| Email |
sbagnas1@jhmi.edu |
| Phone |
(410) 502-0812 |
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Serena M. Bagnasco, M.D.
Primary Appointment in Pathology
My research interests are in the field of renal physiology and pathophysiology, and in the mechanisms of adaptation of renal cells to the environment of the kidney medulla, characterized by high concentration of salt and urea.
We have defined the genomic organization of the gene that encodes the major renal urea transporters, which are essential for the process of urine concentration in the mammalian kidney. We are currently studying the pathways regulating expression and function of these transporters in the kidney and at extrarenal sites.
Publications
Nakayama, Y., T. Peng, J.M. Sands, S.M. Bagnasco. The TonE/TonEBP pathway mediates tonicity-responsive regulation of UT-A urea transporter expression. Journal of Biological Chemistry, 275: 38275-38280, 2000.
Bagnasco, S.M., Tao Peng, M.G. Janech, A. Karakashian, J.M. Sands. Cloning and characterization of the human urea transporter UT-A1, and mapping of the human Slc14a2 gene. American Journal of Physiology- Renal, 281: F400-406, 2001.
Peng, T., J.M.Sands, S.M. Bagnasco. Glucocorticoids inhibit transcription and expression of the UT-A urea transporter gene. American Journal of Physiology- Renal, 282:F859-F865, 2002.
Bagnasco, S.M.. Gene structure of urea transporters. American Journal of Physiology- Renal Physiology, F3-F10, 2003.
Inoue, H., Jackson, S.D., Vikulina,T., Klein, J.D., Tomita, K., Bagnasco, S.M.. Identification and characterization of a Kidd antigen/UT-B urea transporter expressed in human colon. American Journal of Physiology-Cell Physiology, 287:C30-C35, 2004. |
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David M. Berman, M.D., Ph.D.
Primary Appointment in Pathology; Secondary Appointments in Oncology, Urology
Member, Graduate Program in Cellular and Molecular Medicine and Pathobiology
My laboratory focuses on the roles of embryonic patterning pathways in the development and pathophsyiology of urogenital organs. We are particularly interested in the hypothesis that chronic injury leads to activation of these pathways in an effort to regenerate damaged tissue, and that cancers arise in repairative cells that become unable to return to the quiescent state. To study how particular signal transduction pathways contribute to these processes, we study experimental models of prostate and bladder regeneration and carcinogenesis and relate our findings to studies of human tissue.
Publications
He X, Marchionni L, Hansel DE, Yu W, Sood A, Yang J, Parmigiani G, Matsui W, and Berman DM Differentiation of a highly tumorigenic basal cell compartment in urothelial carcinoma. Stem Cells (Advance Online Publication). April 9, 2009
Schaeffer EM, Marchionni L, Huang L, Simons B, Blackman A, Yu W, Parmigiani G, and Berman DM. Androgen induced programs for prostate epithelial growth and invasion arise in embryogenesis and are reactivated in cancer. Oncogene. 2008 27:7180.
Kleeberger W, Bova GS, Nielsen ME, Herawi M, Chuang AY, Epstein JI, Berman DM (2007). Roles for the stem cell associated intermediate filament nestin in prostate cancer migration and metastasis. Cancer Research 2007; 67:9199-206
Beachy PA, Karhadkar SS, Berman DM. (2004) Tissue repair and stem cell renewal in carcinogenesis. Nature. 432:324-331.
Berman DM, Desai N, Wang X, Karhadkar SS, Reynon M, Abate-Shen C, Beachy PA, and Shen MM (2004. Roles for Hedgehog signaling in androgen production and prostate ductal morphogenesis. Developmental Biology. 267:387398
Berman DM, Karhadkar SS, Maitra AM, Montes de Oca R, Gerstenblith MR, Briggs K, Parker AR, Shimada Y, Eshleman JR, Watkins DN, and Beachy PA (2003) Widespread requirement for Hedgehog ligand stimulation in growth of digestive tract tumours. Nature. 425:846-851.
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G. Steven Bova, M.D.
