarajan, S. et al. Heparanase-enhanced shedding of syndecan-1 and its role in driving disease pathogenesis and progression. J. Histochem. Cytochem. 68, 823–840 (2020).
Google Scholar
Yang, Y. et al. Heparanase enhances syndecan-1 shedding: a novel mechanism for stimulation of tumor growth and metastasis. J. Biol. Chem. 282, 13326–13333 (2007).
Google Scholar
Purushothaman, A. & Sanderson, R. D. Heparanase: a dynamic promoter of myeloma progression. Adv. Exp. Med. Biol. 1221, 331–349 (2020).
Google Scholar
An, G. et al. Multiple myeloma patients with low proportion of circulating plasma cells had similar survival with primary plasma cell leukemia patients. Ann. Hematol. 94, 257–264 (2015).
Google Scholar
Matsui, W. et al. Characterization of clonogenic multiple myeloma cells. Blood 103, 2332–2336 (2004).
Google Scholar
Seidel, C. et al. Serum syndecan-1: a new independent prognostic marker in multiple myeloma. Blood 95, 388–392 (2000).
Google Scholar
Dhodapkar, M. V. et al. Elevated levels of shed syndecan-1 correlate with tumour mass and decreased matrix metalloproteinase-9 activity in the serum of patients with multiple myeloma. Br. J. Haematol. 99, 368–371 (1997).
Google Scholar
Beauvais, D. M., Jung, O., Yang, Y., Sanderson, R. D. & Rapraeger, A. C. Syndecan-1 (CD138) suppresses apoptosis in multiple myeloma by activating IGF1 receptor: prevention by SynstatinIGF1R inhibits tumor growth. Cancer Res. 76, 4981–4993 (2016).
Google Scholar
Khotskaya, Y. B. et al. Syndecan-1 is required for robust growth, vascularization, and metastasis of myeloma tumors in vivo. J. Biol. Chem. 284, 26085–26095 (2009).
Google Scholar
Jung, O. et al. Heparanase-induced shedding of syndecan-1/CD138 in myeloma and endothelial cells activates VEGFR2 and an invasive phenotype: prevention by novel synstatins. Oncogenesis 5, e202 (2016).
Google Scholar
Rapraeger, A. C. Synstatin: a selective inhibitor of the syndecan-1-coupled IGF1R-alphavbeta3 integrin complex in tumorigenesis and angiogenesis. FEBS J. 280, 2207–2215 (2013).
Google Scholar
Beauvais, D. M., Ell, B. J., McWhorter, A. R. & Rapraeger, A. C. Syndecan-1 regulates alphavbeta3 and alphavbeta5 integrin activation during angiogenesis and is blocked by synstatin, a novel peptide inhibitor. J. Exp. Med. 206, 691–705 (2009).
Google Scholar
Kusumoto, T. et al. Clinical significance of syndecan-1 and versican expression in human epithelial ovarian cancer. Oncol. Rep. 23, 917–925 (2010).
Google Scholar
Schonfeld, K. et al. Indatuximab ravtansine (BT062) combination treatment in multiple myeloma: pre-clinical studies. J. Hematol. Oncol. 10, 13 (2017).
Google Scholar
Yu, T. et al. VIS832, a novel CD138-targeting monoclonal antibody, potently induces killing of human multiple myeloma and further synergizes with IMiDs or bortezomib in vitro and in vivo. Blood Cancer J. 10, 110 (2020).
Google Scholar
Sun, W. P. et al. A novel anti-human syndecan-1 (CD138) monoclonal antibody 4B3: characterization and application. Cell. Mol. Immunol. 4, 209–214 (2007).
Google Scholar
Sun, C. et al. Safety and efficacy of targeting CD138 with a chimeric antigen receptor for the treatment of multiple myeloma. Oncotarget 10, 2369–2383 (2019).
Google Scholar
Jiang, H. et al. Transfection of chimeric anti-CD138 gene enhances natural killer cell activation and killing of multiple myeloma cells. Mol. Oncol. 8, 297–310 (2014).
