Browse Health
Urologist
16 years of experience
Accepting new patients

Education ?

Medical School
Martin-Luther-Universitaet Halle-Wittenberg (1994)
Foreign school

Awards & Distinctions ?

Associations
American Society of Clinical Oncology
American Urological Association

Affiliations ?

Dr. Nelius is affiliated with 4 hospitals.

Hospital Affilations

Score

Rankings

  • University Medical Center - Lubbock
    Urology
    602 Indiana Ave, Lubbock, TX 79415
    • Currently 1 of 4 crosses
  • University Medical Center
  • Lincoln County Medical Center
  • TX Tech Physicians Associates
  • Publications & Research

    Dr. Nelius has contributed to 20 publications.
    Title Clinical Outcome of Patients with Docetaxel-resistant Hormone-refractory Prostate Cancer Treated with Second-line Cyclophosphamide-based Metronomic Chemotherapy.
    Date January 2011
    Journal Medical Oncology (northwood, London, England)
    Excerpt

    For patients with docetaxel-resistant hormone-refractory prostate cancer (HRPC) no standard chemotherapeutic treatment exists. In this study, we evaluate the efficacy of cyclophosphamide (CP)-based metronomic chemotherapy in this patient population. Patients with metastatic HRPC with disease progression under docetaxel-based chemotherapy were eligible. The primary endpoint was prostate-specific antigen (PSA) response. Secondary endpoints were survival and toxicity. Low-dose CP (50 mg/d) and dexamethasone (1 mg/d) were administered orally in a metronomic manner. Treatment was continued until disease progression or intolerable side effects occurred. Seventeen patients were enrolled in this study. The median follow-up was 12 weeks (range: 4-60). Median age was 68 years (range: 42-85). Median PSA at study entry was 134 ng/ml (range: 46.0-6554). Nine patients had a PSA response (median 44.4%), four patients >or=50% and five patients <50%. Eight patients had a PSA progression. Overall survival was 24 months. Five patients reported a decrease in bone pain after 4 weeks' treatment. No grade 3 and 4 toxicities were noted. In this study, low-dose metronomically administered CP demonstrated efficacy as a second-line treatment in patients with docetaxel-resistant HRPC. The treatment was well tolerated and almost without toxicity. Further advantages of low-dose CP were its convenient oral administration, dosing schedule, low cost, and low-toxicity profile. These attributes in combination with immunoregulatory and antiangiogenic potentials make CP also a prime candidate for combination with other treatment regimens.

    Title Leiomyosarcoma of the Urinary Bladder Presenting As Life Threatening Gross Hematuria.
    Date January 2011
    Journal Medical Oncology (northwood, London, England)
    Excerpt

    Leiomyosarcomas are a relatively rare tumor entity encountered within the urinary bladder. There are just over 100 cases reported in the medical literature. Herein, we describe a case of leiomyosarcoma presenting initially as a urinary tract infection with lower abdominal pain. A life threatening episode of gross hematuria guided to the final diagnosis and treatment. Due to the rarity of this malignancy, we present this case including a review of the existing literature relative to the diagnosis and treatment.

    Title Cross-sectional Study Examining Four Types of Male Penile and Urethral "play".
    Date January 2011
    Journal Urology
    Excerpt

    To provide further quantitative and qualitative evidence about men who insert foreign liquids and objects into their penis and/or urethra.

    Title [self-inflicted Penile Strangulation].
    Date April 2010
    Journal Aktuelle Urologie
    Excerpt

    Constricting devices or misappropriated means are either used to increase sexual performance or for autoerotic actions. They can lead to edema, maceration, to local infections up to Fournier gangrene or penile necrosis with or without involvement of the urethra. Injuries by these means are often challenging for the treating urologist.

    Title Ints6/dice1 Inhibits Growth of Human Androgen-independent Prostate Cancer Cells by Altering the Cell Cycle Profile and Wnt Signaling.
    Date December 2009
    Journal Cancer Cell International
    Excerpt

    The gene encoding integrator complex subunit 6 (INTS6), previously known as deleted in cancer cells 1 (DICE1, OMIM 604331) was found to be frequently affected by allelic deletion and promoter hypermethylation in prostate cancer specimens and cell lines. A missense mutation has been detected in prostate cancer cell line LNCaP. Together, these results suggest INTS6/DICE1 as a putative tumor suppressor gene in prostate cancer. In this study, we examined the growth inhibitory effects of INTS6/DICE1 on prostate cancer cells.