Primary Appointment in Pathology; Secondary Appointments in the Institute of Genetic Medicine, Health Sciences Informatics, Oncology, and Urology.
Our laboratory is working to develop better understanding and treatment of metastatic prostate cancer and cancer in general. We are studying the molecular and clinical basis of cancer in a series of men with metastatic prostate cancer in our laboratory and in collaboration with a number of other laboratories. We are also working to develop novel community and software-based methods to improve cancer research in general. We named our laboratory "PELICAN", which stands for "Project to Eliminate Lethal Cancer". PELICAN seeks to create an integrated clinical-genomic database of lethal prostate cancer that can be used to form a badly needed reference point for the wide spectrum of animal model and cell-line based studies in prostate and other cancers. Our laboratory expertise combines clinical and anatomic pathology methods, genomic analysis techniques and database curation and integration methods to achieve its mission. What makes our lab somewhat unique is that we are working both on improving the fundamental methods used to do cancer research, and to actually use these tools to do research in metastatic prostate cancer. Our April 2009 Nature Medicine paper we believe is a good example of how novel techniques and methods in cancer research and genomics can help bring cancer research into a more fully rational context.
Publications
Liu W, Laitinen S, Khan S, Vihinen M, Kowalski J, Yu G, Chen L, Ewing CM, Eisenberger MA, Carducci MA, Nelson WG, Yegnasubramanian S, Luo J, Wang Y, Xu J, Isaacs WB, Visakorpi T, Bova GS. Copy Number Analysis Indicates Monoclonal Origin of Lethal Metastatic Prostate Cancer. Nature Medicine (published online April 12, 2009).
Hu R, Dunn TA, Wei S, Isharwal S, Veltri RW, Humphreys E, Han M, Partin AW, Vessella RL, Isaacs WB, Bova GS, Luo J. Ligand-Independent Androgen Receptor Variants Derived from Splicing of Cryptic Exons Signify Hormone-Refractory Prostate Cancer. Cancer Res 2009; 69(1):16-22.
Parsons JK, Saria EA, Nakayama M, Vessella RL, Sawyers CL, Isaacs WB, Faith DA, Bova GS, Samathanam CA, Mitchell R, De Marzo AM. Comprehensive mutational analysis and mRNA isoform quantification of TP63 in normal and neoplastic human prostate cells. Prostate 2009. Epub ahead of print
Yegnasubramanian S, Haffner MC, Zhang Y, Gurel B, Cornish TC, Wu Z, Irizarry RA, Morgan J, Hicks J, DeWeese TL, Isaacs WB, Bova GS, De Marzo AM, Nelson WG. DNA hypomethylation arises later in prostate cancer progression than CpG island hypermethylation and contributes to metastatic tumor heterogeneity. Cancer Res 2008; 68(21):8954-8967.
Deutsch EW, Ball CA, Berman JJ, Bova GS, Brazma A, Bumgarner RE, Campbell D, Causton HC, Christiansen J, Davidson DR, Goo YA, Grimmond S, Henrich T, Herrmann BG, Johnson MH, Korb M, Mills JC, Oudes AJ, Parkinson HE, Pascal LE, Pollet N, Quackenbush J, Ramialison M, Ringwald M, Sansone SA, Sherlock G, Stoeckert CJ, Swedlow J, Taylor RC, Walashek L, Warford A, Wilkinson DG, Zhou Y, Zon LI, Liu AY, True LD Minimum Information Specification For In Situ Hybridization and Immunohistochemistry Experiments (MISFISHIE). Nature Biotechnology 2008 26(3): 305-12.
Kleeberger W, Bova GS, Nielsen ME, Herawi M, Chuang AY, Epstein JI, Berman DM Roles for the stem cell associated intermediate filament Nestin in prostate cancer migration and metastasis. Cancer Research. 2007 Oct 1;67(19):199-206. |
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Angelo M. DeMarzo, M.D., Ph.D.
Primary Appointment in Pathology; Secondary Appointments in Oncology and Urology
Member; Graduate Program in Pathobiology
Our basic research is focused on understanding the paradoxical organ selectivity of cancer. Specifically, why is the prostate so commonly targeted for cancer formation?
