Cristoforo L. Cama, M.D., and Inoel Rivera, M.D. are with the University of Florida College of Medicine, Division of Urology in Gainesville, Florida. Zev Wajsman, M.D. is Director Urologic Oncology, Division of Urologyw ith the University of Florida College of Medicine, in Gainesville, Florida.
Tumors of the genitourinary tract in the adult reflect a broad spectrum of altered biological behavior relative to their cell of origin. Modern molecular and cell biology has produced a revolution in our understanding of the cancer cell. This progress is not only extending our basic understanding of urological tumors, but also is resulting in more precise diagnostic and prognostic indicators of tumor behavior. It is our aim to present a current status report regarding the diagnosis and management of penile, testicular and prostate carcinomas. A critical analysis of current data will afford the clinician with insight into treatment options.
Although carcinoma of the penis is an uncommon disease accounting for only two to five percent of genitourinary cancers, it remains the subject of continued debate. The source of this debate include its prevention, treatment of the primary tumor, approach to nodal disease and treatment of metastases.
Squamous cell carcinoma is the most common malignant lesion of the penis. Penile carcinoma constitutes less than 1 per cent of all malignancies among the United States' male population. Incidence rates of carcinoma of the penis vary widely from country to country but in the United States an incidence of 1 to 2 cases per 100,000 per annum is reported. It is most commonly diagnosed during the 6th and 7th decades of life. Penile cancer is the most common genitourinary tumor in Paraguay.
The most common link among cases of cancer of the penis is the
presence of a foreskin. Circumcision has been well established as
a prophylactic measure that virtually eliminates the occurrence
of penile carcinoma. Development of penile cancer among
uncircumcised males has been attributed to the chronic irritative
effects of smegma. Smegma is a by-product of bacterial action on
desquamated cells that are retained within the preputial sac.
Chronic irritation and inflammation are often associated with
cancer of the penis. Most large series report phimosis to occur
in 25 to 75 percent of patients presenting with carcinoma of the
penis.1 Although circumcision at birth seems to be
almost invariably protective, later circumcision at puberty or
during adulthood offers little or no protection against the
future appearance of penile carcinoma.
Carcinoma of the penis is extremely rare among the Jewish
population, among whom neonatal circumcision is customary. It is
somewhat more frequent among Muslims who practice prepubertal
circumcision. The American Academy of Pediatrics Task Force on
circumcision historically reported: "there is no absolute
medical indication for routine circumcision of the newborn."
In 1988, the Task Force revised its assessment as follows:
"Newborn circumcision has potential medical benefits and
advantages as well as disadvantages and risks. When circumcision
is being considered, the benefits and risks should be explained
to the parents and informed consent obtained. It is reasonable to
consider that circumcision is important in countries in which
good hygiene is impractical and soap and water are not readily
available.
Venereal diseases have long been incriminated as causative of penile cancer. However no consistent etiologic relationship of penile carcinoma to venereal disease has been found. An increase in the incidence of cervical cancer among sexual partners of patients with penile cancer has been documented in several series. Penile cancer has also been strongly associated with sexually transmitted human papilloma virus (HPV).
The presenting complaint of a patient with carcinoma of the penis is most frequently a visible penile lesion which is usually painless. The lesion may be papillary and exophytic or flat and ulcerative. The most common site of tumor development is the glans penis, followed by prepuce , and more rarely, the penile shaft. Delayed presentation is not uncommon with the mean delay to diagnosis being eight months and with 15 to 20 per cent of the patients postponing medical evaluation for more than one year.2 Epidemiologic data have provided evidence that penile cancer is associated with low socioeconomic status.
Squamous cell carcinoma of the penis most commonly grows locally with propensity for corporal or urethral invasion. Metastases to the regional femoral and iliac nodes represent the earliest route of dissemination from penile cancer. Clinically detectable distant metastatic lesions to the lung, liver, bone or brain are uncommon and are reported as occurring in 1 to 10 per cent of large series.3
Palpable lymphadenopathy frequently accompanies carcinoma of the penis but is often due to associated inflammatory changes. From 40 to 60 percent of patients with palpably enlarged inguinal lymph nodes will eventually be found to have regional nodal disease.4 Additionally, up to 20% of patients with clinically negative lymph nodes will have disease present at lymphadenectomy. Patient survival is dependent on nodal status with low-stage disease five-year survival approaching 80 percent but with 95 percent of patients with untreated nodal disease dead at three years.5 Death from penile cancer is almost always due to metastatic disease and almost all patients who die will first relapse in the inguinal lymph nodes.