Google Scholar
Bae, J., Tai, Y. T., Anderson, K. C. & Munshi, N. C. Novel epitope evoking CD138 antigen-specific cytotoxic T lymphocytes targeting multiple myeloma and other plasma cell disorders. Br. J. Haematol. 155, 349–361 (2011).
Google Scholar
Jung, O., Beauvais, D. M., Adams, K. M. & Rapraeger, A. C. VLA-4 phosphorylation during tumor and immune cell migration relies on its coupling to VEGFR2 and CXCR4 by syndecan-1. J. Cell Sci. 132, jcs232645 (2019).
Wen, Z. et al. Expression of NrasQ61R and MYC transgene in germinal center B cells induces a highly malignant multiple myeloma in mice. Blood 137, 61–74 (2021).
Google Scholar
Flietner, E. et al. Ponatinib sensitizes myeloma cells to MEK inhibition in the high-risk VQ model. Sci. Rep. 12, 10616 (2022).
Google Scholar
Massia, S. P. & Hubbell, J. A. Vascular endothelial cell adhesion and spreading promoted by the peptide REDV of the IIICS region of plasma fibronectin is mediated by integrin alpha 4 beta 1. J. Biol. Chem. 267, 14019–14026 (1992).
Google Scholar
Wang, H., Jin, H. & Rapraeger, A. C. Syndecan-1 and syndecan-4 capture epidermal growth factor receptor family members and the alpha3beta1 integrin via binding sites in their ectodomains: novel synstatins prevent kinase capture and inhibit alpha6beta4-integrin-dependent epithelial cell motility. J. Biol. Chem. 290, 26103–26113 (2015).
Google Scholar
Wang, H., Leavitt, L., Ramaswamy, R. & Rapraeger, A. C. Interaction of syndecan and alpha6beta4 integrin cytoplasmic domains: regulation of ErbB2-mediated integrin activation. J. Biol. Chem. 285, 13569–13579 (2010).
Google Scholar
Ahani, R. et al. Enhancement of lentiviral vectors gene delivery against VEGFR2 expressing cells by co-display of the binding and fusogenic moieties: a two molecules targeting approach. Virol. J. 22, 300 (2025).
Google Scholar
Ran, S., Mohamedali, K. A., Luster, T. A., Thorpe, P. E. & Rosenblum, M. G. The vascular-ablative agent VEGF(121)/rGel inhibits pulmonary metastases of MDA-MB-231 breast tumors. Neoplasia 7, 486–496 (2005).
Google Scholar
Gu, Y. et al. Low absolute CD4(+) T cell counts in peripheral blood predict poor prognosis in patients with newly diagnosed multiple myeloma. Leuk. Lymphoma 61, 1869–1876 (2020).
Google Scholar
Zelle-Rieser, C. et al. T cells in multiple myeloma display features of exhaustion and senescence at the tumor site. J. Hematol. Oncol. 9, 116 (2016).
Google Scholar
Zheng, Y. et al. Macrophages are an abundant component of myeloma microenvironment and protect myeloma cells from chemotherapy drug-induced apoptosis. Blood 114, 3625–3628 (2009).
Google Scholar
Muthu Raja, K. R. et al. Increased T regulatory cells are associated with adverse clinical features and predict progression in multiple myeloma. PLoS ONE 7, e47077 (2012).
Google Scholar
Feyler, S. et al. CD4(+)CD25(+)FoxP3(+) regulatory T cells are increased whilst CD3(+)CD4(-)CD8(-)alphabetaTCR(+) Double Negative T cells are decreased in the peripheral blood of patients with multiple myeloma which correlates with disease burden. Br. J. Haematol. 144, 686–695 (2009).
Google Scholar
Beyer, M. et al. In vivo peripheral expansion of naive CD4+CD25high FoxP3+ regulatory T cells in patients with multiple myeloma. Blood 107, 3940–3949 (2006).
Google Scholar
Giannopoulos, K., Kaminska, W., Hus, I. & Dmoszynska, A. The frequency of T regulatory cells modulates the survival of multiple myeloma patients: detailed characterisation of immune status in multiple myeloma. Br. J. Cancer 106, 546–552 (2012).
