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Harrison’s Manual of Medicine



Bladder Cancer
Renal Cancer
Testicular Cancer

INCIDENCE AND EPIDEMIOLOGY   Annual incidence in the U.S. is about 53,200 cases with 12,200 deaths. Median age is 65 years. Smoking accounts for 50% of the risk. Exposure to polycyclic aromatic hydrocarbons increases the risk, especially in slow acetylators. Risk is increased in chimney sweeps, dry cleaners, and those involved in aluminum manufacturing. Chronic cyclophosphamide exposure increases risk 9-fold. Schistosoma haematobium infection also increases risk, especially of squamous histology.
ETIOLOGY   Lesions involving chromosome 9q are an early event. Deletions in 17p (p53), 18q (the DCC locus), 13q (RB), 3p, and 5q are characteristic of invasive lesions. Overexpression of epidermal growth factor receptors and HER-2/neu receptors is common.
PATHOLOGY   Over 90% of tumors are derived from transitional epithelium; 3% are squamous, 2% are adenocarcinomas, and <1% are neuroendocrine small cell tumors. Field effects are seen that place all sites lined by transitional epithelium at risk including the renal pelvis, ureter, bladder, and proximal 2/3 of the urethra. 90% of tumors are in the bladder, 8% in the renal pelvis, and 2% in the ureter or urethra. Histologic grade influences survival. Lesion recurrence is influenced by size, number, and growth pattern of the primary tumor.
CLINICAL PRESENTATION   Hematuria is the initial sign in 80–90%; however, cystitis is a more common cause of hematuria (22% of all hematuria) than is bladder cancer (15%). Pts are initially staged and treated by endoscopy. Superficial tumors are removed at endoscopy; muscle invasion requires more extensive surgery.

Management is based on extent of disease: superficial, invasive, or metastatic. Frequency of presentation is 75% superficial, 20% invasive, and 5% metastatic. Superficial lesions are resected at endoscopy. Although complete resection is possible in 80%, 30–80% of cases recur; grade and stage progression occur in 30%. Intravesical instillation of bacille Calmette-Guérin (BCG) reduces the risk of recurrence by 40–45%. Recurrence is monitored every 3 months.
The standard management of muscle-invasive disease is radical cystectomy. 5-year survival is 70% for those without invasion of perivesicular fat or lymph nodes, 50% for those with invasion of fat but not lymph nodes, 35% for those with one node involved, and 10% for those with six or more involved nodes. Pts who cannot withstand radical surgery may have 30–35% 5-year survival with 5000 to 7000-cGy external beam radiation therapy. Bladder sparing may be possible in up to 45% of pts with two cycles of chemotherapy with CMV (methotrexate 30 mg/m2 days 1 and 8, vinblastine 4 mg/m2 days 1 and 8, cisplatin 100 mg/m2 day 2, q21d) followed by 4000-cGy radiation therapy given concurrently with cisplatin.
Metastatic disease is treated with combination chemotherapy, either CMV (see above) or M-VAC (methotrexate 30 mg/m2 days 1, 15, 22; vinblastine 3 mg/m2 days 2, 15, 22; doxorubicin 30 mg/m2 day 2; cisplatin 70 mg/m2 day 2; q28d) or cisplatin plus paclitaxel or gemcitabine. About 70% of pts respond to treatment, and 20% have a complete response; 10–15% have long-term disease-free survival.