    Title Psa Surge/flare-up in Patients with Castration-refractory Prostate Cancer During the Initial Phase of Chemotherapy.
    Date November 2009
    Journal The Prostate
    Excerpt

    Docetaxel-based chemotherapy has shown great promise for the treatment of CRPC and is considered the current standard of care. PSA is mainly used as marker to monitor the treatment response. Several articles were published reporting an initial PSA surge/flare-up after starting chemotherapy. The cause and the impact of this phenomenon are discussed controversially. The intention of this review is to define the significance of initial PSA surge/flare-up and to increase awareness to this phenomenon in the urological community.

    Title Characterization of Pedf: a Multi-functional Serpin Family Protein.
    Date June 2009
    Journal Journal of Cellular Biochemistry
    Excerpt

    Pigment epithelium-derived factor (PEDF) is a 50 kDa secreted glycoprotein that belongs to the non-inhibitory serpin family group. PEDF has been described as a natural angiogenesis inhibitor with neurotrophic and immune-modulation properties; it balances angiogenesis in the eye and blocks tumor progression. The mechanisms underlying most of these events are not completely clear; however, it appears that PEDF acts via multiple high affinity ligands and cell receptors. In this review article, we will summarize the current knowledge on the biochemical properties of PEDF and its receptors, the multimodal activities of PEDF and finally address the therapeutic potential of PEDF in treating angiogenesis-, neurodegeneration- and inflammation-related diseases.

    Title Transitional Cell Carcinoma Due to Chronic Urolume Stent Irritation.
    Date June 2009
    Journal Urology
    Excerpt

    UroLume stents have been used for >15 years to improve the voiding dynamics in patients with benign prostatic hyperplasia and urethral stricture disease. Common complications include stent migration, stricture within the stent, and urothelial hyperplasia, any of which could require stent removal, which itself carries morbidity. We report a case of high-grade urothelial carcinoma associated with chronic UroLume application.

    Title Impact of Psa Flare-up in Patients with Hormone-refractory Prostate Cancer Undergoing Chemotherapy.
    Date September 2008
    Journal International Urology and Nephrology
    Excerpt

    OBJECTIVES: The intention of this study is to describe the impact and underlying potential basis of the prostate-specific antigen (PSA) flare-up phenomenon in patients with hormone-refractory prostate cancer (HRPC) treated with docetaxel-based chemotherapy. METHODS: We retrospectively identified 74 consecutive patients who received docetaxel/estramustine-based chemotherapy at our institution. Patients were evaluated based on modified criteria from the Prostate-Specific Antigen Working Group regarding survival and toxicity. Additionally, two androgen receptor mutations derived from patients with advanced disease were analyzed for promiscuous transactivation activity. RESULTS: The 74 patients were stratified into four groups: response, partial response, flare-up-initial PSA elevation, and progression. Median survival in the flare-up group (n=8) was 20 months and did not differ from the response group (p=0.564). The flare-up group showed a maximum PSA elevation from baseline between 3.4 and 28.3% (between three and six weeks) followed by PSA decline >or=50% from the baseline level in seven of the eight patients. The androgen receptor mutations AR(877) and AR(715) displayed a 37.5- and 5.2-fold increase in transactivation activity by progesterone and a 12.6- and 5.4-fold increase by estrogen compared to the AR(WT), respectively. CONCLUSIONS: A considerable portion of HRPC patients experience an initial PSA flare-up under systemic chemotherapy. In this study, occurrence of flare-up phenomenon did not impact survival. Chemotherapy should be continued a minimum of six weeks before removing patients from a docetaxel-based regimen. We showed evidence that co-medication with dexamethasone/prednisolone and/or estramustine itself can induce an initial PSA flare-up via androgen receptor mutations.