The gold standard of therapy for treatment of the primary lesion is amputation by partial or total penectomy. For superficial tumors localized to the foreskin, circumcision may be an acceptable alternative. Excisional biopsy margins must be examined closely to assure all local disease has been removed. A similar technique suitable for superficial disease known as Mohs micrographic surgery employs tumor excision layer by layer under microscopic control.6 However, this procedure requires an expert in pathological evaluation and precise patient selection is needed. Cure rates are at least equal to partial penectomy and there is less long term functional and cosmetic disability. Additionally, laser destruction of the lesion has been effectively used for superficial tumors.
For tumors of the distal penis in which invasion is present, partial penectomy with a 2 cm proximal margin is the preferred form of therapy. Patients may retain some degree of sexual capability and be able to direct the urinary stream. For primary lesions extending to the base of the penis or in which adequate 2 cm margins are not attainable, total penectomy with perineal urethrostomy is the procedure of choice.
A variety of techniques for delivery of radiotherapy to the penis have been reported. External beam radiation has been reported in some series to have 90 percent local cure rates but others found it unsatisfactory.7,8 These data suggest radiotherapy to be inferior to surgical control of the primary lesion.
The status and management of the inguinal lymph nodes is the most important determinant of patient survival. About 50 percent of patients with inguinal node enlargement have no tumor on histological examination and 20 percent of patients with clinically negative nodes have micrometastases. Controversy still exists regarding early versus delayed lymph node dissection versus no lymph node dissection for carcinoma of the penis. The reason for controversies in management of inguinal nodes is the fact, that groin dissection is associated with high morbidity. However, modern surgery in recent years has resulted in a significant decrease of flap necrosis, skin sloughing and lymphedema.
The data have led many authors to propose the following method of approaching the treatment of inguinal nodes in the patient with penile cancer. These should be regarded as guidelines only; individual considerations may modify therapeutic plans. Patients with lesions that do not invade the corpora (Stage I) and who have no palpable adenopathy should be followed closely at one to two month intervals with physical examination of the inguinal regions after excision of the primary tumor. Ipsilateral ileoinguinal node dissection (ILND) is performed in patients where adenopathy is later detected.
There is controversy in the management of patients with invasive tumors and impalpable nodes. Because of the high incidence of lymph node metastases in patients with lesions invading the corpora, bilateral inguinal and pelvic lymphadenectomy is recommended with clinically negative or positive nodes.
In those patients who present with noninvasive lesions and palpable adenopathy, treatment of the primary lesion should be followed by a course of antibiotics to allow the inflammation to resolve. If a single groin is clinically positive, unilateral ILND should be performed and, if pathologically positive, bilateral ILND is appropriate. If both groins are clinically positive, bilateral ILND is performed. Chemotherapy for metastatic penile cancer is rarely successful and should be administered in a protocol clinical trial.9
Although testicular cancer is a relatively uncommon malignancy overall, accounting for approximately one percent of male cancer, it remains the leading cancer in 15 to 35 year-old males. The significant improvement in survival observed in patients with metastatic germ cell tumors over the past 20 years, has resulted primarily from the development of highly effective combination chemotherapy regimens. Major advances in the therapy of testicular cancer have occurred with an unprecedented increase in long-term disease free survival. Dramatic improvements relate to improved methods of staging and follow-up, improved surgical technique and effective platinum-based combination chemotherapy. Testicular cancer has become a model for the multimodal treatment of solid tumors. Testicular cancer is now one of the most curable solid neoplasms. In the 1990's, long-term disease free survival rates approach 100% for low stage disease. Even for patients with advanced retroperitoneal or pulmonary metastases, survival rates range up to 85 percent. In fact, death from testicular cancer in 1997 almost warrants investigation. Experts in uroradiology, uropathology, radiation oncology and urologic oncology make treatment of testicular cancer at large medical centers imperative.