We have 4 main areas of overlapping interest. - We study gene expression alterations involved in the molecular regulation of the growth of the normal prostate and how this regulation is altered in
neoplastic and pre-neoplastic states.
- The role of inflammation, atrophy and dietary factors in prostate carcinogenesis.
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The role of telomere shortening as a potential mechanism for the generation of genetic instability.
- Using tissue microarrays
we examine the clinical significance of various biomarkers in prostate cancer.
We make extensive use of immunohistochemistry, immunofluorescence, and in situ hybridization. We also employ laser capture microdissection for molecular analysis of individual tissue and cell types.
We collaborate closely with several others in the Brady Urological Research Institute and The Oncology Center.
Publications
Nakayama M, Bennett CJ, Hicks JL, Epstein JI, Platz EA, Nelson WG, and DeMarzo AM. Hypermethylation of the human glutathione S-transferase-pi gene(GSTP1) CpG island is present in a subset of proliferative inflammatory atrophy lesions but not in normal or hyperplastic epithelium of the prostate: a detailed study using laser-capture microdissection. Am J Pathol.,163:923-933, 2003.
Nelson, W.G., De Marzo, A.M., and Isaacs, W.B. Mechanisms of disease. The molecular pathogenesis of prostate cancer: a new role for inflammation? New Eng. J. Med., 349:366-81, 2003.
Meeker, A.K., Hicks, J.L., Platz, E.A., March, G.E., Bennett, C.J.,Delannoy, M.J., De Marzo, A.M. Telomere shortening is an early somatic DNA alteration in human prostate tumorigenesis. Cancer Res., 62:6405-9, 2002.
De Marzo, A.M., Nelson, W.G., Isaacs, W.B., and Epstein, J.I. Pathological and molecular aspects of prostate cancer. Lancet, 361:955-64, 2003.
Meeker, A.K., Hicks, J.L., Iacobuzio-Donahue, C.A., Montgomery, E.A., Westra, W.H., Chan, T.Y., Ronnett, B.M., and De Marzo, A.M. Telomere length abnormalities occur early in the initiation of epithelial carcinogenesis.
Clin Cancer Res., 10:3317-26. 2004 |
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| Email |
jjarow@jhmi.edu |
| Phone |
(410) 955-3617 |
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Jonathan Jarow, M.D.
Primary Appointment in Urology; Secondary Appointments in Pathology, Radiology, Radiological Science and Biochemistry (BSPH)
Our laboratory focuses upon the underpinnings of male infertility. Research projects in our center grant include hormonal control of spermatogenesis and germ cell apoptosis, Sertoli cell-germ cell interactions, and stage-specific androgen receptor activity within the testis. These studies are designed to take basic research to the patient bedside in an effort to develop applicable therapeutic interventions.
Publications
Coviello AD, Bremner WJ, Matsumoto AM, Herbst KL, Amory JK, Anawalt BD, Yan X, Brown TR, Wright WW, Zirkin BR, Jarow JP: Intratesticular Testosterone Concentrations Comparable With Serum Levels Are Not Sufficient to Maintain Normal Sperm Production in Men Receiving a Hormonal Contraceptive Regimen. J Androl. 2004;25(6):931-938.
Sigman M, Jarow JP. Testicular hypotrophy is associated with reduced sperm counts in infertile men with variococeles. J Urology 158:605-607,1997.
Jarow JP, Chen H, Rosner W, Trentacoste S, Zirkin BR: Assessment of the androgen environment within the human testis: Minimally invasive method to obtain intratesticular fluid. J Andrology 22:640-645, 2001.
Zhao M, Baker SD, Yan X, Zhao Y, Wright WW, Zirkin BR and Jarow JP: Simultaneous determination of steroid composition of human testicular fluid using liquid chromatography tandem mass spectrometry. Steroids In Press. |
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| Email |
tlotan1@jhmi.edu |
| Phone |
(410) 434-1003 |
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Tamara Lotan, M.D.