    Title Androgen Receptor Targets Nfkappab and Tsp1 to Suppress Prostate Tumor Growth in Vivo.
    Date October 2007
    Journal International Journal of Cancer. Journal International Du Cancer
    Excerpt

    The androgen role in the maintenance of prostate epithelium is subject to conflicting opinions. While androgen ablation drives the regression of normal and cancerous prostate, testosterone may cause both proliferation and apoptosis. Several investigators note decreased proliferation and stronger response to chemotherapy of the prostate cancer cells stably expressing androgen receptor (AR), however no mechanistic explanation was offered. In this paper we demonstrate in vivo anti-tumor effect of the AR on prostate cancer growth and identify its molecular mediators. We analyzed the effect of AR on the tumorigenicity of prostate cancer cells. Unexpectedly, the AR-expressing cells formed tumors in male mice at a much lower rate than the AR-negative controls. Moreover, the AR-expressing tumors showed decreased vascularity and massive apoptosis. AR expression lowered the angiogenic potential of cancer cells, by increasing secretion of an anti-angiogenic protein, thrombospondin-1. AR activation caused a decrease in RelA, a subunit of the pro-survival transcription factor NFkappaB, reduced its nuclear localization and transcriptional activity. This, in turn, diminished the expression of its anti-apoptotic targets, Bcl-2 and IL-6. Increased apoptosis within AR-expressing tumors was likely due to the NFkappaB suppression, since it was restricted to the cells lacking nuclear (active) NFkappaB. Thus we for the first time identified combined decrease of NFkappaB and increased TSP1 as molecular events underlying the AR anti-tumor activity in vivo. Our data indicate that intermittent androgen ablation is preferable to continuous withdrawal, a standard treatment for early-stage prostate cancer. (c) 2007 Wiley-Liss, Inc.

    Title Evaluation of Peri-operative Peripheral and Renal Venous Levels of Pro- and Anti-angiogenic Factors and Their Relevance in Patients with Renal Cell Carcinoma.
    Date August 2007
    Journal Bju International
    Excerpt

    OBJECTIVE: To evaluate peri-operative peripheral and renal venous plasma levels of vascular endothelial growth factor (VEGF), platelet-derived growth factor type BB (PDGF-BB), transforming growth factor (TGF)-beta1, endostatin, and thrombospondin-1 (TSP-1) in relation to pathological variables and prognosis, as pro- and anti-angiogenic factors are important for tumour growth and treatment of patients with renal cell carcinoma (RCC). PATIENTS AND METHODS: The study included 74 consecutive patients with sporadic RCC who had tumour nephrectomy. Peripheral venous blood was drawn 1 day before, immediately and 1, 3 and 5 days after surgery. Renal venous blood was collected in a subgroup of 33 patients during surgery. The variables were analysed using quantitative enzyme-linked immunoassay kits, and associated with pathological variables and disease-specific survival. RESULTS: Soon after surgery, peripheral venous VEGF, PDGF-BB and TGF-beta1 levels were decreased, whereas endostatin levels were significantly increased. Renal venous VEGF, PDGF-BB and TGF-beta1 levels were higher than in the general venous blood pool. Renal venous VEGF levels were correlated with tumour diameter and associated with grade and vascular invasion. After a mean follow-up of 30 months, higher peripheral preoperative, early peripheral postoperative and renal venous VEGF levels were associated with a poorer prognosis. However, in a multivariate analysis only Tumour-Node-Metastasis stage and Eastern Cooperative Oncology Group performance status were independent prognosticators of disease-specific survival. CONCLUSIONS: Circulating pro- and anti-angiogenic factors change early after nephrectomy. VEGF, PDGF-BB and TGF-beta1 are higher in the renal vein than in the general venous blood pool. Higher renal venous and peripheral levels of VEGF might be associated with a poorer prognosis.

    Title [idiopathic Retroperitoneal Fibrosis (ormond's Disease)]
    Date October 2006
    Journal Aktuelle Urologie
    Excerpt

    INTRODUCTION: Idiopathic retroperitoneal fibrosis (RPF) represents a rare inflammatory disease, which leads to extensive fibrosis of the retroperitoneal space. In the course of the progressive fibrosis, fibrous tissue compresses the retroperitoneal structures with the development of consecutive ureteral obstruction. Because of the unknown aetiology, no consensus between conservative and surgical treatment exists. CASE REPORT: A 60-year-old patient was admitted to hospital with left-sided flank pain, hydronephrosis, and retroperitoneal tumour. A CT scan-guided biopsy revealed RPF. The hydronephrosis was treated by endoluminal urinary diversion. Under simultaneous administration of steroids, an almost complete regression of the RPF was noted. CONCLUSIONS: First goal in the treatment of RPF is urinary diversion to protect the renal function. A simultaneous therapy with steroids can cause a complete regression of the RPF. Surgical intervention is only recommended in refractory cases.