The average annual incidence rate of testicular cancer for American males is 3 per 100,000. It is the most common solid tumor in men between 20 and 34 years of age and accounts for 12% of all cancer deaths in patients in this age group. It is less common in Orientals and American black males and most common in Scandinavians. Peak incidences of testicular tumors occur in late adolescence to early adulthood (20 to 40 years), in late adulthood (over 60 years), and in infancy (0 to 10 years). Ninety five percent of testicular tumors are of germ cell origin (seminoma/nonseminoma), while the remaining are of non germ cell origin (leydig, sertoli and gonado-blastoma). Testicular cancer is seen more frequently on the right side, similar to the greater incidence of right-sided cryptorchidism; the incidence of bilaterality is about 2 to 3 percent.
The etiology of testicular carcinoma is unknown, however, the greatest link is to cryptorchidism, especially to intra-abdominal cryptorchidism with an overall 10-40 times higher incidence than the general population. Approximately 7 to 10 percent of patients with testicular tumors have prior histories of cryptorchidism.10 The risk of developing a testicular tumor is not considered to be decreased by orchiopexy. Tumor in an abdominal testis is more likely to be seminoma, and tumors in testes previously corrected by orchiopexy are more likely to be nonseminomas. Other factors most commonly implicated as possible etiologic agents are trauma and atrophy.
Seminoma is rare in those younger than the age of 10 and above the age of 60, but it is the most common histologic type overall (40%) with a peak incidence between the ages of 35 and 39 years. Embryonal carcinoma and teratocarcinoma occur predominantly between the ages of 25 and 35 years. Choriocarcinoma (1 percent) occurs most often in the 20 to 30 year age group. Yolk sac carcinoma is the most common malignant germ cell tumor of the testis in infants and children. It is frequently found in combination with other germ cell elements in young adults. Teratoma is the second most common testicular tumor in children. There have been no reports of metastatic teratoma in prepubertal children. Adult teratomas may have a propensity for metastases and must be treated accordingly. Secondary tumors in prepubertal testes are most commonly seen in patients with acute lymphoblastic leukemia. In adult patients over 50 years of age, lymphoma constitutes the most common secondary neoplasm of the testis.
In general, survival in patients with germ cell tumors is related to the stage at presentation. Approximately half of patients with nonseminomatous tumors present with metastatic disease.11 Delay in diagnosis of 4 to 6 months is not uncommon. Delay in diagnosis seems to be related directly to patient factors, such as ignorance, denial, and fear, as well as physician factors, such as misdiagnosis. The usual presentation of a testicular tumor is a nodule or painless swelling of one gonad. Approximately 30 to 40 percent of patients may complain of a dull ache or heavy sensation in the lower abdomen or scrotum. In 10 percent of patients, the presenting manifestations may be due to metastases. Gynecomastia is seen in about 5 per cent of patients with testicular germ cell tumors.
Physical examination of the testis is performed by bimanual examination of the scrotal contents and should include palpation of the abdomen for evidence of nodal disease or visceral involvement. The differential diagnosis of a testicular mass includes testicular torsion, epididymitis, orchitis, hydrocele, hernia, hematoma or spermatocele. Ultrasonography of the scrotum typically reveals a hypoechoic testicular lesion within the tunica albuginea. There is a need for high index of suspicion to detect early testicular cancer. A young man who presents with a swollen, painful testicle is frequently treated for weeks and months with antibiotics despite no history of UTI and negative urinalysis. Ultrasound of the scrotum is the most accurate, simple, non-invasive method to differentiate testis tumor from other pathologies.
Radical or inguinal orchiectomy, with early clamping of the spermatic cord at the deep inguinal ring effectively removes the primary tumor and allows staging. In order for staging to be complete, familiarity with the usual sites for metastasis is necessary. The majority of testicular cancers spread through the lymphatics in an orderly fashion. The primary lymphatic drainage is to the retroperitoneal lymph nodes. Distant spread occurs most commonly to the lungs. Subsequent spread may be noted to liver, viscera, brain, or bone.
