Brett Morris, MD, PhD

Radiation Oncology Resident

Department of Human Oncology

Education

Intern, Santa Barbara Cottage Hospital Program, Medicine (2020)

MD/PhD, University of Wisconsin School of Medicine and Public Health , (2019)

BA, Saint Olaf College, (2011)

  • Local Graft Irradiation for Acute, Medication Refractory Transplant Rejection of a Pancreas Alone Graft: A Case Report Advances in radiation oncology
    Morris BA, Alfson A, Davies G, Kaufman D, Bradley KA
    2022 Dec 30;8(2):101168. doi: 10.1016/j.adro.2022.101168. eCollection 2023 Mar-Apr.
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      PMID:36704191 | PMC:PMC9871068 | DOI:10.1016/j.adro.2022.101168


      View details for PubMedID 36704191
  • Late Radiation Related Brachial Plexopathy After Pulsed Reduced Dose Rate Reirradiation of an Axillary Breast Cancer Recurrence Practical radiation oncology
    Morris BA, Burr AR, Anderson BM, Howard SP
    2021 Sep-Oct;11(5):319-322. doi: 10.1016/j.prro.2021.06.003. Epub 2021 Jun 24.
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      Radiation induced brachial plexopathy (RIBP) is an unfortunate complication of radiation involving the axilla and supraclavicular fossa. This case report highlights development of RIBP in a patient 15 years after initial radiation and 11 years after pulsed low dose rate (PRDR) re-irradiation for recurrent disease. PRDR is a radiation technique believed to lower normal tissue toxicity due to improved sublethal intrafraction damage repair of these tissues at low radiation dose rates with good reported long term locoregional control in the re-irradiation setting. However, RIBP, as seen in this patient, is a devastating side effect of high dose radiation to this region, with no effective treatment options outside of symptom management and control. In this case, the patient has remained disease free following her recurrence but has had continued RIBP with minimal improvement using pentoxyfilline for management.

      PMID:34171539 | DOI:10.1016/j.prro.2021.06.003


      View details for PubMedID 34171539
  • Collagen Matrix Density Drives the Metabolic Shift in Breast Cancer Cells EBioMedicine
    Morris BA, Burkel B, Ponik SM, Fan J, Condeelis JS, Aguirre-Ghiso JA, Castracane J, Denu JM, Keely PJ
    2016 Nov;13:146-156. doi: 10.1016/j.ebiom.2016.10.012. Epub 2016 Oct 8.
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      Increased breast density attributed to collagen I deposition is associated with a 4-6 fold increased risk of developing breast cancer. Here, we assessed cellular metabolic reprogramming of mammary carcinoma cells in response to increased collagen matrix density using an in vitro 3D model. Our initial observations demonstrated changes in functional metabolism in both normal mammary epithelial cells and mammary carcinoma cells in response to changes in matrix density. Further, mammary carcinoma cells grown in high density collagen matrices displayed decreased oxygen consumption and glucose metabolism via the tricarboxylic acid (TCA) cycle compared to cells cultured in low density matrices. Despite decreased glucose entry into the TCA cycle, levels of glucose uptake, cell viability, and ROS were not different between high and low density matrices. Interestingly, under high density conditions the contribution of glutamine as a fuel source to drive the TCA cycle was significantly enhanced. These alterations in functional metabolism mirrored significant changes in the expression of metabolic genes involved in glycolysis, oxidative phosphorylation, and the serine synthesis pathway. This study highlights the broad importance of the collagen microenvironment to cellular expression profiles, and shows that changes in density of the collagen microenvironment can modulate metabolic shifts of cancer cells.

      PMID:27743905 | PMC:PMC5264313 | DOI:10.1016/j.ebiom.2016.10.012


      View details for PubMedID 27743905
  • Preparation of 3D Collagen Gels and Microchannels for the Study of 3D Interactions In Vivo Journal of visualized experiments : JoVE
    Burkel B, Morris BA, Ponik SM, Riching KM, Eliceiri KW, Keely PJ
    2016 May 9;(111):53989. doi: 10.3791/53989.
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      Historically, most cellular processes have been studied in only 2 dimensions. While these studies have been informative about general cell signaling mechanisms, they neglect important cellular cues received from the structural and mechanical properties of the local microenvironment and extracellular matrix (ECM). To understand how cells interact within a physiological ECM, it is important to study them in the context of 3 dimensional assays. Cell migration, cell differentiation, and cell proliferation are only a few processes that have been shown to be impacted by local changes in the mechanical properties of a 3-dimensional ECM. Collagen I, a core fibrillar component of the ECM, is more than a simple structural element of a tissue. Under normal conditions, mechanical cues from the collagen network direct morphogenesis and maintain cellular structures. In diseased microenvironments, such as the tumor microenvironment, the collagen network is often dramatically remodeled, demonstrating altered composition, enhanced deposition and altered fiber organization. In breast cancer, the degree of fiber alignment is important, as an increase in aligned fibers perpendicular to the tumor boundary has been correlated to poorer patient prognosis(1). Aligned collagen matrices result in increased dissemination of tumor cells via persistent migration(2,3). The following is a simple protocol for embedding cells within a 3-dimensional, fibrillar collagen hydrogel. This protocol is readily adaptable to many platforms, and can reproducibly generate both aligned and random collagen matrices for investigation of cell migration, cell division, and other cellular processes in a tunable, 3-dimensional, physiological microenvironment.

