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Paul Meyer
- Assistant Professor, Pathology - (Clinical Scholar Track)
Contact
- (520) 792-1450
- AHSC, Rm. 5205
- paulnmeyer@arizona.edu
Degrees
- M.D.
- Pennsylvania State University College of Medicine, Hershey, Pennsylvania, United States
- Ph.D. Cell and Molecular Biology
- Pennsylvania State University College of Medicine, Hershey, Pennsylvania, United States
- Murine tissue distribution of an antigen recognized by an antibody against the hemochromatosis gene product, HFE, and the role of HFE in intestinal immunology and diabetes.
Work Experience
- SAVAHCS (2012 - Ongoing)
- Skagit Pathology (2010 - 2012)
Awards
- Veterans Health Affairs LEAN Healthcare
- Department of Veterans Affairs, Spring 2014
- Excellence in Laboratory Management
- Loyola University Medical Center, Spring 2006
- Chrysalis Grant
- American Academy of Allergy Asthma and Immunology (AAAA1), Spring 2000
Licensure & Certification
- Board Certified (2008)
- Board Certified (2009)
Interests
No activities entered.
Courses
No activities entered.
Scholarly Contributions
Journals/Publications
- Caponetti, G. C., Dave, B. J., Perry, A. M., Smith, L. M., Jain, S., Meyer, P. N., Bast, M., Bierman, P. J., Bociek, R. G., Vose, J. M., Armitage, J. O., Aoun, P., Fu, K., Greiner, T. C., Chan, W. C., Sanger, W. G., & Weisenburger, D. D. (2015). Isolated MYC cytogenetic abnormalities in diffuse large B-cell lymphoma do not predict an adverse clinical outcome. Leukemia & lymphoma, 56(11), 3082-9.More infoIn this study, we investigated the significance of MYC, BCL2 and BCL6 gene abnormalities in a cohort of 205 diffuse large B-cell lymphoma (DLBCL) patients studied by conventional and/or fluorescence in situ hybridization cytogenetic analysis. Combining these methods, 172 cases (84%) were classified as MYC-, 17 (8%) were MYC+/BCL2-/BCL6-, and 16 (8%) were double/triple-hit lymphomas (i.e. MYC+/BCL2+, MYC+/BCL6+, or MYC+/BCL2+/BCL6+). We found a significant difference in event-free survival (EFS) among the three groups (p = 0.02), with the double/triple-hit group having the worst EFS. Patients who were MYC+, but BCL2- and BCL6-, had the best EFS. We conclude that patients with MYC+ DLBCL, but without BCL2 or BCL6 abnormalities, do not have a worse outcome when compared to those who are MYC-. However, patients with double/triple-hit DLBCL have a very poor outcome and should be treated with aggressive or novel therapies.
- Taverna, J. A., Babiker, H. M., Yun, S., Bishop, M. C., Lau-Braunhut, S., Meyer, P. N., & Enzler, T. (2014). The great masquerader of malignancy: chronic intestinal pseudo-obstruction. Biomarker research, 2(1), 23.More infoParaneoplastic syndromes can precede the initial manifestation and diagnosis of cancer. Paraneoplastic syndromes are a heterogeneous group of disorders caused by mechanisms other than the local presence of tumor cells. These phenomena are mediated by humoral factors secreted by tumor cells or by tumor mediated immune responses. Among paraneoplastic syndromes, chronic intestinal pseudo-obstruction (CIPO) is rare and represents a particularly difficult clinical challenge. Paraneoplastic CIPO is a highly morbid syndrome characterized by impaired gastrointestinal propulsion with symptoms and signs of mechanical bowel obstruction. Clinical outcomes of paraneoplastic CIPO are often deleterious. The current standard of care for the management of CIPO includes supportive treatment with promotility and anti-secretory agents. However, the majority of patients with CIPO eventually require the resection of the non-functioning gut segment. Here, we present a 62-year-old patient with anti-Hu antibody associated paraneoplastic CIPO and underlying small cell lung cancer who underwent treatment with cisplatin and etoposide. Herein, we discuss diagnosis, prognosis, proposed mechanisms, treatment options, and future potential therapeutic strategies of paraneoplastic CIPO.
- Johnson, N. A., Slack, G. W., Savage, K. J., Connors, J. M., Ben-Neriah, S., Rogic, S., Scott, D. W., Tan, K. L., Steidl, C., Sehn, L. H., Chan, W. C., Iqbal, J., Meyer, P. N., Lenz, G., Wright, G., Rimsza, L. M., Valentino, C., Brunhoeber, P., Grogan, T. M., , Braziel, R. M., et al. (2012). Concurrent expression of MYC and BCL2 in diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 30(28), 3452-9.More infoDiffuse large B-cell lymphoma (DLBCL) is curable in 60% of patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP). MYC translocations, with or without BCL2 translocations, have been associated with inferior survival in DLBCL. We investigated whether expression of MYC protein, with or without BCL2 protein expression, could risk-stratify patients at diagnosis.
