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484
LETTERS TO THE EDITOR
RE: THE CLINICAL IMPLICATIONS OF PROCEDURAL DEVIATIONS DURING ORCHIECTOMY FOR NONSEMINOMATOUS TESTIS CANCER
I. Leibovitch, J . Baniel, R. S. Foster and J . P. Donohue J . Urol., 154: 935939, 1995 To the Editor. This article makes it clear t h a t transscrotal removal of testicular tumors is not to be done. Capelouto et a1 "suggest t h a t scrotal violation does not impart a significantly worse overall prognosis."' Recently I advocated the transscrotal approach to testicular tumors.2 I believe t h a t there are 3 import a n t reasons not to perform radical inguinal orchiectomy for suspected testicular cancer: 1) a benign lesion can unnecessarily and unknowingly be treated by orchiectomy, 2) alternate routes of tumor dissemination, t h a t is the superficial external pudendal veins, are not clamped or destroyed before the tumor bearing testes are brought up through the external inguinal ring and 3) the act of squeezing the testes through the external inguinal ring may be a n important cause of tumor spread. My article, in which I present a n anatomical method of transscrotal orchiectomy associated with inguinal ligation of the spermatic cord, is a significant contribution that should be considered by these and other authors as a n alternate to inguinal orchiectomy. Respectfully, John A. Arcadi Huntington Medical Research Institutes 99 North El Molino Avenue Pasadena, California 91101-1830
pSA velocity after prostatectomy has been used to distinguish local recurrence and distant metastasis. Metastasis has a shorter PSA doubling time and a velocity greater than 0.75 ng./ml. per year.8 The median PSA doubling time of 10 to 15 months for stage T2 recurrences compared to 5 years before radiation suggests a combination of massive tumor volume (widespread metastasis) and higher tumor grade. Recurrence stems from a nidus of heterogeneous tumor cells. From the same starting point, the rapidly dividing cells with a short cell cycle will soon be the predominant cell type, which is noted after surgery, radiation or chemotherapy. Thus, a more rapid PSA increase in recurrences is not unexpected and is unrelated to any effects of treatment on the tumor. Urologists and radiation oncologists face a dichotomy in viewing prostate cancer a s a slowly Bowing tumor with a progression rate of 40 to 8 0 8 after any treatment. As in all cancers, tumor control is a n important end point to which clinical or biochemical disease-free survival for various therapeutic approaches should be added. This is especially important in the case of locally advanced tumors, including those with nodal involvement and elevated PSA. The major benefit of curative therapy in these cases is improved disease-free survival with the lesser benefit in cure rates. Increased disease-free survival delays and may obviate the need for hormonal manipulation, especially when used for clinical recurrence. In the current health care environment, therapeutic benefit, morbidity and cost should be commensurate with each other. However, one cannot watch a tumor progress to incurability and major benefit cannot be obtained by controlling clinical cancer for significantly longer periods than actuarial patient survival. PSA failure rate and PSA velocity after surgery or radiation therapy should end the myth that prostate cancer is "benign."
1. Ca elouto, C. C., Clark, P. E., Ransil, B. J . and Loughlin, K. R.: A) review of scrotal violation in testicular cancer: is adjuvant local therapy necessary? J . Urol., part 2, 1 5 3 981, 1995. 2. Arcadi, J . A.: Transscrotal approach to testicular tumors: a n anatomical approach. J . Surg. Oncol., 57: 261, 1994.
Reply by Authors. The most important concept from our article is t h a t tumor spillage during orchiectomy may result in more treatment than would otherwise be necessary. We believe, along with Pizzocaro in the Editorial Comment, t h a t tumor spillage is less likely if inguinal orchiectomy is performed. Since inguinal orchiectomy probably has no greater morbidity than does scrotal orchiectomy, and probably decreases the chance of contamination of the scrotum and inguinal floor, we believe that i t remains the standard of care.