      PMID:27213771 | PMC:PMC4942088 | DOI:10.3791/53989


      View details for PubMedID 27213771
  • Increased tumor response to neoadjuvant therapy among rectal cancer patients taking angiotensin-converting enzyme inhibitors or angiotensin receptor blockers Cancer
    Morris ZS, Saha S, Magnuson WJ, Morris BA, Borkenhagen JF, Ching A, Hirose G, McMurry V, Francis DM, Harari PM, Chappell R, Tsuji S, Ritter MA
    2016 Aug 15;122(16):2487-95. doi: 10.1002/cncr.30079. Epub 2016 May 20.
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      BACKGROUND: Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are commonly used antihypertensive medications that have been reported to affect aberrant angiogenesis and the dysregulated inflammatory response. Because of such mechanisms, it was hypothesized that these medications might affect the tumor response to neoadjuvant radiation in patients with rectal cancer.

      METHODS: One hundred fifteen patients who were treated with neoadjuvant radiation at the University of Wisconsin (UW) between 1999 and 2012 were identified. Univariate analyses were performed with anonymized patient data. In a second independent data set, 186 patients with rectal cancer who were treated with neoadjuvant radiation at the Queen's Medical Center of the University of Hawaii (UH) between 1995 and 2010 were identified. These data were independently analyzed as before. Multivariate analyses were performed with aggregate data.

      RESULTS: Among patients taking ACEIs/ARBs in the UW data set, a significant 3-fold increase in the rate of pathologic complete response (pCR) to neoadjuvant therapy (52% vs 17%, P = .001) was observed. This finding was confirmed in the UH data set, in which a significant 2-fold-increased pCR rate (24% vs 12%, P = .03) was observed. Identified patient and treatment characteristics were otherwise balanced between patients taking and not taking ACEIs/ARBs. No significant effect was observed on pCR rates with other medications, including statins, metformin, and aspirin. Multivariate analyses of aggregate data identified ACEI/ARB use as a strong predictor of pCR (odds ratio, 4.02; 95% confidence interval, 2.06-7.82; P < .001).

      CONCLUSIONS: The incidental use of ACEIs/ARBs among patients with rectal cancer is associated with a significantly increased rate of pCR after neoadjuvant treatment. Cancer 2016;122:2487-95. © 2016 American Cancer Society.

      PMID:27203227 | PMC:PMC4998053 | DOI:10.1002/cncr.30079


      View details for PubMedID 27203227
  • Impact of a Contralateral Tumor Nodule on Survival in Non-Small-Cell Lung Cancer Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
    Morris ZS, Cannon DM, Morris BA, Bentzen SM, Kozak KR
    2015 Nov;10(11):1608-15. doi: 10.1097/JTO.0000000000000655.
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      INTRODUCTION: Contralateral lung tumors in non-small-cell lung cancer (NSCLC) are classified as stage M1a yet may represent hematogenous metastases or synchronous primary tumors. The impact of these tumors on overall survival (OS) is poorly understood. Here, we aim to determine whether NSCLC patients with M1a disease due only to a contralateral tumor nodule exhibit a favorable prognosis relative to other M1a or M1b patients.

      METHODS: Retrospective evaluation of the impact of contralateral tumor nodules on OS in NSCLC stratified by primary tumor size and N stage attained from Surveillance, Epidemiology, and End Results database.

      RESULTS: Of 173,640 patients, 5161 M1a-contra patients were identified. Median and 3-year OS for these patients exceeded that of patients with M1b (p < 0.0001) or other M1a disease (p < 0.0001). Primary tumor size and N stage were strongly associated with OS in M1a-contra patients. Three-year OS demonstrated a delayed convergence between M1a-contra and other M1a patients with primary tumors greater than or equal to 3 cm or mediastinal lymph node involvement. Proportional hazard modeling indicated that T1-2N0-1M1a-contra patients exhibit OS not significantly different (p = 0.258) from that predicted with comparable T and N stage disease plus a second early-stage primary.

      CONCLUSIONS: Contralateral tumors in NSCLC carry a more favorable prognosis than other M1a or M1b disease. Primary tumor size and N stage may help distinguish M1a-contra patients with hematogenous metastasis from those with a synchronous, second primary.

      PMID:26317917 | PMC:PMC4636460 | DOI:10.1097/JTO.0000000000000655


      View details for PubMedID 26317917

Contact Information

Brett A Morris, MD

600 Highland Avenue ,
Madison, WI 53792
Email