- Perry, A. M., Cardesa-Salzmann, T. M., Meyer, P. N., Colomo, L., Smith, L. M., Fu, K., Greiner, T. C., Delabie, J., Gascoyne, R. D., Rimsza, L., Jaffe, E. S., Ott, G., Rosenwald, A., Braziel, R. M., Tubbs, R., Cook, J. R., Staudt, L. M., Connors, J. M., Sehn, L. H., , Vose, J. M., et al. (2012). A new biologic prognostic model based on immunohistochemistry predicts survival in patients with diffuse large B-cell lymphoma. Blood, 120(11), 2290-6.More infoBiologic factors that predict the survival of patients with a diffuse large B-cell lymphoma, such as cell of origin and stromal signatures, have been discovered by gene expression profiling. We attempted to simulate these gene expression profiling findings and create a new biologic prognostic model based on immunohistochemistry. We studied 199 patients (125 in the training set, 74 in the validation set) with de novo diffuse large B-cell lymphoma treated with rituximab and CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) or CHOP-like therapies, and immunohistochemical stains were performed on paraffin-embedded tissue microarrays. In the model, 1 point was awarded for each adverse prognostic factor: nongerminal center B cell-like subtype, SPARC (secreted protein, acidic, and rich in cysteine) < 5%, and microvascular density quartile 4. The model using these 3 biologic markers was highly predictive of overall survival and event-free survival in multivariate analysis after adjusting for the International Prognostic Index in both the training and validation sets. This new model delineates 2 groups of patients, 1 with a low biologic score (0-1) and good survival and the other with a high score (2-3) and poor survival. This new biologic prognostic model could be used with the International Prognostic Index to stratify patients for novel or risk-adapted therapies.
- Iqbal, J., Meyer, P. N., Smith, L. M., Johnson, N. A., Vose, J. M., Greiner, T. C., Connors, J. M., Staudt, L. M., Rimsza, L., Jaffe, E., Rosenwald, A., Ott, G., Delabie, J., Campo, E., Braziel, R. M., Cook, J. R., Tubbs, R. R., Gascoyne, R. D., Armitage, J. O., , Weisenburger, D. D., et al. (2011). BCL2 predicts survival in germinal center B-cell-like diffuse large B-cell lymphoma treated with CHOP-like therapy and rituximab. Clinical cancer research : an official journal of the American Association for Cancer Research, 17(24), 7785-95.More infoWe have previously shown the prognostic significance of BCL2 expression in the activated B-cell-like diffuse large B-cell lymphoma (ABC-DLBCL) patients treated with cyclophosphamide-Adriamycin-vincristine-prednisone (CHOP) or CHOP-like therapy. However, after the inclusion of rituximab (R) in the CHOP regimen, several conflicting observations about the prognostic value of BCL2 expression have been reported.
- Meyer, P. N., Fu, K., Greiner, T. C., Smith, L. M., Delabie, J., Gascoyne, R. D., Ott, G., Rosenwald, A., Braziel, R. M., Campo, E., Vose, J. M., Lenz, G., Staudt, L. M., Chan, W. C., & Weisenburger, D. D. (2011). Immunohistochemical methods for predicting cell of origin and survival in patients with diffuse large B-cell lymphoma treated with rituximab. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 29(2), 200-7.More infoPatients with diffuse large B-cell lymphoma (DLBCL) can be divided into prognostic groups based on the cell of origin of the tumor as determined by microarray analysis. Various immunohistochemical algorithms have been developed to replicate these microarray results and/or stratify patients according to survival. This study compares some of those algorithms and also proposes some modifications.
- Meyer, P. N., Fu, K., Greiner, T., Smith, L., Delabie, J., Gascoyne, R., Ott, G., Rosenwald, A., Braziel, R., Campo, E., Vose, J., Lenz, G., Staudt, L., Chan, W., & Weisenburger, D. D. (2011). The stromal cell marker SPARC predicts for survival in patients with diffuse large B-cell lymphoma treated with rituximab. American journal of clinical pathology, 135(1), 54-61.More infoThe cellular composition of the tumor microenvironment may affect survival in diffuse large B-cell lymphoma (DLBCL). We performed immunostains for 2 stromal cell markers, CD68 and SPARC (secreted protein, acidic and rich in cysteine), in 262 patients with DLBCL treated with rituximab and cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or CHOP-like therapies. Patients with any SPARC+ cells in the microenvironment had a significantly longer overall survival, and patients with high SPARC positivity in the microenvironment also had a significantly longer event-free survival. Survival differences were mainly due to the prognostic effect of SPARC+ cells in activated B-cell (ABC)-type DLBCL, with no effect found in the germinal center B-cell-type DLBCL. Of clinical features examined, only the number of extranodal sites was significantly associated with SPARC expression. Multivariate analysis revealed that SPARC expression predicted patient survival independent of the International Prognostic Index or tumor cell of origin. SPARC expression in the microenvironment of DLBCL can be used for prognostic purposes, determining a subgroup of patients with ABC DLBCL who have significantly longer survival. More aggressive chemotherapy protocols should be considered for patients with ABC DLBCL without SPARC+ stromal cells. CD68 expression by cells in the microenvironment did not predict survival.