Primary Appointment in Pathology
My laboratory focuses on the cellular mechanisms controlling prostate epithelial cell migration in cancer and development. We are currently developing three-dimensional culture systems that model in vivo prostate epithelial architecture and using these systems to study the signaling pathways and cellular mechanisms that regulate and drive prostate epithelial cell movements. We are particularly interested in utilizing state-of-the-art time lapse microscopic imaging to capture detailed cell movements during directed epithelial migration, both under normal conditions and in various mouse knock-out models that perturb specific signaling pathways of interest. Once we understand the cellular mechanisms and signaling pathways that drive normal prostatic epithelial migration, we will gain insight into how cancer cells adapt and dysregulate these same processes during Gleason grade progression and metastasis.
In the area of clinical research, I am particularly interested in identifying and evaluating immunohistochemical biomarkers and genetic aberrations that characterize unusual subtypes of prostatic adenocarcinoma, such as ductal adenocarcinoma and prostatic small cell carcinoma. Additionally, I am interested in the cellular mechanisms that regulate micropapillary carcinoma tumor architecture and metastatic propensity.
Publications
Lotan TL, Lyon M, Huo D, Taxy JB, Brendler C, Foster B, Stadler W, Rinker-Schaeffer CW. Upregulation of MKK4, MKK6 and MKK7 during Prostate Cancer Progression: An Important Role for SAPK Signaling in Prostatic Neoplasia. Journal of Pathology 2007; 212(4):386-394.
Lotan TL, Tefs K, Schuster V, Miller JL, Manaligod J, Filstead A, Yamada D, Krausz T. Inherited Plasminogen Deficiency Presenting as Ligneous Vaginitis: A Case Report with Molecular Correlation and Review of the Literature. Human Pathology 2007; 38(10):1569-1575.
Lotan TL, Hickson J, Souris J, Huo D, Taylor J, Li T, Otto K, Yamada SD, Macleod K, Rinker-Schaeffer CW. Taylor J, Otto K. Suppression of Ovarian Cancer Metastatic Colonization by JNKK1/MKK4 is Associated with Cellular Growth Arrest and Upregulation of p21. Cancer Research 2008; 68(7):2166-75.
Lotan TL and Epstein JI. Diffuse Adenosis of the Prostate Peripheral Zone in Needle Biopsy and Prostatectomy Specimens. American Journal of Surgical Pathology 2008; 32(9):1360-6. |
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| Email |
ameeker@mail.jhmi.edu |
| Phone |
(410) 502-3398 |
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Alan K. Meeker, Ph.D.
Primary Appointment in Pathology; Secondary Appointment in Urology
Telomere Shortening in Cancer
The genesis and progression of cancer is thought to depend upon genetic instability. This is clearly seen at the chromosomal level in epithelial cancers, such as prostate and breast cancers, which show chromosomal instability as reflected by aberrations in both chromosomal number and structure, yet the molecular mechanisms responsible for chromosome destabilization during carcinogenesis and progression are largely unknown. Our lab is examining defective telomeres which appear to be an important route to chromosomal instability. Telomeres are specialized chromosomal structures consisting of terminal DNA tracts and associated binding proteins. Telomeres protect chromosome ends from fusing with other chromosome ends or other chromosomes containing DNA double strand breaks. In the absence of the telomere synthetic enzyme telomerase, telomeric DNA is subject to loss during cell division. Results from telomerase knockout mouse models indicate that telomere shortening can lead to an increased incidence of cancer in these animals, thus apparently playing a role in cancer initiation.
In close collaboration with Angelo De Marzos lab in the John Hopkins Pathology Department, we developed a novel quantitative fluorescence microscopy technique to measure telomere lengths directly in archival tissues, in order to find out if telomere shortening is playing a role in the initiation of human cancers. Making use of this technique in collaborative efforts with other faculty members in the Johns Hopkins Department of Pathology (Drs. Pedram Argani, Theresa Chan, Christine Iacobuzio-Donahue, Elizabeth Montgomery, Bridgette Ronnett and William Westra) we found that, indeed, telomeres are abnormally short in the vast majority of microscopic cancer precursor lesions in common epithelial cancers, including those of the bladder, breast, cervix, colon, esophagus, gall bladder, oral cavity and prostate.
