17 years of experience
Video profile
Accepting new patients
La Sierra
10683 Magnolia Ave
Ste B
Riverside, CA 92505
Locations and availability (6)

Education ?

Medical School Score Rankings
University of Southern California (1993)
  • Currently 4 of 4 apples
Top 25%

Awards & Distinctions ?

Patients' Choice Award (2011)
Compassionate Doctor Recognition (2011 - 2012)
American Urological Association
American Board of Urology

Affiliations ?

Dr. Highshaw is affiliated with 12 hospitals.

Hospital Affilations



  • Pomona Valley Hospital Medical Center
    1798 N Garey Ave, Pomona, CA 91767
    • Currently 4 of 4 crosses
    Top 25%
  • Anaheim Memorial Medical Center
    1111 W La Palma Ave, Anaheim, CA 92801
    • Currently 4 of 4 crosses
    Top 25%
  • Corona Regional Medical Center
    800 S Main St, Corona, CA 92882
    • Currently 3 of 4 crosses
    Top 50%
  • Parkview Community Hospital Medical Center
    3865 Jackson St, Riverside, CA 92503
    • Currently 3 of 4 crosses
    Top 50%
  • Huntington Beach Hospital
    17772 Beach Blvd, Huntington Beach, CA 92647
    • Currently 3 of 4 crosses
    Top 50%
  • Orange Coast Memorial Medical Center
    9920 Talbert Ave, Fountain Valley, CA 92708
    • Currently 2 of 4 crosses
  • Riverside Community Hospital
    4445 Magnolia Ave, Riverside, CA 92501
    • Currently 2 of 4 crosses
  • Menifee Valley Medical Center
    28400 McCall Blvd, Sun City, CA 92585
    • Currently 2 of 4 crosses
  • La Palma Intercommunity Hospital
    7901 Walker St, La Palma, CA 90623
    • Currently 2 of 4 crosses
  • Fountain Valley Regional Hospital & Medical Center
    17100 Euclid St, Fountain Valley, CA 92708
    • Currently 1 of 4 crosses
  • Hemet Valley Medical Center
    1117 E Devonshire Ave, Hemet, CA 92543
    • Currently 1 of 4 crosses
  • San Bernardino Mountains Community Hospital District
    29101 Hospital Rd, Lake Arrowhead, CA 92352
  • Publications & Research

    Dr. Highshaw has contributed to 9 publications.
    Title Aggresome Disruption: a Novel Strategy to Enhance Bortezomib-induced Apoptosis in Pancreatic Cancer Cells.
    Date May 2006
    Journal Cancer Research

    The proteasome inhibitor bortezomib (formerly known as PS-341) recently received Food and Drug Administration approval for the treatment of multiple myeloma, and its activity is currently being evaluated in solid tumors. Bortezomib triggers apoptosis in pancreatic cancer cells, but the mechanisms involved have not been fully elucidated. Here, we show that pancreatic cancer cells exposed to bortezomib formed aggregates of ubiquitin-conjugated proteins ("aggresomes") in vitro and in vivo. Bortezomib-induced aggresome formation was determined to be cytoprotective and could be disrupted using histone deacetylase (HDAC) 6 small interfering RNA or chemical HDAC inhibitors, which resulted in endoplasmic reticulum stress and synergistic levels of apoptosis in vitro and in an orthotopic pancreatic cancer xenograft model in vivo. Interestingly, bortezomib did not induce aggresome formation in immortalized normal human pancreatic epithelial cells in vitro or in murine pancreatic epithelial cells in vivo. In addition, these cells did not undergo apoptosis following treatment with bortezomib, suberoylanilide hydroxamic acid, or the combination, showing tumor selectivity. Taken together, our study shows that inhibition of aggresome formation can strongly potentiate the efficacy of bortezomib and provides the foundation for clinical trials of bortezomib in combination with HDAC inhibitors for the treatment of pancreatic cancer.

    Title Bortezomib Sensitizes Pancreatic Cancer Cells to Endoplasmic Reticulum Stress-mediated Apoptosis.
    Date February 2006
    Journal Cancer Research

    Bortezomib (PS-341, Velcade) is a potent and selective inhibitor of the proteasome that is currently under investigation for the treatment of solid malignancies. We have shown previously that bortezomib has activity in pancreatic cancer models and that the drug induces endoplasmic reticulum (ER) stress but also suppresses the unfolded protein response (UPR). Because the UPR is an important cytoprotective mechanism, we hypothesized that bortezomib would sensitize pancreatic cancer cells to ER stress-mediated apoptosis. Here, we show that bortezomib promotes apoptosis triggered by classic ER stress inducers (tunicamycin and thapsigargin) via a c-Jun NH(2)-terminal kinase (JNK)-dependent mechanism. We also show that cisplatin stimulates ER stress and interacts with bortezomib to increase ER dilation, intracellular Ca(2+) levels, and cell death. Importantly, combined therapy with bortezomib plus cisplatin induced JNK activation and apoptosis in orthotopic pancreatic tumors resulting in a reduction in tumor burden. Taken together, our data establish that bortezomib sensitizes pancreatic cancer cells to ER stress-induced apoptosis and show that bortezomib strongly enhances the anticancer activity of cisplatin.