- Meyer, P. (2010). Diffuse large B-cell lymphoma with both CD5 and Cyclin D1 expression -- A case report and review of the literature. Journal of Hematopathology, 3(4), 145-148. doi:10.1007/s12308-010-0072-6
- Meyer, P. N., Cao, Y., Jacobson, K., Krausz, T., Flanigan, R. C., & Picken, M. M. (2008). Chromosome 1 analysis in chromophobe renal cell carcinomas with tissue microarray (TMA)-facilitated fluorescence in situ hybridization (FISH) demonstrates loss of 1p/1 which is also present in renal oncocytomas. Diagnostic molecular pathology : the American journal of surgical pathology, part B, 17(3), 141-4.More infoMorphologic overlap between chromophobe renal cell carcinoma (ChRCC) and renal oncocytomas (RO) has been widely recognized. Whether these tumors are genetically related and represent a spectrum of benign to malignant tumor progression remains an open question. We previously showed by conventional cytogenetics and fluorescent in situ hybridization (FISH) that the most common chromosomal abnormality in RO is loss of chromosome 1 or 1p. In this study, we evaluated chromosome 1 in ChRCC using the same set of FISH probes. Twenty-one ChRCCs from 13 men and 8 women were studied. Formalin-fixed, paraffin-embedded tissue blocks were used to construct tissue microarrays. A subtelomeric 1p36.3 probe was used in tandem with 1q25 probes for FISH studies. The patients ranged in age from 34 to 82 years (mean 62.8 y, median 61 y). FISH analysis showed an abnormal chromosome 1 in 20/21 (95%) ChRCCs as follows: 18 tumors (85%) had loss of entire chromosome 1, 2 tumors (10%) had loss of 1p36.3 only, and 1 tumor (5%) was apparently diploid for chromosome 1. In this study, 95% of ChRCCs showed abnormality of chromosome 1 by FISH. The progression of chromosome 1 abnormalities, from diploid to loss of 1p to loss of entire chromosome, is also present in oncocytomas. These results provide further evidence to support a genetic similarity between chromophobe carcinoma and oncocytoma. Whether abnormalities of chromosome 1 are associated with RO tumorigenesis or its progression to carcinoma requires further studies.
- Meyer, P. N., Roychowdhury, S., Kini, A. R., & Alkan, S. (2008). HSP90 inhibitor 17AAG causes apoptosis in ATRA-resistant acute promyelocytic leukemia cells. Leukemia research, 32(1), 143-9.More infoThe effects of a novel heat shock protein inhibitor, 17AAG, on established APL cell lines (NB4 and R1) were analyzed. 17AAG induces apoptosis in APL cell lines both sensitive (NB4) and resistant (R1) to ATRA after 72 h of incubation. Apoptosis occurs by a mechanism different than ATRA-mediated response, as the cells do not undergo differentiation before apoptosis. Analysis of bax and bcl-2 shows that pro-apoptotic (bax) and anti-apoptotic (bcl-2) proteins are decreased in expression after incubation with 17AAG. We believe this data supports potential clinical use of agents that target HSP90 in APL patients failing conventional therapy.
- Meyer, P. (2007). Xp11.2 Translocation Renal Cell Carcinoma With Very Aggressive Course in Five Adults. American Journal of Clinical Pathology, 128, 70-79. doi:http://dx.doi.org/10.1309/LR5G1VMXPY3G0CUK
- Meyer, P. N., Al-Masri, H., & Alkan, S. (2007). Osseous metaplasia in diffuse large B-cell lymphoma of the kidney. AMERICAN JOURNAL OF HEMATOLOGY, 82(4), 321-324.
- Ozpuyan, F., Meyer, P., Ni, H., Al-Masri, H., & Alkan, S. (2007). Bortezomib induces apoptosis in T-cell prolymphocytic leukemia (T-PLL). LEUKEMIA & LYMPHOMA, 48(11), 2247-2250.
- Chorney, M. J., Yoshida, Y., Meyer, P. N., Yoshida, M., & Gerhard, G. S. (2003). The enigmatic role of the hemochromatosis protein (HFE) in iron absorption. TRENDS IN MOLECULAR MEDICINE, 9(3), 118-125.
- Meyer, P. N., Gerhard, G. S., Yoshida, Y., Yoshida, M., Chorney, K. A., Beard, J., Kauffman, E. J., Weiss, G., & Chorney, M. J. (2002). Hemochromatosis protein (HFE) and tumor necrosis factor receptor 2 (TNFR2) influence tissue iron levels: Elements of a common gut pathway?. BLOOD CELLS MOLECULES AND DISEASES, 29(3), 274-285.
- Meyer, P. N., Wilmes-Riesenberg, M., Stathopoulos, C., & Curtiss, R. (1998). Virulence of a Salmonella typhimurium OmpD mutant. INFECTION AND IMMUNITY, 66(1), 387-390.