Telomere length abnormalities appear to be one of the earliest and most prevalent molecular genetic alterations acquired in the multi-step process of tumorigenesis. These findings support a model whereby telomere dysfunction induces a mutator phenotype that acts at the chromosomal and sub-chromosomal levels to accelerate tumor development. We hypothesize that pre-malignant lesions displaying short telomeres are poised on the edge of genetic instability, and are therefore at risk of progressing on to fully invasive carcinomas.
Practically speaking, telomere shortening may have utility in cancer diagnosis, as well as an intermediate endpoint marker in chemoprevention studies. In addition, if telomere shortening is indeed playing a causal role in cancer initiation, then it represents a valid prevention target in its own right.
Telomere Shortening in Aging
Cells normally respond to short telomeres by halting their cell division activities or by committing cellular suicide (apoptosis). It is thought that these responses evolved in long-lived multicellular organisms to prevent the outgrowth of potentially cancerous cell populations. It has been postulated that a loss of division potential due to telomere shortening in proliferating tissues might contribute to certain age-related pathologies, such as the decreased wound healing seen in the elderly. This theory has been difficult to evaluate, as previous methods of telomere length measurement only gave information on the average telomere length of a large number of cells combined.
We believe that our telomere length assay, which features single cell resolution, can be used to test the hypothesized link between telomere shortening and human aging.
Publications
Meeker, A.K., Gage, W.R., Simon, I., Coffman, J.R., Platz, E.A., March, G., and DeMarzo, A.M. Telomere Length Assessment in Human Archival Tissues: Combined Telomere Fluorescent in Situ Hybridization and Immunostaining. American Journal of Pathology. 160:1259-1268, 2002.
Meeker, A.K., Hicks, J.L., Platz, E.A., March, G.E., Bennett, C.J., and De Marzo, A.M. Telomere Shortening is an Early Somatic DNA Alteration in Human Prostate Tumorigenesis. Cancer Research. 62:6405-6409, 2002.
Montgomery, E.A., Argani, P., Hicks, J.L., DeMarzo, A.M., and Meeker, A.K. Telomere Lengths of Translocation Associated and Non-Translocation Associated Sarcomas Differ Dramatically. American Journal of Pathology. 164:1523-1529, 2004.
Meeker, A.K., Hicks, J.L., Iacobuzio-Donahue, C.A., Montgomery, E.A., Westra, W.H., Chan, T.Y., Ronnett, B.M., and DeMarzo, A.M. Telomere Length Abnormalities Occur Early in the Initiation of Epithelial Carcinogenesis. Clinical Cancer Research. 10:3317-3326, 2004.
Meeker, A.K., Hicks, J.L., Gabrielson, E., Strauss, W.M., De Marzo, A.M., and Argani, P. Telomere Shortening Occurs in Subsets of Normal Breast Epithelium as well as In Situ and Invasive Carcinoma. American Journal of Pathology. 164:925-935, 2004. |
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| Email |
bnelson@jhmi.edu |
| Phone |
(410) 614-1661 |
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William G. Nelson, M.D., Ph.D.
Primary Appointment in Oncology; Secondary Appointments in Pathology, Urology, Pharmacology, Medicine, and Radiation Oncology
Member, Graduate Program in Cellular and Molecular Biology; Member, Graduate Program in Pharmacology & Molecular Science
My laboratory is dedicated to the discovery of new targets for cancer treatment and prevention via studies of the molecular pathogenesis of the disease. We have found that somatic inactivation of GSTP1, encoding a carcinogen-detoxification enzyme, by CpG island hypermethylation, likely initiates carcinogenesis in the prostate, liver, and breast via a phenotype of oxidative genome damage tolerance. In the prostate, GSTP1 is normally expressed in basal epithelial cells, the stem cells for the prostatic epithelium, but not in columnar secretory epithelial cells. In proliferative inflammatory atrophy (PIA) lesions, a likely precursor to prostatic intraepithelial neoplasia (PIN) and to prostate cancer, GSTP1 appears induced as part of a stress response associated with exposure to inflammatory oxidants. Loss of GSTP1 expression, attributable to GSTP1 CpG island hypermethylation, is characteristic of some 70% of PIN lesions and >90% of prostate cancers. When compared to cells capable of expressing GSTP1, cancer cells devoid of GSTP1 accumulate more genome damage upon exposure to oxidant carcinogens, yet exhibit improved clonogenic survival.