    Title Port-site Metastasis: the Influence of Biology.
    Date July 2005
    Journal European Urology

    OBJECTIVE: Several surgical and technical mechanisms have been proposed for the development of port-site metastasis, but the influence of tumor and host biologic factors has not been emphasized. We present a case of a pelvic chordoma that metastasized to a prior laparoscopic radical nephrectomy port-site. METHODS: A 62-year-old woman underwent laparoscopic radical nephrectomy (LRN) for a pT1b grade 3 renal cell carcinoma, followed 6 weeks later by resection of a sacral chordoma. The incisions and areas of dissection for the two procedures were discontinuous. RESULTS: Eight months following the LRN she developed a nodule in one of the laparoscopic port-sites. The port-site metastasis was treated with wide surgical resection, which was confirmed as metastatic chordoma on histologic examination. CONCLUSION: Based on the chronological sequence and physical distance between surgical sites, only biological factors could have contributed to this port-site metastasis. This unusual case highlights the important role that tumor and host biologic mechanisms play in the development of port-site metastasis.

    Title Integrating Basic Science and Clinical Research in Bladder Cancer: Update from the First Bladder Specialized Program of Research Excellence (spore).
    Date January 2005
    Journal Current Opinion in Urology

    PURPOSE OF REVIEW: To review the progress of the genitourinary SPORE (Specialized Program of Research Excellence) in bladder cancer. RECENT FINDINGS: The optimal management of bladder cancer depends on the accurate assessment of the biological potential of the disease. Methotrexate, vincristine, adriamycin and cisplatin (M-VAC) chemotherapy has been the standard of therapy for over a decade. However, there has been no improvement in patient survival. Encouraging preclinical data have resulted in the rapid translation of epidermal growth factor receptor antagonists into the clinic. However, phase I and II single-agent clinical trials in head and neck, lung, and colon cancer failed to match the hope generated by laboratory investigations since only a minority of patients seemed to benefit from this approach. Nonetheless, recent data revealed that non-small-cell lung cancer tumors that responded to single-agent Iressa possessed activating epidermal growth factor receptor mutations. These findings have generated refound interest for epidermal growth factor receptor-dependent tumors that are identified by molecular and pharmacodynamic approaches prior to or early in the course of therapy. SUMMARY: Targeted therapy against epidermal growth factor receptor has become one of the primary focuses of the genitourinary SPORE in bladder cancer. The SPORE grant scheme is designed to encourage rapid development of new and innovative cancer research in areas of high priority, in this case bladder cancer. The SPORE has facilitated the advancement of novel epidermal growth factor receptor-targeted therapy, such as the monoclonal antibody IMC-225 and the tyrosine kinase inhibitor ZD1839 (Iressa), from the laboratory to clinical trials. The integration of these new biological agents in combination with chemotherapy, in order to abrogate the progression of advanced bladder cancer, is the prime directive of our current phase II Iressa/docetaxel trial.

    Title The Phosphatidylinositol-3 Kinase Pathway Regulates Bladder Cancer Cell Invasion.
    Date February 2004
    Journal Bju International

    OBJECTIVES: To investigate the role of the phosphatidylinositol (PI)-3 kinase pathway in the invasion of bladder cancer cell lines, and to assess the activation of this pathway in primary human bladder tumours. MATERIALS AND METHODS: Human bladder cancer cells were treated with pathway specific inhibitors or were transfected with PI-3 kinase pathway components. The invasion of cultured bladder cancer cells was analysed by an invasion assay. Bladder cancer cells lines and primary human bladder tumours were analysed for pathway activation by western blotting. RESULTS: A specific inhibitor of PI-3 kinase enzyme activity, Ly294002, potently suppressed the invasive properties of three highly invasive bladder tumour cell lines. Restoration of the PTEN gene to invasive UM-UC-3 bladder tumour cells or expression of a dominant-negative version of the PI-3 kinase target, Akt, also potently inhibited invasion, indicating a central role for the PI-3 kinase/Akt pathway in this process. In addition, 55% of primary tumours from patients with bladder cancer had markedly high levels of phosphorylated Akt. CONCLUSION: Pharmacological or biochemical inhibition of the PI-3 kinase pathway drastically reduced the invasive capacity of bladder cancer cell lines; over half of primary human bladder tumours had high Akt phosphorylation, suggesting that the aberrant activation of this pathway may contribute to the invasion of a significant subset of bladder cancers.