Google Scholar
Hadjiaggelidou, C. & Katodritou, E. Regulatory T-cells and multiple myeloma: implications in tumor immune biology and treatment. J. Clin. Med. 10, 4588 (2021).
Sun, J. et al. Tumor-associated macrophages in multiple myeloma: advances in biology and therapy. J. Immunother. Cancer 10, e003975 (2022).
Benner, B. et al. Generation of monocyte-derived tumor-associated macrophages using tumor-conditioned media provides a novel method to study tumor-associated macrophages in vitro. J. Immunother. Cancer 7, 140 (2019).
Google Scholar
Yao, L. et al. Single-cell discovery and multiomic characterization of therapeutic targets in multiple myeloma. Cancer Res 83, 1214–1233 (2023).
Google Scholar
Luo, M., Zhao, F., Cheng, H., Su, M. & Wang, Y. Macrophage polarization: an important role in inflammatory diseases. Front. Immunol. 15, 1352946 (2024).
Google Scholar
Liu, Y. C., Zou, X. B., Chai, Y. F. & Yao, Y. M. Macrophage polarization in inflammatory diseases. Int. J. Biol. Sci. 10, 520–529 (2014).
Google Scholar
Flietner, E. et al. Molecular characterization stratifies VQ myeloma cells into two clusters with distinct risk signatures and drug responses. Oncogene 42, 1751–1762 (2023).
Google Scholar
Meregalli, C. An overview of bortezomib-induced neurotoxicity. Toxics 3, 294–303 (2015).
Google Scholar
Bruna, J. et al. Neurophysiological, histological and immunohistochemical characterization of bortezomib-induced neuropathy in mice. Exp. Neurol. 223, 599–608 (2010).
Google Scholar
Kawano, Y. et al. Targeting the bone marrow microenvironment in multiple myeloma. Immunol. Rev. 263, 160–172 (2015).
Google Scholar
Liu, L. et al. Multiple myeloma hinders erythropoiesis and causes anaemia owing to high levels of CCL3 in the bone marrow microenvironment. Sci. Rep. 10, 20508 (2020).
Google Scholar
Bruns, I. et al. Multiple myeloma-related deregulation of bone marrow-derived CD34(+) hematopoietic stem and progenitor cells. Blood 120, 2620–2630 (2012).
Google Scholar
Laurenzana, I. et al. Multiple myeloma-derived extracellular vesicles impair normal hematopoiesis by acting on hematopoietic stem and progenitor cells. Front. Med. 8, 793040 (2021).
Google Scholar
Rajkumar, S. V. Multiple myeloma: 2020 update on diagnosis, risk-stratification and management. Am. J. Hematol. 95, 548–567 (2020).
Google Scholar
Turinelli, V., Rossi, G. & Gavazza, A. Retrospective study of 613 canine cytologically normal bone marrows associated to altered hemograms: description, possible interpretation, and review of the principal physiological hematopoietic mechanisms. Open Vet. J. 13, 233–240 (2023).
Google Scholar
Bouchnita, A., Eymard, N., Moyo, T. K., Koury, M. J. & Volpert, V. Bone marrow infiltration by multiple myeloma causes anemia by reversible disruption of erythropoiesis. Am. J. Hematol. 91, 371–378 (2016).
Google Scholar
Fredriksson, S. et al. Protein detection using proximity-dependent DNA ligation assays. Nat. Biotechnol. 20, 473–477 (2002).
Google Scholar
Su, W., Yang, L., Luo, X., Chen, M. & Liu, J. Elimination of autofluorescence in archival formaldehyde-fixed, paraffin-embedded bone marrow biopsies. Arch. Pathol. Lab. Med. 143, 362–369 (2019).
Google Scholar
Blade, J. et al. Extramedullary disease in multiple myeloma: a systematic literature review. Blood Cancer J. 12, 45 (2022).
Google Scholar
Touzeau, C. & Moreau, P. How I treat extramedullary myeloma. Blood 127, 971–976 (2016).
Google Scholar
Kumar, L. et al. Multiple myeloma with extramedullary disease: impact of autologous stem cell transplantation on outcome. Bone Marrow Transplant. 52, 1473–1475 (2017).