RE: EDITOR= THE CENTRAL ROLE OF PROSTATE SPECIFIC ANTIGEN IN DIAGNOSIS AND PROGRESSION OF PROSTATE CANCER T . A . Stamey J . Urol., 154. 1418-1419, 1995 To the Editor. I read this editorial on the role of posttreatment prostate specific antigen (PSA) with interest. PSA levels permit a 5-year lead time over clinical signs of prostate cancer. However, an increase in PSA does not necessarily indicate local disease. A failure rate of 82% for PSA greater than 1.1 ng./ml. compared to 22% for PSA less than 1.1 ng./ml. is noted in prostatectomy series when postoperative radiation is started at the tumor bed, which suggests the start of metastasis when the tumor volume is minimal and PSA levels are low.' Studies have reported more undifferentiated cancer in nodes and a t other metastatic sites compared to the primary.2 Several articles have correlated the activation and expression of proto-oncogenes with neoplastic transformation and progression to metastatic p h e n ~ t y p e Stage .~ D disease is not a n extension of stage B/C cancer a s noted on survival curves. The metastatic cascade has been well described in in vivo s t u d i e ~ .The ~ . ~larger the initial tumor burden (PSA level), and the more aggressive and higher the percentage of anaplastic tumor cells, the higher the failure rate regardless of which occurs in all urological and nonurological cancers.
Respectfully, Gilbert Lawrence Life Care Cancer Center 4352 GreenuilleSandy Lake Road Stoneboro, Pennsylvania 16153 1. Schild, S. E., Wong, W. W., Grado, G. L., Buskirk, S. J., Robinow, J. S., k i c k , L. M. and Ferrigni, R. G.: Radiotherapy for isolated increases in serum prostate-specific antigen levels after radical prostatectomy. Mayo Clin. Proc., 69: 613, 1994. 2. Sternberg, S. S.: Prostate and seminal vesicles. In: Diagnostic Surgical Pathology. Rowen Press, p. 1837, 1994. 3. Fidler, I. J. and Kripke, M. L.: Metastasis results from preexisting variant cells within a malignant tumor. Science, 191: 893, 1977. 4. Liotta, L. A. and Settler-Stevenson, W. G.: Principles of molecular cell biology of cancer: cancer metastases. In: Cancer: Principles and Practice of Oncology, 3rd ed. Edited by V. T. DeVita, Jr., S. Hellman and S. A. Rosenberg. Philadelphia: J. B. Lippincott Co., chapt. 7, pp. 98-115, 1989. 5. Perez, C. A., Fair, W. R. and Ihde, D. C.: Carcinoma of the prostate. In: Cancer: Principles and Practice of Oncology, 3rd ed. Edited by V. T. DeVita, Jr., S. Hellman and S. A. Rosenberg. Philadelphia: J . B. Lippincott Co., chapt. 33, pp. 1023-1058, 1989. 6. Partin, A. W., Pound, R. C., Clemens, J. Q., Epstein, J . I. and Walsh, P. C.: Serum PSA after anatomic radical prostatectomy. The Johns Hopkins experience after 10 years. Urol. Clin. N. Amer., 2 0 713, 1993. 7. Zagars, G. K.: Serum PSA as a tumor marker for patients undergoing definitive radiation therapy. Urol. Clin. N. Amer., 2 0 737, 1993. 8. Partin, A. W., Pearson, J . D., Landis, P. K., Carter, H. B., Pound, C. R., Clemens, J . Q., Epstein, J. I. and Walsh, P. C.: Evaluation of serum prostate-specific antigen velocity after radical prostatectomy to distinguish local recurrence from distant metastases. Urology, 43: 649, 1994.