Chest radiographs should be the initial procedure performed. Chest CT scanning is usually unnecessary, and may be misleading when granulomas are present. A negative chest x-ray is sufficient. Abdominal CT scanning is the procedure of choice for evaluation of retroperitoneal lymph node involvement. The study of biochemical markers substances, particularly alpha-feto protein (AFP), human chorionic gonadotropin (B-hCG), and lactic acid dehydrogenase (LDH), is clinically useful in staging and monitoring of treatment responses in patients with germ cell neoplasms.
Principal treatment strategies for patients with testicular tumors have evolved from clinical staging and effectiveness of treatment. Each of the major treatment alternatives - surgery, irradiation, and chemotherapy has a defined role in the management. The established treatment for low-stage seminoma (stage I and II A) is inguinal orchiectomy followed by therapeutic or adjuvant radiation therapy. Approximately 75 per cent of seminomas are confined to the testis (stage I) at clinical presentation. The optimum treatment of patients who present with distant metastasis (stage III) or bulk retroperitoneal disease (stage IIB > 5cm) is chemotherapy initially.
External beam radiation (2000 to 2500 cGy) is delivered over a 3-week period to the periaortic and ipsilateral pelvic nodes. In stage I and low-volume stage II seminoma, 5-year survival rates are 90 to 95 percent and 80 percent, respectively. The combination of cis-platinum, etoposide, and bleomycin has been found to be effective against disseminated testicular seminomas as well as nonseminomatous tumors. In patients with advanced seminoma (stage III) approximately 90 percent will achieve a complete response to chemotherapy. One difficulty is the lack of complete resolution of retroperitoneal masses on CT scan. In most patients explored after chemotherapy, only residual necrosis or fibrosis is found. Therefore, with post-chemotherapy residual mass, in contrast to nonseminomas, careful observation is favored as opposed to consolidation with radiation therapy or surgical excision.
Nonseminomas follow a potentially less favorable course than do pure seminomas. In patients with clinical stage I or low stage II nonseminomatous germ cell tumors, following inguinal orchiectomy, retroperitoneal lymphadenectomy (RPLND) remains the mainstay of surgical therapy. The cure rate for patients with pathologically confirmed stage I disease is 95 percent with surgery alone. Relapse generally occurs within the first 2 years and RPLND virtually eliminates the possibility of retroperitoneal relapse. Careful follow-up is necessary with monthly chest radiographs and tumor markers for the 1st year and every other month for the 2nd year.
With the advent of effective chemotherapy, postorchiectomy observation or surveillance for clinical stage I has emerged as a viable option in highly select patients. Prognostic factors that are associated with relapse and are a contraindication for the surveillance program include; a significant percentage of embryonal carcinoma in the primary tumor, invasion of epididymis or tunica albuginea, and lymphatic or vascular invasion. Embryonal carcinoma is associated with higher incidence of retroperitoneal metastasis. Many young patients however are noncompliant and surveillance in this group may result in late detection of metastasis. These patients should be treated initially with RPLND and chemotherapy when indicated.
Combination chemotherapy is the initial therapy for those with bulky retroperitoneal disease or pulmonary metastases. Chemotherapy is capable of sterilizing bulky disease, with resultant tumor necrosis and fibrosis in 30 to 40 percent of cases. Another 20 percent harbor residual malignant elements and the remainder, teratoma. Therefore, surgical excision of residual nodal tissue or extranodal masses following treatment with multidrug chemotherapy is recommended when mass is persistent on CT scan after chemotherapy. In summary, proper early diagnosis and treatment in major medical centers is required to obtain cure rates approaching 100% in these young healthy men.
Adenocarcinoma of the prostate is the most common malignancy in men and, after lung cancer, is the second leading cause of death from cancer in men. The American Cancer Society projects that approximately 334,000 new cases will be diagnosed and more than 40,000 associated deaths will occur from prostate cancer in 1997. In comparison with other cancers, the prevalence and incidence of prostate cancer increase most rapidly with age. Improved life expectancy and a shifting age distribution favoring an older population will increase the number of patients with and dying of prostate cancer. Currently, for American men, the lifetime risk of developing clinically evident prostate cancer is approximately 10 percent, and the risk of dying of prostate cancer is three percent.