Google Scholar
Dallavalasa, S. et al. The role of tumor associated macrophages (TAMs) in cancer progression, chemoresistance, angiogenesis and metastasis—current status. Curr. Med. Chem. 28, 8203–8236 (2021).
Google Scholar
Sun, M. et al. Tumor-associated macrophages modulate angiogenesis and tumor growth in a xenograft mouse model of multiple myeloma. Leuk. Res. 110, 106709 (2021).
Google Scholar
Cencini, E. et al. Tumor-associated macrophages in multiple myeloma: key role in disease biology and potential therapeutic implications. Curr. Oncol. 30, 6111–6133 (2023).
Google Scholar
Suyani, E. et al. Tumor-associated macrophages as a prognostic parameter in multiple myeloma. Ann. Hematol. 92, 669–677 (2013).
Google Scholar
Panchabhai, S. et al. Tumor-associated macrophages and extracellular matrix metalloproteinase inducer in prognosis of multiple myeloma. Leukemia 30, 951–954 (2016).
Google Scholar
Zhang, J. et al. Tumor-associated macrophages regulate the function of cytotoxic T lymphocyte through PD-1/PD-L1 pathway in multiple myeloma. Cancer Med. 11, 4838–4848 (2022).
Google Scholar
Wang, H. et al. High numbers of CD163+ tumor-associated macrophages correlate with poor prognosis in multiple myeloma patients receiving bortezomib-based regimens. J. Cancer 10, 3239–3245 (2019).
Google Scholar
Kawano, Y. The role of regulatory T cells in multiple myeloma progression. Rinsho Ketsueki 62, 299–304 (2021).
Google Scholar
Chen, H., Wang, X., Wang, Y. & Chang, X. What happens to regulatory T cells in multiple myeloma. Cell Death Discov. 9, 468 (2023).
Google Scholar
Feng, X. et al. Targeting CD38 suppresses induction and function of T regulatory cells to mitigate immunosuppression in multiple myeloma. Clin. Cancer Res. 23, 4290–4300 (2017).
Google Scholar
Wang, D. et al. Macrophage-derived CCL22 promotes an immunosuppressive tumor microenvironment via IL-8 in malignant pleural effusion. Cancer Lett. 452, 244–253 (2019).
Google Scholar
Kos, K. et al. Tumor-associated macrophages promote intratumoral conversion of conventional CD4(+) T cells into regulatory T cells via PD-1 signalling. Oncoimmunology 11, 2063225 (2022).
Google Scholar
Sanderson, R. D. & Yang, Y. Syndecan-1: a dynamic regulator of the myeloma microenvironment. Clin. Exp. Metastasis 25, 149–159 (2008).
Google Scholar
Akl, M. R. et al. Molecular and clinical profiles of syndecan-1 in solid and hematological cancer for prognosis and precision medicine. Oncotarget 6, 28693–28715 (2015).
Google Scholar
Agrahari, A. K., Dikshit, M. & Asthana, S. Crystallographic mining of ASK1 regulators to unravel the intricate PPI interfaces for the discovery of small molecule. Comput. Struct. Biotechnol. J. 20, 3734–3754 (2022).
Google Scholar
Kim, H. et al. Cyclophilin A regulates JNK/p38-MAPK signaling through its physical interaction with ASK1. Biochem. Biophys. Res. Commun. 464, 112–117 (2015).
Google Scholar
Garcia-Ortiz, A. et al. The role of tumor microenvironment in multiple myeloma development and progression. Cancers 13, 217 (2021).
Yang, W. C. & Lin, S. F. Mechanisms of drug resistance in relapse and refractory multiple myeloma. Biomed. Res. Int. 2015, 341430 (2015).
Google Scholar
Sun, J. et al. IL-10R inhibition reprograms tumor-associated macrophages and reverses drug resistance in multiple myeloma. Leukemia 38, 2355–2365 (2024).
Azab, A. K. et al. CXCR4 inhibitor AMD3100 disrupts the interaction of multiple myeloma cells with the bone marrow microenvironment and enhances their sensitivity to therapy. Blood. 2009;113:4341-4351. Blood 143, 2673 (2024).