RE: CUTANEOUS METASTASIS FOLLOWING LAPAROSCOPIC PELVIC LYMPHADENECTOMY FOR PROSTATIC CARCINOMA C. H. Bangma,
W.J . Kirkels, S. Chadha and F. H . Schroder J. Urol., 1 5 3 1635-1636, 1995
To the Editor. Port site recurrence has been well documented and There are presently more than 20 cases reported in the
LETTERS TO THE EDITOR
RE: THE CLINICAL IMPLICATIONS OF PROCEDURAL DEVIATIONS DURING ORCHIECTOMY FOR NONSEMINOMATOUS TESTIS CANCER
I. Leibovitch, J . Baniel, R. S. Foster and J . P. Donohue J . Urol., 154: 935939, 1995 To the Editor. This article makes it clear t h a t transscrotal removal of testicular tumors is not to be done. Capelouto et a1 "suggest t h a t scrotal violation does not impart a significantly worse overall prognosis."' Recently I advocated the transscrotal approach to testicular tumors.2 I believe t h a t there are 3 import a n t reasons not to perform radical inguinal orchiectomy for suspected testicular cancer: 1) a benign lesion can unnecessarily and unknowingly be treated by orchiectomy, 2) alternate routes of tumor dissemination, t h a t is the superficial external pudendal veins, are not clamped or destroyed before the tumor bearing testes are brought up through the external inguinal ring and 3) the act of squeezing the testes through the external inguinal ring may be a n important cause of tumor spread. My article, in which I present a n anatomical method of transscrotal orchiectomy associated with inguinal ligation of the spermatic cord, is a significant contribution that should be considered by these and other authors as a n alternate to inguinal orchiectomy. Respectfully, John A. Arcadi Huntington Medical Research Institutes 99 North El Molino Avenue Pasadena, California 91101-1830
pSA velocity after prostatectomy has been used to distinguish local recurrence and distant metastasis. Metastasis has a shorter PSA doubling time and a velocity greater than 0.75 ng./ml. per year.8 The median PSA doubling time of 10 to 15 months for stage T2 recurrences compared to 5 years before radiation suggests a combination of massive tumor volume (widespread metastasis) and higher tumor grade. Recurrence stems from a nidus of heterogeneous tumor cells. From the same starting point, the rapidly dividing cells with a short cell cycle will soon be the predominant cell type, which is noted after surgery, radiation or chemotherapy. Thus, a more rapid PSA increase in recurrences is not unexpected and is unrelated to any effects of treatment on the tumor. Urologists and radiation oncologists face a dichotomy in viewing prostate cancer a s a slowly Bowing tumor with a progression rate of 40 to 8 0 8 after any treatment. As in all cancers, tumor control is a n important end point to which clinical or biochemical disease-free survival for various therapeutic approaches should be added. This is especially important in the case of locally advanced tumors, including those with nodal involvement and elevated PSA. The major benefit of curative therapy in these cases is improved disease-free survival with the lesser benefit in cure rates. Increased disease-free survival delays and may obviate the need for hormonal manipulation, especially when used for clinical recurrence. In the current health care environment, therapeutic benefit, morbidity and cost should be commensurate with each other. However, one cannot watch a tumor progress to incurability and major benefit cannot be obtained by controlling clinical cancer for significantly longer periods than actuarial patient survival. PSA failure rate and PSA velocity after surgery or radiation therapy should end the myth that prostate cancer is "benign."
1. Ca elouto, C. C., Clark, P. E., Ransil, B. J . and Loughlin, K. R.: A) review of scrotal violation in testicular cancer: is adjuvant local therapy necessary? J . Urol., part 2, 1 5 3 981, 1995. 2. Arcadi, J . A.: Transscrotal approach to testicular tumors: a n anatomical approach. J . Surg. Oncol., 57: 261, 1994.
Reply by Authors. The most important concept from our article is t h a t tumor spillage during orchiectomy may result in more treatment than would otherwise be necessary. We believe, along with Pizzocaro in the Editorial Comment, t h a t tumor spillage is less likely if inguinal orchiectomy is performed. Since inguinal orchiectomy probably has no greater morbidity than does scrotal orchiectomy, and probably decreases the chance of contamination of the scrotum and inguinal floor, we believe that i t remains the standard of care.