The exact etiology of prostate cancer is unknown. Prostate cancer is a disease with a high prevalence and variable biologic behavior. In general, overall cancer incidence and mortality are greater in the African American population than in White Americans. Men of Asian descent have the lowest incidence of clinical prostate cancer. Geographic studies suggest a decreased incidence of prostate cancer in the sun belt region possibly related to vitamin D. Increased alcohol consumption has been associated with a lower incidence of clinical prostate cancer. We do not recommend increasing your intake of alcohol for this purpose. Family history is important and a man with one first degree relative with prostate cancer has a 2.1 to 2.8 fold greater risk of being diagnosed with prostate cancer than the general population. Diets high in fat may increase the relative risk of prostate cancer. Studies on the relationship between smoking and prostate cancer have been conflicting. No clear relationship between sexual activity and prostate cancer has been defined.
The traditional clinical evaluation of prostate cancer patients has included digital rectal examination (DRE), serum prostate specific antigen (PSA) level, CT examination of the pelvis and or a bone scan. Unfortunately many biologically significant prostate tumors are not signaled by symptoms and signs. Prior to availablility of PSA, most patients with prostate malignancy were identified by findings on rectal palpation. Today, most prostate cancer is detected using serum PSA. Prostate carcinoma typically develops as a peripherally located multifocal lesion. The DRE characteristically underestimates tumor volume and the extent of progression. Symptoms of bladder outlet obstruction from early tumors of small mass is rare.
Hematuria is an uncommon nonspecific symptom occurring in less than 15% of prostate cancer patients. Rectal involvement and priapism are rare late manifestations of local extension. Distal ureteral obstruction from tumor extension and invasion of the trigone is indicative of advanced disease.
Approximately 30 percent of patients present with disseminated disease and symptoms of distant spread may be the first manifestation of prostate carcinoma. Persistent, often severe bone pain in the back or hip region is one of the common presenting symptoms of stage D disease. The pelvic lymph nodes are a common site of metastatic spread. Neurologic symptoms are not uncommon with advanced disease and spinal cord compression from epidural metastases is a urologic emergency. Involvement of organs other than bone and the lymphatics is rare.
The natural history of adenocarcinoma of the prostate has been stated to be unpredictable. For other malignancies, a fatal outcome for untreated disease is assumed. For prostate cancer, it is often assumed that localized disease in some cases will have little or no effect on quality or duration of life. Prediction then focuses on identifying clinically localized prostate cancer that is likely to progress to metastatic disease. This is the need of the hour. With advent of PSA, the most important tumor marker in urology, prostate cancer screening has become a highly debated subject. Screening using PSA can detect clinically significant disease, however at present there is no evidence yet that this impacts survival.
The American Urologic Association (AUA) as well as The American Cancer Society currently recommend an annual DRE and serum PSA level in men beginning at age 50 years. In African American males and those with a family history of prostate cancer, this should being at age 35. Recent emphasis has been placed on early detection. Several methods for improving the clinical usefulness of PSA have emerged. These include age-specific PSA reference ranges, PSA density (PSAD), PSA velocity and free/total PSA.
Age specific reference ranges increase the sensitivity of PSA for detecting prostate cancer in younger men and increase the specificity of PSA in older men. The reference range for men 40 to 49 years of age (0 - 2.5), for men 50 to 59 years of age (0 - 3.5), for men 60 to 69 years of age (0 - 4.5), and for men 70 to 79 years of age (0 - 6.5). The age adjusted use of PSA will reduce the need for prostate biopsies in the older population with a small risk of missing some cancers. On the other hand, this concept results in a higher number of biopsies performed in younger men, with the benefit of detecting cancer in a population with an otherwise long life expectancy. Still it is easy to apply and reasonable for routine practice.
PSA density (PSAD) is the serum PSA concentration divided by the volume of the prostate gland, as determined from transrectal ultrasound. Initial studies suggested PSAD was useful in distinguishing benign prostatic hyperplasia (BPH) (<0.15) from clinically localized prostate cancer (>0.15).13 The problem with the PSAD concept is that the determination of prostate volume by transrectal ultrasound is highly operator dependent and it varies considerably. PSA velocity is the rate of change in serum PSA over time. It was found that an annual PSA slope >0.75 ng/ml/yr best distinguished between men with and without prostate cancer using three measurements.14 One difficulty with this concept is that laboratory variation exists and it is too early to judge its clinical significance.
