{"id":131380,"date":"2026-04-14T15:30:00","date_gmt":"2026-04-14T20:30:00","guid":{"rendered":"https:\/\/www.unmc.edu\/newsroom\/?p=131380"},"modified":"2026-04-14T15:27:32","modified_gmt":"2026-04-14T20:27:32","slug":"pathology-trainees-contribute-to-departments-research-output","status":"publish","type":"post","link":"https:\/\/www.unmc.edu\/newsroom\/2026\/04\/14\/pathology-trainees-contribute-to-departments-research-output\/","title":{"rendered":"Pathology trainees contribute to department\u2019s research output"},"content":{"rendered":"
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Recent publications and grants from PMI residents and predoctoral and postdoctoral trainees:<\/p>\n\n\n\n

Arumugam P, <\/strong>Heim CE, Fallet RW, Shinde DD, Thomas VC, Arg\u00fcello RJ, Kielian T. Mitochondrial transfer to granulocytic myeloid-derived suppressor cells augments immunosuppressive activity. Cell Rep. 2026 Mar 24;45(3):117057. doi: 10.1016\/j.celrep.2026.117057. Epub 2026 Mar 10. PMID: 41811849<\/p>\n\n\n\n

Dr. Prabhakar  Arumugam, a postdoctoral trainee in Professor Tammy Kielian\u2019s laboratory, has published a seminal study published in Cell Reports. Previous studies in Dr. Kielian\u2019s laboratory have documented that the anti-inflammatory properties of granulocytic myeloid derived suppressor cells (G-MDSCs) function to promote S. aureus <\/em>biofilm persistence.  This anti-inflammatory property is driven by staphylococcal metabolites in addition to cellular metabolic programs. The investigative team found that increasing mitochondrial abundance in G-MDSC\u2019s enhances their suppressive activity and increases bacterial burden in mouse models of infection. Importantly, their suppressive activity is reversed when macrophages with non-functional mitochondria are introduced into G-MDSC\u2019s.  These data document that G-MDSC\u2019s acquire mitochondria from macrophages that function to increase their suppressive activity during a S. aureus <\/em>biofilm infection.   <\/p>\n\n\n\n

Ihedioha OC<\/strong>, Sivakoses A, Marcarian HQ, Sajeev M, McMahon-Pratt D, Bothwell ALM. Platelet DKK1 promotes tolerogenic dendritic cells and non-healing responses in cutaneous leishmaniasis. iScience. 2026 Feb 26;29(4):115090. doi: 10.1016\/j.isci.2026.115090. eCollection 2026 Apr 17. PMID: 41858624<\/p>\n\n\n\n

Dr. Olivia Ihedioha, a postdoctoral trainee with Professor Alfred Bothwell, published a manuscript in iScience assessing the immunological response against Leishmania.  <\/em>Clinical manifestations following infection can result in wounds that heal to those that are chronic. It is unclear how the innate immune cells function to regulate this outcome. These studies found that platelet-derived DKK1 promotes tolerogenic dendritic cells and the non-healing responses found in cutaneous leishmaniasis.<\/p>\n\n\n\n

Auen T<\/strong>, Chen J, Shonka N, Cathcart S A. Case of IDH-Mutant Astrocytoma Harboring an IDH2 R172_H173delinsSN Variant. Neuropathology. 2026 Apr;46(2):e70048. doi: 10.1111\/neup.70048. PMID: 41736408au<\/p>\n\n\n\n

Dr. Thomas Auen and faculty colleagues in the department wrote a case of a patient with IDH-mutant astrocytoma. IDH-mutant gliomas typically harbor canonical mutations including IDH1<\/em> p.R132H mutation, followed by less common mutations involving IDH1<\/em> p.R132 or IDH2<\/em> p.R172 codons. A case is presented in a patient with an atypical molecular presentation including a previously uncharacterized IDH2 <\/em>mutation, ATRX expression yet lacking MGMT <\/em>promoter hypermethylation.  <\/p>\n\n\n\n

Bhola R, <\/strong>Sturgeon R, Singh RK. Cutting to the core: Proteases in the tumor-bone interface and metastatic progression. Biochim Biophys Acta Rev Cancer. 2026 Apr;1881(2):189567. doi: 10.1016\/j.bbcan.2026.189567. Epub 2026 Feb 27. PMID: 41765208<\/p>\n\n\n\n

Ridhi Bhola, a pre-doctoral trainee in Professor Singh\u2019s laboratory, has published a review in Biochimica et Biophysica ACTA-Reviews on Cancer investigating proteases at the tumor-bone interface including MMPs and cathepsins. These proteases contribute to multiple steps during metastasis and tumor growth including intravasion, immune evasion, extravasion, and bone destruction. Therefore, inhibitions of these proteases remain a viable therapeutic target. <\/p>\n\n\n\n

Love M,<\/strong> Dang RC, Xie J, Zhang P. The Rab5 effector Rabankyrin-5 mediates endosomal fusion and trafficking of human papillomavirus during early entry. Proc Natl Acad Sci U S A. 2026 Mar 3;123(9):e2524765123. doi: 10.1073\/pnas.2524765123. Epub 2026 Feb 26. PMID: 41746727<\/p>\n\n\n\n

Maddie Love, a pre-doctoral trainee in Dr. Zhang\u2019s laboratory, has published her initial first author manuscript in PNAS studying Human papillomavirus (HPV) endosomal fusion.  Fusion of HPV endosomal vesicles following endocytosis eventually leads to viral replication. However, fusion of these vesicles is not well understood. These studies led by Maddie found that Rabankyrin-5 is essential for fusion of HPV carrying endosomes following viral entry. In addition, Rabankyrin-5 also functions to promote virus movement via microtubules. By coupling endosomal fusion with directed transport, HPV ensures efficient trafficking within the endosomal system during early infection thus leading to efficient replication.<\/p>\n\n\n\n

Congratulations to:<\/p>\n\n\n\n