Key research objectives under current scrutiny include: (i) elucidating the mechanism(s) of oxidative genome damage tolerance in cells devoid of GSTP1, (ii) ascertaining how CpG island hypermethylation leads to GSTP1 gene silencing in prostate cancer cells, (iii) discovering the manner by which the GSTP1 CpG island accumulates abnormally methylated CpG dinucleotides, and (iv) exploring new avenues for the prevention and treatment of cancers, like prostate cancer, by targeting abnormal DNA methylation, enhancement of genome damage repair enzyme capacity, and reduction of inflammation.
Publications
Lin, X., and Nelson, W.G. Methyl-CpG-binding domain protein-2 mediates transcriptional repression associated with hypermethylated GSTP1 CpG islands in MCF-7 breast cancer cells. Cancer Res. 63: 498-504 (2003).
Nakayama, M., Bennett, C.J., Hicks, J.L., Epstein, J.I., Platz, E.A., Nelson, W.G., and De Marzo, A.M. Hypermethylation of the human glutathione S-transferase-pi gene (GSTP1) CpG island is present in a subset of proliferative inflammatory atrophy lesions but not in normal or hyperplastic epithelium of the prostate: a detailed study using laser-capture microdissection. Am. J. Pathol. 163: 923-933 (2003).
De Marzo, A.M., Nelson, W.G., Isaacs, W.B., and Epstein, J.I. Pathological and molecular aspects of prostate cancer. Lancet 361: 955-964 (2003).
Nelson, W.G., De Marzo, A.M., and Isaacs, W.B. Prostate cancer. New Engl. J. Med. 349: 366-381 (2003).
Yegnasubramanian, S., Kowalski, J., Gonzalgo, M.L., Zahurak, M., Piantadosi, S., Walsh, P.C., Bova, G.S., De Marzo, A.M., Isaacs, W.B., and Nelson, W.G. Hypermethylation of CpG islands in primary and metastatic human prostate cancer. Cancer Res. 64: 1975-1986 (2004).
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| Email |
gnetto1@jhmi.edu |
| Phone |
(410) 955-5082 |
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Georges J. Netto, M.D.
Primary Appointment in Pathology; Secondary Appointment in Urology
Current research is focused on the evaluation of molecular biomarkers that can serve as potential prognosticators and or therapeutic targets in the management of urologic malignancies. These studies are facilitated by the construction of Tissue Micro Arrays coupled with Image Analysis technology to be used for immunohistochemistry and FISH analysis of prostatic, bladder, renal and testicular cancers. Molecular Diagnostic applications with potential role in screening and early detection of urologic malignancies are also investigated.
Ongoing prostate cancer studies include the evaluation of the role of TMPRSS2-ERG translocation, proliferation markers (MCM2 and Ki67) and members of the mTOR pathway in predicting progression of prostate cancer in a large well characterized nested case-control cohort of prostate carcinoma patients. The studies are funded by several grants awarded from the Prostate Cancer Foundation and the Patrick C Walsh Foundation in addition to the NIH/NCI sponsored Johns Hopkins Prostate SPORE.
Studies on urothelial carcinoma involve evaluation of biomarkers in a newly constructed tissue array from a well characterized cohort of cystectomy patients treated at the Brady Institute of Urology. Markers under study include: cell cycle control elements, EGFR expression and mutation analysis, PIK3CA mutation analysis and DNA damage response elements and mTOR pathway members. Studies are supported by several philanthropic and NIH/NCI sponsored grants including a PO1 program award.