Multiple molecular forms of PSA in serum have been identified. Serum PSA complexed to alpha-1 antichymotrypsin was found in significantly higher proportions in prostate cancer patients compared to patients with BPH. Moreover, studies reported that the free/total PSA ratio in serum was significantly lower in prostate cancer than BPH. An abnormally low free/total PSA ratio (<25%) may increase the ability of serum PSA (in the range between 4 and 10) in distinguishing subjects with prostate cancer from those with BPH.15 More recently, attempts at molecular staging of prostate cancer using a reverse transcriptase polymerase chain reaction assay (RT-PCR) for PSA have been reported.16 This data is still experimental and needs to be validated and verified in more centers.
Current imaging modalities used to clinically stage prostate cancer fail to detect extracapsular disease in a significant subset of patients. CT examination is reserved for advanced stage disease, mostly for detection of lymph node metastasis or for planning radiation therapy. Radionuclide bone scans may be avoided if the PSA is <20 ng ml.17 The incidence of bone metastasis in this group is exceedingly rare.
Treatment alternatives for clinically localized prostate cancer include radical prostatectomy, external beam radiation therapy, watchful waiting and interstitial seed implantation (brachytherapy). For over a century, radical prostatectomy has been proven to be an effective cure for patients with localized prostate cancer and excellent long-term cancer-specific survival is expected.
Late complications including bladder neck contracture, incontinence and impotence have been reduced with improved surgical technique. Using the anatomic nerve-sparing approach, potency may be preserved in selected patients.
Two radiation modalities are currently used in the treatment of early stage prostate cancer; external beam therapy and interstitial isotopic transperineal implantation using permanently placed iodine-125 or palladium-103 radioactive seeds. Most recently, conformal radiation therapy techniques result in less acute side effects including urinary frequency, dysuria, diarrhea, and occasional rectal bleeding. Urethral stricture and incontinence have decreased. Interstitial seed implantation may result in acute irritative voiding symptoms, although usually temporary and easily managed clinically. Some authors recommend against implant in TURP patients.
A comparison between radical prostatectomy and radiation remains less than exact outside a randomized study. Outcome appears quite similar by both clinical and biochemical (PSA) endpoints when treatment groups are as similar as possible. We favor radical surgery for the younger patient (<70) with excellent performance status and a life expectancy more than 10 years. This affords the patient the opportunity to receive either immediate or delayed postoperative adjuvant irradiation when indicated. This can reduce local recurrence, although evidence on improved disease-free survival is inconclusive. At 5 years post treatment, it appears that transperineal seed implantation may be as good as external beam radiation. Combination of external beam radiation and seed implantation show encouraging results.
In the case of metastatic prostate cancer, treatment has remained palliative and the disease incurable. Although hormonal therapy results in successful palliation in the vast majority of patients, it is not effective in preventing progressive disease. Androgen deprivation can be achieved using one of several approaches: bilateral orchiectomy, the use of analogs of luteinizing hormone releasing hormone (LHRH), the use of antiandrogens, systemic estrogens, or by combinations. Hormone therapy results in stabilization or regression of the disease. A rising PSA level, despite complete androgen blockade, is a sign of treatment failure or relapse.
After the initiation of hormonal therapy, PSA levels typically decrease over a period of 3-4 months. Tumor shrinkage can be achieved in approximately 80 percent of cases. Early versus delayed hormonal therapy has been a long debated topic. Current evidence favors early androgen ablation therapy.
Regardless of the method of hormone treatment, the median time of progression is 12 to 18 months, and the median time for survival is 24 to 30 months.19 The benefit of combined androgen blockade over monotherapy remains unclear. Current data do not support total or combined androgen blockade (LHRH analog - Lupron + antiandrogen - Flutamide or Casodex). Morbidity of treatment is not insignificant and side effects include sweating, hot flashes, loss of libido, impotence, weight gain, and gynecomastia.
Almost all patients who initially respond to androgen deprivation eventually relapse to a state of unresponsiveness (hormone-refractory prostate cancer). Secondary hormonal therapy (ketoconazole, corticosteroids, megestrol) is of limited benefit.