RE: EDITOR= THE CENTRAL ROLE OF PROSTATE SPECIFIC ANTIGEN IN DIAGNOSIS AND PROGRESSION OF PROSTATE CANCER T . A . Stamey J . Urol., 154. 1418-1419, 1995 To the Editor. I read this editorial on the role of posttreatment prostate specific antigen (PSA) with interest. PSA levels permit a 5-year lead time over clinical signs of prostate cancer. However, an increase in PSA does not necessarily indicate local disease. A failure rate of 82% for PSA greater than 1.1 ng./ml. compared to 22% for PSA less than 1.1 ng./ml. is noted in prostatectomy series when postoperative radiation is started at the tumor bed, which suggests the start of metastasis when the tumor volume is minimal and PSA levels are low.' Studies have reported more undifferentiated cancer in nodes and a t other metastatic sites compared to the primary.2 Several articles have correlated the activation and expression of proto-oncogenes with neoplastic transformation and progression to metastatic p h e n ~ t y p e Stage .~ D disease is not a n extension of stage B/C cancer a s noted on survival curves. The metastatic cascade has been well described in in vivo s t u d i e ~ .The ~ . ~larger the initial tumor burden (PSA level), and the more aggressive and higher the percentage of anaplastic tumor cells, the higher the failure rate regardless of which occurs in all urological and nonurological cancers.
Respectfully, Gilbert Lawrence Life Care Cancer Center 4352 GreenuilleSandy Lake Road Stoneboro, Pennsylvania 16153 1. Schild, S. E., Wong, W. W., Grado, G. L., Buskirk, S. J., Robinow, J. S., k i c k , L. M. and Ferrigni, R. G.: Radiotherapy for isolated increases in serum prostate-specific antigen levels after radical prostatectomy. Mayo Clin. Proc., 69: 613, 1994. 2. Sternberg, S. S.: Prostate and seminal vesicles. In: Diagnostic Surgical Pathology. Rowen Press, p. 1837, 1994. 3. Fidler, I. J. and Kripke, M. L.: Metastasis results from preexisting variant cells within a malignant tumor. Science, 191: 893, 1977. 4. Liotta, L. A. and Settler-Stevenson, W. G.: Principles of molecular cell biology of cancer: cancer metastases. In: Cancer: Principles and Practice of Oncology, 3rd ed. Edited by V. T. DeVita, Jr., S. Hellman and S. A. Rosenberg. Philadelphia: J. B. Lippincott Co., chapt. 7, pp. 98-115, 1989. 5. Perez, C. A., Fair, W. R. and Ihde, D. C.: Carcinoma of the prostate. In: Cancer: Principles and Practice of Oncology, 3rd ed. Edited by V. T. DeVita, Jr., S. Hellman and S. A. Rosenberg. Philadelphia: J . B. Lippincott Co., chapt. 33, pp. 1023-1058, 1989. 6. Partin, A. W., Pound, R. C., Clemens, J. Q., Epstein, J . I. and Walsh, P. C.: Serum PSA after anatomic radical prostatectomy. The Johns Hopkins experience after 10 years. Urol. Clin. N. Amer., 2 0 713, 1993. 7. Zagars, G. K.: Serum PSA as a tumor marker for patients undergoing definitive radiation therapy. Urol. Clin. N. Amer., 2 0 737, 1993. 8. Partin, A. W., Pearson, J . D., Landis, P. K., Carter, H. B., Pound, C. R., Clemens, J . Q., Epstein, J. I. and Walsh, P. C.: Evaluation of serum prostate-specific antigen velocity after radical prostatectomy to distinguish local recurrence from distant metastases. Urology, 43: 649, 1994.
RE: CUTANEOUS METASTASIS FOLLOWING LAPAROSCOPIC PELVIC LYMPHADENECTOMY FOR PROSTATIC CARCINOMA C. H. Bangma,
W.J . Kirkels, S. Chadha and F. H . Schroder J. Urol., 1 5 3 1635-1636, 1995
To the Editor. Port site recurrence has been well documented and There are presently more than 20 cases reported in the