    Title A Randomized Study of Docetaxel and Dexamethasone with Low- or High-dose Estramustine for Patients with Advanced Hormone-refractory Prostate Cancer.
    Date September 2006
    Journal Bju International
    Excerpt

    OBJECTIVE: To test the combination of docetaxel with two different doses of estramustine in patients with hormone-refractory prostate cancer (HRPC), to improve response rates and to lower side-effects, as docetaxel-based chemotherapy is an increasing option for men with advanced HRPC, and alone or combined with estramustine, docetaxel improves median survival. PATIENTS AND METHODS: In all, 72 patients with metastatic HRPC were randomly assigned to receive docetaxel (70 mg/m(2) intravenously, on day 2 every 21 days) and estramustine (3 x 280 mg/day oral starting 1 day before docetaxel, for 5 consecutive days) for arm A, or estramustine (3 x 140 mg/day oral starting 1 day before docetaxel, for 3 consecutive days) for arm B. Premedication with oral dexamethasone at a total daily dose of 16 mg, in divided doses twice a day was administered in arm A on day 1-5 and in arm B on day 1-3. Initially, six cycles were administered. Chemotherapy was restarted after a significant increase in prostate-specific antigen (PSA) level. Patients were monitored for any measurable PSA response and toxicity. RESULTS: Between the arms there was no statistically significant difference in time to progression and overall survival. However, treatment B had less treatment-related toxicity than A. Independent prognostic variables were baseline factors like PSA level, haemoglobin level, Eastern Cooperative Oncology Group performance status, and bone pain at presentation. CONCLUSIONS: In this randomized phase II study the combination of docetaxel and estramustine had substantial activity in HRPC, with a significant incidence of severe toxicity, both haematological and not. Nevertheless, treatment-related toxicity was predictable and manageable. There was no better effect with a higher dose of estramustine with docetaxel than for a lower dose. There was a slight tendency to higher toxicity for high-dose estramustine but this was not statistically significant. The present results support the assertion that estramustine is not necessary in docetaxel-based treatment regimens.

    Title Characterization of Prognostic Factors and Efficacy in a Phase-ii Study with Docetaxel and Estramustine for Advanced Hormone Refractory Prostate Cancer.
    Date January 2006
    Journal Onkologie
    Excerpt

    BACKGROUND: Docetaxel based chemotherapy not only reduces pain and improves quality of life in advanced hormone refractory prostate cancer (HRPC), but it also improves survival. We investigated the combination of docetaxel and estramustine in patients with HRPC regarding efficacy and prognostic parameters. PATIENTS AND METHODS: We conducted a phase-II trial, administering docetaxel (70 mg/m(2) i.v., day 2, every 3 weeks) and estramustine (280 mg 3 times daily p.o., 1 day prior to docetaxel, on 5 consecutive days) to patients with HRPC. Patients were monitored for PSA (prostate-specific antigen) response and toxicity. RESULTS: 62 patients were treated. The median age was 67.5 years, the median PSA was 177.9 ng/ml. The median number of cycles was 6. The median time to progression (TTP) and median survival time were 14 (+/-2) and 24 (+/-5) months, respectively. A = 50% decrease in PSA levels from baseline occurred in 38 (61.3%) patients of whom 25 (40.3%) had a = 75% PSA decrease. The main grade 3-4 hematologic toxicities were neutropenia 34% and anemia 18%. CONCLUSIONS: The combination of docetaxel and estramustine exerts substantial activity in HRPC suggesting an overall survival benefit with manageable toxicity. This trial also demonstrated a survival advantage for patients with early chemotherapeutic intervention. We identified PSA relapse, baseline PSA and hemoglobin as valuable prognostic factors in this setting.

