Male breast cancer (MaBC) is a rare clinical entity, which makes up approximately 1% of all breast cancers. However, the incidence of MaBC has been steadily increasing over the past few decades. The risk factors for MaBC include age, black race, family history of breast cancer, genetic mutations, liver cirrhosis, and testicular abnormalities. The majority of patients with MaBC present with painless lumps, and about half of the patients have at least one lymph node involved at the time of diagnosis. The treatment of MaBC models that of female breast cancer (FeBC), but this is mainly due to lack of prospective studies for MaBC patients. The treatment modality includes surgery, adjuvant radiation, endocrine therapy, and chemotherapy. However, there are some distinct features of MaBC, both clinically and molecularly, that may warrant a different clinical approach. Ongoing multinational effort is required, to conduct clinical trials for MaBC, or the inclusion of MaBC patients in FeBC trials, to help clinicians improve care for MaBC patients.

Ag-specific tolerizing immunotherapy is considered the optimal strategy to control type 1 diabetes, a childhood disease involving autoimmunity toward multiple islet antigenic peptides. To understand whether tolerizing immunotherapy with a single peptide could control diabetes driven by multiple Ags, we coencapsulated the high-affinity CD4 + mimotope (BDC2.5 mim ) of islet autoantigen chromogranin A (ChgA) with or without calcitriol (1a,25-dihydroxyvitamin D3) into liposomes. After liposome administration, we followed the endogenous ChgA-specific immune response with specific tetramers. Liposome administration s.c., but not i.v., induced ChgA-specific Foxp3 + and Foxp3 2 PD1 + CD73 + ICOS + IL-10 + peripheral regulatory T cells in prediabetic mice, and liposome administration at the onset of hyperglycemia significantly delayed diabetes progression. After BDC2.5 mim /calcitriol liposome administration, adoptive transfer of CD4 + T cells suppressed the development of diabetes in NOD severe combined immunodeficiency mice receiving diabetogenic splenocytes. After BDC2.5 mim /calcitriol liposome treatment and expansion of ChgA-specific peripheral regulatory T cells. IFN-g production and expansion of islet-specific glucose-6-phosphatase catalytic subunit-related protein-specific CD8 + T cells were also suppressed in pancreatic draining lymph node, demonstrating bystander tolerance at the site of Ag presentation. Thus, liposomes encapsulating the single CD4 + peptide, BDC2.5 mim , and calcitriol induce ChgA-specific CD4 + T cells that regulate CD4 + and CD8 + self-antigen specificities and autoimmune diabetes in NOD mice.

<b><i>Introduction:</i></b> Oncogenic osteomalacia (Onc-Ost) is a paraneoplastic phenomenon characterized by hypophosphatemia due to elevated fibroblast growth factor-23 (FGF-23). Onc-Ost has been previously reported in patients with germ line mesenchymal tumors and solid organ malignancies. This is the first report of aggressive natural killer (NK) T-cell lymphoma presenting as Onc-Ost. <b><i>Case Description:</i></b> A 33-year-old Vietnamese female with active hepatitis B and <i>Mycobacterium avium</i> complex, on ongoing therapy with tenofovir disoproxil, azithromycin, and ethambutol, presented with persistent fevers and developed refractory hypophosphatemia. Workup confirmed severe renal phosphate wasting. Tenofovir disoproxil was initially suspected; however, presence of isolated phosphaturia without Fanconi syndrome and persistence of hypophosphatemia despite discontinuation of medication led to clinical suspicion of Onc-Ost. Elevated FGF-23 warranted further workup, leading to a definitive diagnosis of clinically subtle NK T-cell lymphoma. Chemotherapy was initiated; however, patient continued to deteriorate clinically and expired. <b><i>Conclusion:</i></b> Along with commonly reported germ line mesenchymal tumors and solid malignancies, NK T-cell lymphoma can also present as Onc-Ost. Timely detection of associated tumors and subsequent antitumor therapy would likely reverse hypophosphatemia and improve clinical outcomes.