The M1/M2 macrophage paradigm plays a key role in tumor progression. M1 macrophages are historically regarded as anti-tumor, while M2-polarized macrophages, commonly deemed tumor-associated macrophages (TAMs), are contributors to many pro-tumorigenic outcomes in cancer through angiogenic and lymphangiogenic regulation, immune suppression, hypoxia induction, tumor cell proliferation, and metastasis. The tumor microenvironment (TME) can influence macrophage recruitment and polarization, giving way to these pro-tumorigenic outcomes. Investigating TME-induced macrophage polarization is critical for further understanding of TAM-related pro-tumor outcomes and potential development of new therapeutic approaches. This review explores the current understanding of TME-induced macrophage polarization and the role of M2-polarized macrophages in promoting tumor progression.

Waldenström macroglobulinemia is an indolent, B-cell lymphoma without a known cure. The bone marrow microenvironment and cytokines both play key roles in Waldenström macroglobulinemia (WM) tumor progression. Only one FDA-approved drug exists for the treatment of WM, Ibrutinib, but treatment plans involve a variety of drugs and inhibitors. This review explores avenues of tumor progression and targeted drug therapy that have been investigated in WM and related B-cell lymphomas.

Aim(s): To assess barriers and facilitators to seeking inpatient psychiatric treatment among transgender and nonbinary people.Design: Qualitative interview study.Methods: Semi‐structured interviews were conducted from March 2019 to June 2022 with transgender and nonbinary people admitted to an inpatient psychiatric hospital in the United States during the past 5 years. Data were analysed using thematic analysis and constructed within a modified social‐ecological model of stigma. Standards for Reporting Qualitative Research were used for this study.Results: Participants (N = 15) described barriers and facilitators across all three social‐ecological levels. i) Individual themes included distrust of the mental healthcare system, feeling unsafe, loss of autonomy, minimizing one's own mental health needs, and feelings of accountability to others. ii) Interpersonal themes included: lack of support for transgender/nonbinary identity, limited transgender/nonbinary knowledge among mental healthcare professionals, and allyship. iii) Structural themes included: carceral setting, financial costs, and availability of non‐profit treatment options.Conclusion: Multi‐level themes were identified as barriers and facilitators to seeking inpatient psychiatric care for transgender and nonbinary people, providing opportunities among inpatient settings to improve care delivery and engagement. Greater health equity can be achieved by addressing barriers to care.Implications: Incorporating inclusive and affirming practices in inpatient psychiatric services presents an opportunity to reduce barriers to seeking care.Impact: The present study describes the experiences of transgender and nonbinary people as they determine whether to voluntarily seek inpatient psychiatric treatment. This perspective allows nurses, health systems, and policymakers to integrate transgender and nonbinary people's needs to improve healthcare delivery.Patient/Public Contribution: Transgender and nonbinary participants were recruited in collaboration with community organizations. Members of the transgender and nonbinary community participated in study design development and analysis and were part of the study team.

Waldenstrom macroglobulinemia (WM) is a non-Hodgkin B-cell lymphoma, characterized by bone marrow infiltration with plasma cells and lymphocytes. The tumor microenvironment (TME) plays an important role in mediating WM cell biology, but the effects of macrophages on WM biology remains unclear. Here, we investigated the effects of macrophages on WM growth and survival and identified a novel role for transcription factor GLI3 in macrophage polarization. We found that co-culture of M0 and M2 macrophages promoted WM cell growth and survival, and co-culture WM cells with M0 macrophages induced M2-like phenotypes. Interestingly, GLI3 expression was induced in M2 macrophages (not M1), leading us to perform analysis of macrophages from mice lacking Gli3 in myeloid cells (M-Gli3^−/− mice). A subset of differentially expressed genes implicated a role for GLI3 in macrophage polarization. Macrophages from M-Gli3^−/− mice did not induce WM cell proliferation and reduced survival compared to M2 macrophages from WT mice. In addition, in vitro polarization of M0 macrophages from M-Gli3^−/− was not able to induce M2 markers such as CD163, despite inducing iNos expression (M1 marker). Taken together, these results suggest a role for M2 macrophages in promoting WM cell growth and identify GLI3 as a modulator of macrophage polarization.