Browsing by Author "Burgin, Callie"

Now showing 1 - 6 of 6
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    Cutaneous collagenous vasculopathy: development after coronary artery bypass surgery
    (eScholarship Publishing, University of California, 2018) Rahnama-Moghadam, Sahand; Burgin, Callie; Gilbert, Juliana; Warren, Simon; Dermatology, School of Medicine
    Cutaneous collagenous vasculopathy (CCV) is a rare benign microangiopathy of the superficial dermal vessels. Clinically, it is characterized by widespread, asymptomatic development of cutaneous telangiectasia in the absence of systemic symptoms. Morphologically, it most resembles generalized essential telangiectasia and other telangiectatic syndromes such as telangiectasia macularis eruptiva perstans (TMEP), ataxia telangiectasia, and hereditary hemorrhagic telangiectasia. It is distinctive in its histology, showing characteristic dilated thick-walled blood vessels in the superficial dermis. The thickened walls of these superficial dermal blood vessels demonstrate reduplication of the basement membrane on PAS staining. We report a 63-year-old man with CCV with this condition for 20 years, starting in 1996. He was diagnosed in the past as having essential telangiectasia. The development of the telangectasias occurred after coronary artery bypass grafting, also performed in 1996. This case not only demonstrates the characteristic clinical and histologic findings, but also suggests a possible mechanism. Moreover, it illustrates that cases of generalized essential telangiectasia may in fact be CCV that are misclassified.
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    From Case Selection to Publication: A Comprehensive Guide to Dermatology Case
    (2024-11-01) Bari, Mariam; Watters, Jennifer; Rumancik, Brad; Burgin, Callie; Rahnama-Moghadam, Sahand
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    No Protractor, No Problem: A different angle on z-plasties
    (Wolters Kluwer, 2018-10) Burgin, Callie; Somani, Ally-Khan; Dermatology, School of Medicine
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    PAK1 inhibition reduces tumor size and extends the lifespan of mice in a genetically engineered mouse model of Neurofibromatosis Type 2 (NF2)
    (Oxford University Press, 2021) Hawley, Eric; Gehlhausen, Jeffrey; Karchugina, Sofiia; Chow, Hoi-Yee; Araiza-Olivera, Daniela; Radu, Maria; Smith, Abbi; Burks, Ciersten; Jiang, Li; Li, Xiaohong; Bessler, Waylan; Masters, Andrea; Edwards, Donna; Burgin, Callie; Jones, David; Yates, Charles; Clapp, D. Wade; Chernoff, Jonathan; Park, Su-Jung; Biochemistry and Molecular Biology, School of Medicine
    Neurofibromatosis Type II (NF2) is an autosomal dominant cancer predisposition syndrome in which germline haploinsufficiency at the NF2 gene confers a greatly increased propensity for tumor development arising from tissues of neural crest derived origin. NF2 encodes the tumor suppressor, Merlin, and its biochemical function is incompletely understood. One well-established function of Merlin is as a negative regulator of group A serine/threonine p21-activated kinases (PAKs). In these studies we explore the role of PAK1 and its closely related paralog, PAK2, both pharmacologically and genetically, in Merlin-deficient Schwann cells and in a genetically engineered mouse model (GEMM) that develops spontaneous vestibular and spinal schwannomas. We demonstrate that PAK1 and PAK2 are both hyper activated in Merlin-deficient murine schwannomas. In preclinical trials, a pan Group A PAK inhibitor, FRAX-1036, transiently reduced PAK1 and PAK2 phosphorylation in vitro, but had insignificant efficacy in vivo. NVS-PAK1-1, a PAK1 selective inhibitor, had a greater but still minimal effect on our GEMM phenotype. However, genetic ablation of Pak1 but not Pak2 reduced tumor formation in our NF2 GEMM. Moreover, germline genetic deletion of Pak1 was well tolerated, while conditional deletion of Pak2 in Schwann cells resulted in significant morbidity and mortality. These data support the further development of PAK1-specific small molecule inhibitors and the therapeutic targeting of PAK1 in vestibular schwannomas and argue against PAK1 and PAK2 existing as functionally redundant protein isoforms in Schwann cells.
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    Primary cutaneous peripheral T-cell lymphoma, not otherwise specified with mammalian target of rapamycin mutation: A novel finding for targeted treatment
    (Elsevier, 2020-12) De la Sancha, Carlo; Burgin, Callie; Warren, Simon; Hoffmann, Kristin; Davé, Utpal; Nassiri, Mehdi; Pathology and Laboratory Medicine, School of Medicine
    Primary cutaneous peripheral T-cell lymphoma, not otherwise specified (pcPTCL-NOS) is a rare, progressive, and often fatal disease with no specific treatment regimen that presents as rapidly enlarging plaques or nodules. Here, we present a case of progressive pcPTCL-NOS with mammalian target of rapamycin (mTOR) mutation and variable T-cell antigen expression. mTOR mutation in pcPTCL-NOS may represent a new therapeutic target.
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    Repair of a Large Sternal Notch Defect
    (Wolters Kluwer, 2019-09) Kandula, Prasanthi; Burgin, Callie; Somani, Ally-Khan; Dermatology, School of Medicine