    Title In Vivo Upregulation of Cd95 and Cd95l Causes Synergistic Inhibition of Angiogenesis by Tsp1 Peptide and Metronomic Doxorubicin Treatment.
    Date October 2005
    Journal Cell Death and Differentiation
    Excerpt

    Antiangiogenic thrombospondin-1 (TSP1) induces endothelial cell death via a CD95-mediated cascade. We used this signaling pathway, where CD95/Fas is a rate-limiting intermediate, as a target to optimize the efficacy of TSP1 active peptide, DI-TSP. Like TSP1, DI-TSP upregulated endothelial CD95L in vivo. To modulate CD95 levels, we chose chemotherapy agent doxorubicin (DXR). DXR caused sustained upregulation of CD95 in the activated endothelium at 1/100 of the maximal tolerated dose. DI-TSP and DXR synergistically induced endothelial apoptosis in vitro, and in vivo, in developing murine vessels. Fas decoy, TSP1 receptor antibody and Pifithrin, a p53 inhibitor, severely decreased apoptosis and restored angiogenesis by DXR-DI-TSP combination, evidencing critical roles of CD95 and TSP1. Combined therapy synergistically blocked neovascularization and progression of the bladder and prostate carcinoma. Such informed design of a complex antiangiogenic therapy based on the rate-limiting molecular targets is a novel concept, which may yield new approaches to cancer treatment.

    Title Two Functional Epitopes of Pigment Epithelial-derived Factor Block Angiogenesis and Induce Differentiation in Prostate Cancer.
    Date August 2005
    Journal Cancer Research
    Excerpt

    Pigment epithelial-derived factor (PEDF), an angiogenesis inhibitor with neurotrophic properties, balances angiogenesis in the eye and blocks tumor progression. Its neurotrophic function and the ability to block vascular leakage is replicated by the PEDF 44-mer peptide (residues 58-101). We analyzed PEDFs' three-dimensional structure and identified a potential receptor-binding surface. Seeking PEDF-based antiangiogenic agents we generated and tested peptides representing the middle and lower regions of this surface. We identified previously unknown antiangiogenic epitopes consisting of the 34-mer (residues 24-57) and a shorter proximal peptide (TGA, residues 16-26) with the critical stretch L19VEEED24 and a fragment within the 44-mer (ERT, residues 78-94), which retained neurotrophic activity. The 34-mer and TGA, but not the 44-mer reproduced PEDF angioinhibitory signals hinged on c-jun-NH2-kinase-dependent nuclear factor of activated T cell deactivation and caused apoptosis. Conversely, the ERT, but not the 34-mer/TGA induced neuronal differentiation. For the 44-mer/ERT, we showed a novel ability to cause neuroendocrine differentiation in prostate cancer cells. PEDF and the peptides bound endothelial and PC-3 prostate cancer cells. Bound peptides were displaced by PEDF, but not by each other, suggesting multiple receptors. PEDF and its active fragments blocked tumor formation when conditionally expressed by PC-3 cells. The 34- and 44-mer used distinct mechanisms: the 34-mer acted on endothelial cells, blocked angiogenesis, and induced apoptosis whereas 44-mer prompted neuroendocrine differentiation in cancer cells. Our results map active regions for the two PEDF functions, signaling via distinct receptors, identify candidate peptides, and provide their mechanism of action for future development of PEDF-based tumor therapies.

    Title Peroxisome Proliferator-activated Receptor Gamma Ligands Improve the Antitumor Efficacy of Thrombospondin Peptide Abt510.
    Date March 2005
    Journal Molecular Cancer Research : Mcr
    Excerpt

    An expanding capillary network is critical for several pathologic conditions. In cancer, the decrease of antiangiogenic thrombospondin-1 (TSP1) often enables an angiogenic switch, which can be reversed with exogenous TSP1 or its peptide derivative ABT510. TSP1 acts by inducing endothelial cell apoptosis via signaling cascade initiated at CD36, a TSP1 antiangiogenic receptor. Here, we show that the ligands of nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma), 15-deoxy-delta(12,14)-prostaglandin J2, troglitazone, and rosiglitazone increased PPARgamma and CD36 expression in endothelial cells and improved the efficacy of TSP1 and ABT510 in a CD36-dependent manner. The ABT510 and PPARgamma ligands cooperatively blocked angiogenic endothelial functions in vitro and neovascularization in vivo. In tumor xenografts, 15-deoxy-delta(12,14)-prostaglandin J2 and troglitazone synergistically improved antiangiogenic and antitumor effects of ABT510. Our data provide one mechanism for the in vivo angioinhibitory effect of PPARgamma ligands and show fine-tuning of the antiangiogenic efficacy via targeted up-regulation of the endothelial receptor.