    Title Is Bladder Biopsy Necessary at Three or Six Months Post Bcg Therapy?
    Date October 2003
    Journal Urologic Oncology

    The standard of practice set by the SWOG investigation of BCG therapy for superficial bladder cancer has been to evaluate response at 3 months with cystoscopy and bladder biopsy. This study is to determine if all patients require a biopsy post therapy at 3 or 6 months. We reviewed the charts of 43 patients who had received a 6-weekly course of BCG (Connaught strain) for high grade or recurrent Ta, T1, or Tis transitional cell carcinoma of the bladder. The patients with Ta recurrent, T1 or Tis disease received maintenance therapy. All patients were followed through 6 months. At 3 months, 32/43 patients had negative cystoscopies. All 32 patients had corresponding negative biopsies. Eight patients had visible papillary tumors, while three patients had erythematous lesions, which were biopsy negative. At 6 months, eight different patients had visible lesions on cystoscopy that were biopsy proven superficial bladder cancer. The positive predictive value at 3 and 6 months post BCG therapy was 72.6% and 100%, respectively. The false positive rate was 7% at the 3-month checkpoint. Bladder biopsy is not necessary at the 3 or 6 month period following BCG therapy in the face of negative cystoscopic findings.

    Title Initial Report of Bladder Carcinoma Following Combined Bladder-drained Pancreas and Kidney Transplantation.
    Date October 2002
    Journal Clinical Transplantation

    Although long-term survival of a functional allograft requiring long-term immunosuppressive therapy is responsible for higher incidence of non-urothelial cancers in renal allograft recipients than in normal population, the incidence of bladder cancer is uncommon and carcinoma of the bladder in the setting of combined kidney-pancreas transplantation has not been reported to date. We herein report a case of poorly differentiated invasive adeno-squamous cell carcinoma of the bladder following renal and bladder-drained pancreatic transplantation in a 44-yr-old lady with long-standing insulin dependent diabetes mellitus, which necessitated radical extirpation. Management implications are reviewed.

    Title Somatic Mutations at the Srd5a2 Locus Encoding Prostatic Steroid 5alpha-reductase During Prostate Cancer Progression.
    Date April 1999
    Journal The Journal of Urology

    Prostate cancer is a serious public health problem in many industrialized countries. Androgens appear to play a critical role in its etiology. Specifically, the active androgen in the prostate, dihydrotestosterone (DHT) which is synthesized by the enzyme steroid 5alpha-reductase from testosterone (T), acts as a mitogen. Hence androgen-deprivation is commonly used during prostate cancer therapy. Two isozymes for steroid 5alpha-reductase have been reported. The type II enzyme is prostate-specific and encoded by the SRD5A2 gene. We have investigated a polymorphic (TA)n dinucleotide repeat in the 3' UTR (untranslated region) of the SRD5A2 gene in 30 matched samples of constitutional ("germline") DNA from peripheral blood lymphocytes and microdissected, pure tumor DNA. We report here 8 LOH (loss of heterozygosity) events and 9 cases of microsatellite instability at this marker. Therefore, almost 57% of the samples examined showed evidence of somatic mutations at the 3' UTR of the SRD5A2 locus. Our data suggest that the SRD5A2 gene may be involved in prostate cancer progression and that this may have relevance for treatment of the disease.

    Title Benign Ectopic Prostatic Tissue Involving the Seminal Vesicle in a Patient with Prostate Cancer: Recognition and Implications for Staging.
    Date October 1996
    Journal Urology

    We report the finding of benign, ectopic prostatic tissue in the seminal vesicle of a 67-year-old man who underwent a radical cystoprostatectomy for transitional cell carcinoma of the bladder and in whom carcinoma of the prostate was incidentally identified. The benign nature of the ectopic prostatic epithelium within the seminal vesicle was confirmed by its morphologic features and by the identification of an intact basal cell layer surrounding the prostatic epithelium. In this patient with prostatic carcinoma, it was essential to distinguish benign prostatic epithelium from adenocarcinoma to assign a correct tumor stage and determine appropriate treatment.

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