Chemotherapy strategies (suramin, estramustine, vinblastine) show some promise in clinical trials. At the earliest sign of disease progression these men should be considered candidates for clinical trials designed to develop improved therapy for metastatic prostate cancer.
In summary, early detection and management of prostate cancer continue to be controversial. Many prostate cancer patients will live with disease and not die from disease. In such patients the need for diagnosis and treatment is debatable. However, prostate cancer remains a deadly disease for many thousands of younger patients and over forty thousand deaths from prostate cancer are projected for 1997. It is likely that the majority of prostate cancers detected by current methods are clinically significant lesions. Because we lack the capability of distinguishing aggressive lesions from more indolent cancers, we recommend early detection and treatment of prostate cancer in patients with a life expectancy of ten years or longer.
REFERENCES
1. Hanash KA, Furlow WL, Utz DC, et al: Carcinoma of the penis: A clinicopathologic study. J Urol 1970; 104:291-7.
2. McDougal WS, Kirchner FK, Edwards RH, et al: Treatment of carcinoma of the penis: The case of primary lymphadenectomy. J Urol 1986; 136:38-41.
3. Puras A, Gonzalez-Flores B, et al. Treatment of carcinoma of the penis. Proc. Kimbrough Urol. Semin., 12: 143, 1978.
4. Skinner DG, Leadbetter WF, Kelley SB: The surgical management of squamous cell carcinoma of thepenis. J Urol 1972; 107:273-7.
5. Fraley EE, Zhang G, Sazama R, et al: Cancer of the penis. Cancer 1985;55:1618-24.
6. Mohs FE, Snow SN, Messing EM, et al. Microscopically controlled surgery in the treatment of carcinoma of the penis. J. Urol 1985; 133:961-6.
7. Kelley CD, Arthur K, Rogoff E, et al: Radiation therapy of penile cancer. Urology 1974; 4:571-3.
8. Duncan W, Jackson SM: The treatment of early cancer of the penis with megavoltage x-rays. Clin Radial 1972;23:246-8.
9. Ahmed T, Sklaroff R, Yagoda A: Sequential trials of methotrexate, cisplatin and bleomycin for penile cancer. J Urol 1984; 132:465-8:
10. Whitaker RH: Management of the undescended testis. Br. J. Hosp. Med., 4:25, 1970.
11. Bosl GJ, Vegelzang NJ, Goldman A, et al. Impact of delay in diagnosis on clinical stage of testicular cancer. Lancet, 2:970, 1981.
12. Barzell WE, Whitmore WF Jr.: Clinical significance of biological markers: Memorial Hospital experience. Semi Oncol., 6:48, 1979.
13. Benson MC, Whang, IS, Pantuck A, et al. Prostate-specific antigen density: a means of distinguishing benign prostate hypertrophy from prostate cancer. J. Urol. 1992; 147: 815-816.
14. Carter HB, Pearson JD, Metter EJ, et al. Longitudinal evaluation of prostate-specific antigen levels in men with and without prostate disease. JAMA 1992; 267: 2215.
15. Christensson A, Bjork T, Nilsson O, et al. Serum prostate-specific antigen complexed to alpha,- antichymotrypsin as an indicator of prostate cancer. J Urol. 1993; 150: 100-105.
16. Cama C., Olsson CA, Raffo A, et al. Molecular staging of prostate cancer II. a comparison of the application of an enhanced reverse transcriptase polymerase chain reaction assay for prostate specific antigen versus prostate specific membrane antigen. J. Urol. 1995; 153: 1373-1378
17. Oesterling JE. Using PSA to eliminate the staging radionuclide bone scan. Urol Clin North Am. 1993: 20: 705-711.
18. Blasko J. Clinical results. A: Treatment with implantation alone. B: Combined external beam irradiation with permanent implantation boost. Prostate cancer: horizons in transperineal therapy, fifth annual symposium, Seattle, 1994.
19. Ahmann FR, Dalkin BL. Controverries in the management of newly diagnosed metastatic prostate cancer. In: Dawson NA, Vogelzzang NJ, eds. Prostate Cancer. New York: Wiley-Liss, 1994: 215-233.
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