Google Scholar
Jurczyszyn, A. et al. HGF, sIL-6R and TGF-beta1 play a significant role in the progression of multiple myeloma. J. Cancer 5, 518–524 (2014).
Google Scholar
Yu, M., Zhou, V., Pisano, M. D., Janz, S. & Cui, X. Changes in the immune microenvironment during plasma cell tumor development in the IL6Myc mouse model of human multiple myeloma. Exp. Cell Res. 442, 114273 (2024).
Larrayoz, M. et al. Preclinical models for prediction of immunotherapy outcomes and immune evasion mechanisms in genetically heterogeneous multiple myeloma. Nat. Med. 29, 632–645 (2023).
Google Scholar
Bouyssou, J. M., Ghobrial, I. M. & Roccaro, A. M. Targeting SDF-1 in multiple myeloma tumor microenvironment. Cancer Lett. 380, 315–318 (2016).
Google Scholar
Colombo, F. et al. In vitro models of the crosstalk between multiple myeloma and stromal cells recapitulate the mild NF-kappaB activation observed in vivo. Cell Death Dis. 15, 731 (2024).
Google Scholar
Ren, Z. et al. Correction to: The CXCL12gamma chemokine immobilized by heparan sulfate on stromal niche cells controls adhesion and mediates drug resistance in multiple myeloma. J. Hematol. Oncol. 14, 29 (2021).
Google Scholar
Ria, R. & Vacca, A. Bone marrow stromal cells-induced drug resistance in multiple myeloma. Int. J. Mol. Sci. 21, 613 (2020).
Kwantwi, L. B. & Tandoh, T. Focal adhesion kinase-mediated interaction between tumor and immune cells in the tumor microenvironment: implications for cancer-associated therapies and tumor progression. Clin. Transl. Oncol. 27, 1398–1405 (2025).
George, L. L. et al. Emerging targets and cellular therapy for relapsed refractory multiple myeloma: a systematic review. Clin. Lymphoma Myeloma Leuk. 21, 741–751 (2021).
Google Scholar
Radhakrishnan, V., Golla, U. & Kudva, A. K. Role of immune cells and immunotherapy in multiple myeloma. Life 14, 461 (2024).
Chen, J. et al. BAFF is involved in macrophage-induced bortezomib resistance in myeloma. Cell Death Dis. 8, e3161 (2017).
Google Scholar
Sabol, H. M. et al. A NOTCH3-CXCL12-driven myeloma-tumor niche signaling axis promotes chemoresistance in multiple myeloma. Haematologica 109, 2606–2618 (2024).
Google Scholar
De Bruyne, E. et al. IGF-1 suppresses Bim expression in multiple myeloma via epigenetic and posttranslational mechanisms. Blood. 2010;115(12):2430-2440. Blood 142, 1027 (2023).
Google Scholar
Cao, Y. et al. The cytokine/chemokine pattern in the bone marrow environment of multiple myeloma patients. Exp. Hematol. 38, 860–867 (2010).
Google Scholar
Rapraeger, A. C. Syndecans and their synstatins: targeting an organizer of receptor tyrosine kinase signaling at the cell-matrix interface. Front. Oncol. 11, 775349 (2021).
Google Scholar
Beauvais, D. M. & Rapraeger, A. C. Syndecan-1 couples the insulin-like growth factor-1 receptor to inside-out integrin activation. J. Cell Sci. 123, 3796–3807 (2010).
Google Scholar
Dore, J. M., Morard, F., Vita, N. & Wijdenes, J. Identification and location on syndecan-1 core protein of the epitopes of B-B2 and B-B4 monoclonal antibodies. FEBS Lett. 426, 67–70 (1998).
Google Scholar
Orecchia, P. et al. A novel human anti-syndecan-1 antibody inhibits vascular maturation and tumour growth in melanoma. Eur. J. Cancer 49, 2022–2033 (2013).
Google Scholar
Orecchia, P. et al. Targeting Syndecan-1, a molecule implicated in the process of vasculogenic mimicry, enhances the therapeutic efficacy of the L19-IL2 immunocytokine in human melanoma xenografts. Oncotarget 6, 37426–37442 (2015).
