Urologists
12 years of experience

Accepting new patients
Urologic Health Associates
2031 N Broad St
Ste 141
Lansdale, PA 19446
215-855-9135
Locations and availability (4)

Education ?

Medical School Score
State University of New York Downstate (1998)
  • Currently 2 of 4 apples

Awards & Distinctions ?

Associations
American Board of Urology
American Urological Association

Affiliations ?

Dr. Gerstein is affiliated with 13 hospitals.

Hospital Affilations

Score

Rankings

  • St. Luke's Hospital/Bethlehem
    Urology
    801 Ostrum St, Bethlehem, PA 18015
    • Currently 4 of 4 crosses
    Top 25%
  • Grand View Hospital
    700 Lawn Ave, Sellersville, PA 18960
    • Currently 3 of 4 crosses
    Top 50%
  • Central Montgomery Medical Center
    100 Medical Campus Dr, Lansdale, PA 19446
    • Currently 2 of 4 crosses
  • St Luke's Quakertown Hospital
    300 S 11th St, Quakertown, PA 18951
    • Currently 2 of 4 crosses
  • St. Luke's Miners Memorial Hospital
    360 W Ruddle St, Coaldale, PA 18218
    • Currently 2 of 4 crosses
  • Lehigh Valley Hospital - Muhlenberg
    Urology
    2545 Schoenersville Rd, Bethlehem, PA 18017
    • Currently 1 of 4 crosses
  • Lansdale Hospital
  • Saint Luke's Hospital - Allentown Campus
    1736 W Hamilton St, Allentown, PA 18104
  • Urologic Health Associates
  • Abington Health-Lansdale Hospital
  • St Lukes Qtown
  • UroCare Associates, PC
  • Southampton Hospital
  • Publications & Research

    Dr. Gerstein has contributed to 2 publications.
    Title Effect of Obese and Lean Zucker Rat Sera on Human and Rat Prostate Cancer Cells: Implications in Obesity-related Prostate Tumor Biology.
    Date February 2007
    Journal Urology
    Excerpt

    OBJECTIVES: Several reports have demonstrated the effects of obesity on prostate cancer. Also several reports have linked expression of vascular endothelial cell growth factor (VEGF) and basic fibroblast growth factor (FGF-2) to prostate cancer aggressiveness. The objective of this study was to determine whether a difference exists between lean and obese Zucker rat sera on proliferation prostate cancer cell lines, as well as to examine the differences in FGF-2 and VEGF concentrations. METHODS: Ten-week-old female obese and lean Zucker rat sera were subjected to charcoal stripping and tested for the proliferation of human LNCaP and rat AT3B-1 prostate cancer cells. An acetonitrile extract of the charcoal used to strip the sera was also tested for mitogenicity. VEGF and FGF-2 concentrations were determined by enzyme-linked immunosorbent assay. RESULTS: Both unstripped and charcoal-stripped obese rat sera had a greater mitogenic effect than did the lean sera on the LNCaP cell line. Charcoal stripping of both obese and lean sera reduced the mitogenic effect on the AT3B-1 cell line. The acetonitrile extract of the charcoal used to strip the sera was unable to recover this proliferative effect. The concentration of VEGF was greater in the obese serum than in the lean serum, and charcoal stripping reduced the concentrations of both FGF-2 and VEGF. CONCLUSIONS: The finding of greater VEGF in obese rat sera, as well as greater mitogenic responses on human prostate cancer cells in vitro, suggests this as one of the many possible mechanisms involved in obesity-related prostate cancer biology.

    Title Immune Function, Mitogenicity, and Angiogenic Growth Factor Concentrations in Lean and Obese Rodent Sera: Implications in Obesity-related Prostate Tumor Biology.
    Date August 2004
    Journal Prostate Cancer and Prostatic Diseases
    Excerpt

    Some studies suggest that several tumors have a greater incidence in those patients with a high fat diet, such as colon, breast, and prostate. However, we wanted to determine the effects of obesity alone, independent of diet, on the progression of prostate tumor growth. Using a genetic model of obese and lean Zucker rats, we wanted to demonstrate any sera differences in the concentration of basic fibroblast growth factor (FGF-2) and vascular endothelial cell growth factor (VEGF), two important factors involved in the growth and progression of prostate cancer. We also wanted to investigate if there were any differences in immune function between the two sera, which could also account for uninhibited tumor growth, as well as differences in mitogenic stimulation. Female Zucker rat obese and lean sera were analyzed using ELISA assays for FGF-2, VEGF, and macrophage inflammatory protein-1 alpha (MIP-1a), as a measure of macrophage function. In addition, the sera of lean and obese sera were plated on wells growing LNCaP prostate cancer cells to determine differences in mitogenicity. We found a greater concentration of FGF-2 in the sera from obese Zucker rats compared to lean Zucker rats: 6.32+/-0.56 vs 3.48+/-0.34 pg/ml, respectively, P<0.05). We also demonstrated a greater concentration of VEGF in obese rat sera compared to lean sera: 54.4+/-4.1 vs 38.0+/-2.9 pg/mL, respectively, P<0.05). We detected a trend in mitogenic stimulation among LNCaP cells along the higher concentrations of the dose-response curve (0.72+/-0.06 vs 0.51+/-0.5). However, this was not statistically significant. In addition, we did not find a significant difference in MIP-1a macrophage activity levels between sera. To conclude, we speculate that the greater concentrations of VEGF and FGF-2 in the sera of obese rodents vs lean rodents may account for some of the differences seen in obesity-related tumor growth seen in the human condition. However, the lack of any sera differences of immune function, as measured by macrophage activity, as well as no significant differences on mitogenic proliferation on LNCaP prostate cancer cells, suggests that other mechanisms may exist to explain differences seen in obesity-related prostate tumor biology.


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