INCIDENCE AND EPIDEMIOLOGY   Annual incidence in U.S. is about 31,200 cases with 11,900 deaths. Cigarette smoking accounts for 20– 30% of cases. Risk is increased in acquired renal cystic disease. There are two familial forms: a rare autosomal dominant syndrome and von Hippel-Lindau disease. About 35% of pts with von Hippel-Lindau disease develop renal cancer. Incidence is also increased in tuberous sclerosis and polycystic kidney disease.
ETIOLOGY   Most cases are sporadic; however, the most frequent chromosomal abnormality (occurs in 60%) is deletion or rearrangement of 3p21-26. The von Hippel-Lindau gene has been mapped to that region and appears to have novel activities, regulation of speed of transcription and participation in turnover of damaged proteins. It is unclear how lesions in the gene lead to cancer.
PATHOLOGY   Five variants are recognized: clear cell tumors (75%), chromophilic tumors (15%), chromophobic tumors (5%), oncocytic tumors (3%), and collecting duct tumors (2%). Clear cell tumors arise from cells of the proximal convoluted tubules. Chromophilic tumors tend to be bilateral and multifocal and often show trisomy 7 and/or trisomy 17. Chromophobic and eosinophilic tumors less frequently have chromosomal aberrations and follow a more indolent course.
CLINICAL PRESENTATION   The classic triad of hematuria, flank pain, and flank mass is seen in only 10–20% of pts; hematuria (40%), flank pain (40%), palpable mass (33%), weight loss (33%) are the most common individual symptoms. Paraneoplastic syndromes of erythrocytosis (3%), hypercalcemia (5%), and nonmetastatic hepatic dysfunction (Stauffers’ syndrome) (15%) may also occur. Workup should include IV pyelography, renal ultrasonography, CT of abdomen and pelvis, CXR, urinalysis, and urine cytology. Stage I is disease restricted to the kidney, stage II is disease contained within Gerota’s fascia, stage III is locally invasive disease involving nodes and/or inferior vena cava, stage IV is invasion of adjacent organs or metastatic sites. Prognosis is related to stage: 66% 5-year survival for I, 64% for II, 42% for III, and 11% for IV.

Radical nephrectomy is standard for stages I, II, and most stage III pts. Surgery may also be indicated in the setting of metastatic disease for intractable local symptoms (bleeding, pain). About 10–15% of pts with advanced stage disease may benefit from interleukin 2 and/or interferon-a. Some remissions are durable. Chemotherapy is of little or no benefit.

INCIDENCE AND EPIDEMIOLOGY   Annual incidence is about 6900 cases with 300 deaths. Peak age incidence is 20–40. Occurs 4–5 times more frequently in white than black men. Cryptorchid testes are at increased risk. Early orchiopexy may protect against testis cancer. Risk is also increased in testicular femininization syndromes, and Klinefelter’s syndrome is associated with mediastinal germ cell tumor.
ETIOLOGY   The cause is unknown. Disease is associated with a characteristic cytogenetic defect, isochromosome 12p.
PATHOLOGY   Two main subtypes are noted; seminoma and nonseminoma. Each accounts for about ~50% of cases. Seminoma has a more indolent natural history and is highly sensitive to radiation therapy. Four subtypes of nonseminoma are defined; embryonal carcinoma, teratoma, choriocarcinoma, and endodermal sinus (yolk sac) tumor.
CLINICAL PRESENTATION   Painless testicular mass is the classic initial sign. In the presence of pain, differential diagnosis includes epididymitis or orchitis; a brief trial of antibiotics may be undertaken. Staging evaluation includes measurement of serum tumor markers alphafetoprotein (AFP) and b- human chorionic gonadotropin (hCG), CXR, and CT scan of abdomen and pelvis. Lymph nodes are staged at resection of the primary tumor through an inguinal approach. Stage I disease is limited to the testis, epididymis, or spermatic cord; stage II involves retroperitoneal nodes; and stage III is disease outside the retroperitoneum. Among seminoma pts, 70% are stage I, 20% are stage II, and 10% are stage III. Among nonseminoma germ cell tumor pts, 33% are found in each stage. hCG may be elevated in either seminoma or nonseminoma, but AFP is elevated only in nonseminoma. 95% of pts are cured if treated appropriately.

For stages I and II seminoma, inguinal orchiectomy followed by retroperitoneal radiation therapy to 2500–3000 cGy is effective. For stages I and II nonseminoma germ cell tumors, inguinal orchiectomy followed by retroperitoneal lymph node dissection is effective. For pts of either histology with bulky nodes or stage III disease, chemotherapy is given. Cisplatin (20 mg/m2 days 1–5), etoposide (100 mg/m2 days 1–5), and bleomycin (30 U days 2, 9, 16) given every 21 d for four cycles is the standard therapy. If tumor markers return to zero, residual masses are resected. Most are necrotic debris or teratomas. Salvage therapy rescues about 25% of those not cured with primary therapy.


For more detailed discussion, see Scher HI, Motzer RJ: Bladder and Renal Cell Carcinomas, Chap. 94, p. 604; and Motzer RJ, Bosl GL: Testicular Cancer, Chap. 96, p. 616, in HPIM-15.



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