Google Scholar
Jagannath, S. et al. Indatuximab ravtansine (BT062) monotherapy in patients with relapsed and/or refractory multiple myeloma. Clin. Lymphoma Myeloma Leuk. 19, 372–380 (2019).
Google Scholar
Kelly, K. R. et al. Indatuximab ravtansine plus dexamethasone with lenalidomide or pomalidomide in relapsed or refractory multiple myeloma: a multicentre, phase 1/2a study. Lancet Haematol. 8, e794–e807 (2021).
Google Scholar
Rousseau, C. et al. Dosimetry results suggest feasibility of radioimmunotherapy using anti-CD138 (B-B4) antibody in multiple myeloma patients. Tumour Biol. 33, 679–688 (2012).
Google Scholar
Thul, P. J. et al. A subcellular map of the human proteome. Science 356, eaal3321 (2017).
Li, Q., Park, P. W., Wilson, C. L. & Parks, W. C. Matrilysin shedding of syndecan-1 regulates chemokine mobilization and transepithelial efflux of neutrophils in acute lung injury. Cell 111, 635–646 (2002).
Google Scholar
Wang, L. et al. Therapeutic peptides: current applications and future directions. Signal Transduct. Target. Ther. 7, 48 (2022).
Google Scholar
Craik, D. J., Fairlie, D. P., Liras, S. & Price, D. The future of peptide-based drugs. Chem. Biol. Drug Des. 81, 136–147 (2013).
Google Scholar
Reddy, D. N. et al. Design, synthesis, and biological evaluation of stable beta(6.3)-Helices: discovery of non-hemolytic antibacterial peptides. Eur. J. Med. Chem. 149, 193–210 (2018).
Google Scholar
Dima, D. et al. Multiple myeloma therapy: emerging trends and challenges. Cancers 14, 4082 (2022).
Papadimitriou, K. et al. Deep phenotyping reveals distinct immune signatures correlating with prognostication, treatment responses, and MRD status in multiple myeloma. Cancers 12, 3245 (2020).
Hideshima, T. et al. Biologic sequelae of c-Jun NH(2)-terminal kinase (JNK) activation in multiple myeloma cell lines. Oncogene 22, 8797–8801 (2003).
Google Scholar
Chauhan, D. et al. JNK-dependent release of mitochondrial protein, Smac, during apoptosis in multiple myeloma (MM) cells. J. Biol. Chem. 278, 17593–17596 (2003).
Google Scholar
Obeng, E. A. et al. Proteasome inhibitors induce a terminal unfolded protein response in multiple myeloma cells. Blood 107, 4907–4916 (2006).
Google Scholar
Fribley, A. & Wang, C. Y. Proteasome inhibitor induces apoptosis through induction of endoplasmic reticulum stress. Cancer Biol. Ther. 5, 745–748 (2006).
Google Scholar
Fribley, A., Zeng, Q. & Wang, C. Y. Proteasome inhibitor PS-341 induces apoptosis through induction of endoplasmic reticulum stress-reactive oxygen species in head and neck squamous cell carcinoma cells. Mol. Cell. Biol. 24, 9695–9704 (2004).
Google Scholar
Akhmetzyanova, I. et al. Dynamic CD138 surface expression regulates switch between myeloma growth and dissemination. Leukemia 34, 245–256 (2020).
Google Scholar
Yang, S. Y. et al. Characterization of organ-specific regulatory B cells using single-cell RNA sequencing. Front. Immunol. 12, 711980 (2021).
Google Scholar
Orecchioni, M., Ghosheh, Y., Pramod, A. B. & Ley, K. Macrophage polarization: different gene signatures in M1(LPS+) vs. classically and M2(LPS-) vs. alternatively activated macrophages. Front. Immunol. 10, 1084 (2019).
Google Scholar
Welte, T. et al. A heparan-sulfate-bearing syndecan-1 glycoform is a distinct surface marker for intra-tumoral myeloid-derived suppressor cells. iScience 24, 103349 (2021).
Google Scholar