Additional urologic oncology studies involve the evaluation of biomarkers of targeted therapy in renal cell carcinoma including TOPOIIa, HIF1a/VEGF pathway and global and promoter methylation in Germ cell tumors of testis.
Publications
W Wang, F Tavora, R Sharma, M Eisenberger and GJ Netto. PSMA Expression in Schwannoma: A Potential Clinical Mimicker of Metastatic Prostate Carcinoma. Urol Oncology (in Press)
Lane Z, Epstein JI, Ayub S and Netto GJ : Prostatic Adenocarcinoma In Colorectal Biopsy: Clinical And Pathologic Features. Hum Pathol. 2008 Apr;39(4):543-9
Osunkoya AO, Hansel DE, Sun X, Netto GJ, Epstein JI. Aberrant diffuse expression of p63 in adenocarcinoma of the prostate on needle biopsy and radical prostatectomy: report of 21 cases. Am J Surg Pathol. 2008 Mar;32(3):461-7.
Goodwin AC, Jadallah S, Toubaji A, Lecksell K, Hicks J, Kowalski J, Bova GS, 3, De Marzo AM, Netto GJ, and Casero RA Jr: Increased Spermine Oxidase Expression in Human Prostate Cancer and Prostatic Intraepithelial Neoplasia Tissues. Prostate (In Press)
Hansel DE, DeMarzo AM, Platz EA, Jadallah S , Hicks J, Epstein1JI, Partin AW, and Netto GJ: Early Prostate Cancer Antigen (EPCA) Expression in Predicting Presence of Prostate Cancer among Men with Histologically Negative Biopsies. J Urol 2007: 177(5): 1736-1740
Owens C, Epstein JI and Netto GJ: Distinguishing Prostatic From Colorectal Adenocarcinoma on Biopsy Samples: The Role of Morphology and Immunohistochemistry. Arch Pathol Lab Med 2007:131(4);599-603
Osunkoya AO, Netto GJ, Epstein JI. Colorectal adenocarcinoma involving the prostate: report of 9 cases. Hum Pathol. 2007 Dec;38(12):1836-41
Netto GJ, Epstein JI: Widespread High Grade Prostatic Intraepithelial Neoplasia on Prostatic Needle Biopsy: A Significant Likelihood of Subsequently Diagnosed Adenocarcinoma. Am J Surg Pathol 2006: 30(9):1184-1188
E Kuhn, J De Anda, S Manoni, G Netto and J Rosai: Renal Cell Carcinoma Associated with Prominent Angioleiomyoma-Like Proliferation: Report of Five cases and review of The Literature. Am J Surg Pathol 2006: 30(11): 1372-1361 |
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| Email |
lracusen@jhmi.edu |
| Phone |
(410) 955-3437 |
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Lorraine C. Racusen, M.D.
Primary Appointment in Pathology
The focus of our research is on injury to the kidney. We are also studying morphologic aspects of native kidney and renal allograft injury and rejection, utilizing in-house biopsies and consultant cases, and computerized morphometric techniques. Current projects include pathologic correlates of antibody mediated rejection, assessment of chronic changes in renal allografts, and urinary molecule markers of renal allograft rejection. We are also collaborating with colleagues in nephrology to characterize animal models of acute and chronic renal injury.
Publications
Messias NC, Eustace J, Zachary AA, Tucker PC, Charney D, Racusen LC. Cohost study of the prognostic significance of acute transplant glomerulitisin acutely rejecting renal allografts. Transplantation 74: 655-60, 2001.
Solez K, Racusen LC. Role of renal biopsy in acute renal failure. Contrib. Nephrol. 132: 68-75, 2001.
Racusen LC, Solez K, Colvin R. Fibrosis and atrophy in the renal allograft - Interim report and new directions. Am J Transplan 2:203-6, 2002
Racusen LD, Colvin RB, Solez K, et al. Antibody-mediated rejection criteria - An addition to the Banff 97 classification of renal allograft rejection. Am J Transplant 3:708-14, 2003 |
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