    Title Alpha1-antitrypsin Inhibits Angiogenesis and Tumor Growth.
    Date November 2004
    Journal International Journal of Cancer. Journal International Du Cancer
    Excerpt

    Disturbances of the ratio between angiogenic inducers and inhibitors in tumor microenvironment are the driving force behind angiogenic switch critical for tumor progression. Angiogenic inhibitors may vary depending on organismal age and the tissue of origin. We showed that alpha(1)-antitrypsin (AAT), a serine protease inhibitor (serpin) is an inhibitor of angiogenesis, which induced apoptosis and inhibited chemotaxis of endothelial cells. S- and Z-type mutations that cause abnormal folding and defective serpin activity abrogated AAT antiangiogenic activity. Removal of the C-terminal reactive site loop had no effect on its angiostatic activity. Both native AAT and AAT truncated on C-terminus (AATDelta) inhibited neovascularization in the rat cornea and delayed the growth of subcutaneous tumors in mice. Treatment with native AAT and truncated AATDelta, but not control vehicle reduced tumor microvessel density, while increasing apoptosis within tumor endothelium. Comparative analysis of the human tumors and normal tissues of origin showed correlation between reduced local alpha(1)-antitrypsin expression and more aggressive tumor growth.

    Title Nuclear Factor of Activated T Cells Balances Angiogenesis Activation and Inhibition.
    Date August 2004
    Journal The Journal of Experimental Medicine
    Excerpt

    It has been demonstrated that vascular endothelial cell growth factor (VEGF) induction of angiogenesis requires activation of the nuclear factor of activated T cells (NFAT). We show that NFATc2 is also activated by basic fibroblast growth factor and blocked by the inhibitor of angiogenesis pigment epithelial-derived factor (PEDF). This suggests a pivotal role for this transcription factor as a convergence point between stimulatory and inhibitory signals in the regulation of angiogenesis. We identified c-Jun NH2-terminal kinases (JNKs) as essential upstream regulators of NFAT activity in angiogenesis. We distinguished JNK-2 as responsible for NFATc2 cytoplasmic retention by PEDF and JNK-1 and JNK-2 as mediators of PEDF-driven NFAT nuclear export. We identified a novel NFAT target, caspase-8 inhibitor cellular Fas-associated death domain-like interleukin 1beta-converting enzyme inhibitory protein (c-FLIP), whose expression was coregulated by VEGF and PEDF. Chromatin immunoprecipitation showed VEGF-dependent increase of NFATc2 binding to the c-FLIP promoter in vivo, which was attenuated by PEDF. We propose that one possible mechanism of concerted angiogenesis regulation by activators and inhibitors may be modulation of the endothelial cell apoptosis via c-FLIP controlled by NFAT and its upstream regulator JNK.

    Title Id1 Regulates Angiogenesis Through Transcriptional Repression of Thrombospondin-1.
    Date June 2003
    Journal Cancer Cell
    Excerpt

    Id proteins are helix-loop-helix transcription factors that regulate tumor angiogenesis. In order to identify downstream effectors of Id1 involved in the regulation of angiogenesis, we performed PCR-select subtractive hybridization on wild-type and Id1 knockout mouse embryo fibroblasts (MEFs). Here we demonstrate that thrombospondin-1 (TSP-1), a potent inhibitor of angiogenesis, is a target of transcriptional repression by Id1. We also show that Id1-null MEFs secrete an inhibitor of endothelial cell migration, which is completely inactivated by depletion of TSP-1. Furthermore, in vivo studies revealed decreased neovascularization in matrigel assays in Id1-null mice compared to their wild-type littermates. This decrease was completely reversed by a TSP-1 neutralizing antibody. We conclude that TSP-1 is a major target for Id1 effects on angiogenesis.

    Similar doctors nearby

    Dr. James Cammack

    Surgery
    23 years experience
    Lubbock, TX

    Dr. Michael Crone

    Urology
    11 years experience
    Lubbock, TX

    Dr. Jonathan Sawyer Vordermark

    Urology
    36 years experience
    Lubbock, TX

    Dr. Jorge Brothers

    Urology
    40 years experience
    Lubbock, TX

    Dr. Thomas Nicholson

    Urology
    43 years experience
    Lubbock, TX

    Dr. James Kirk

    Urology
    34 years experience
    Lubbock, TX
    Search All Similar Doctors