Search

Treatments for clinically localized prostate carcinoma are accompanied by sexual, urinary, and bowel dysfunction and other sequelae that can result in significant distress and reduced well being. Methods capable of improving quality of life are needed that can be integrated into clinical practice. To address this need, a nurse‐driven, cancer care intervention was developed and tested.Within 6 weeks after completing treatment, 99 patients, along with their partners, were enrolled into a prospective, controlled trial and were randomized to receive the cancer care intervention or to receive standard care. Participants in the intervention arm met once each month for 6 months with an oncology nurse intervenor, who helped patients identify their quality‐of‐life needs using an interactive computer program. The intervener then provided education and support tailored to participants' needs. Primary outcome variables included 1) disease‐specific quality of life, including sexual, urinary, and bowel outcomes and cancer worry; 2) depression; 3) dyadic adjustment; and 4) general quality of life. Outcomes data were collected prior to randomization and again at 4 months, 7 months, and 12 months posttreatment.Patients in the intervention arm experienced long‐term improvements in quality‐of‐life outcomes related to sexual functioning and cancer worry compared with patients who received standard care. Baseline depression moderated the impact of the intervention on several other quality‐of‐life outcomes.The findings of the current study indicated that a computer‐assisted, nurse‐driven intervention was capable of providing durable improvements in the quality of life of men who underwent treatment for clinically localized prostate carcinoma. Cancer 2005. © 2005 American Cancer Society.

Urothelial carcinoma commonly manifested loss of heterozygosity (LOH) at different regions of chromosomes 17p, 3p, and 9q. Recent studies suggested that bladder stromal cells may be implicated in the growth and progression of urothelial carcinoma. To better understand the genetic alterations in the stromal cells in patients with bladder carcinoma, the authors evaluated the prevalence of allelic loss at three microsatellite polymorphic markers on chromosomes 17p13 (TP53), 3p25-26 (D3S3050), and 9q32-33 (D9S177). In addition, the pattern of X-chromosome inactivation of the stromal cells was evaluated by analyzing the DNA methylation pattern at a polymorphic site on the androgen receptor gene. The authors studied 18 female patients who underwent either transurethral resection (n = 2) or radical cystectomy (n = 16) for high-grade muscle-invasive urothelial carcinoma of the urinary bladder. Genomic DNA samples from the stromal cells immediately adjacent to the tumor and the tumor itself were prepared from formalin-fixed, paraffin-processed tissues using laser-assisted microdissection and LOH was determined. The stromal cells showed a high frequency of LOH on chromosomes 17p13 (29%), 3p25-26 (61%), and 9q32-33 (47%) with no clear concordance with the adjacent tumor cells. Fourteen specimens (78%) showed LOH in the stroma in at least 1 of 3 markers examined. Nonrandom X-chromosome inactivation was frequent in the stromal cells (50% of informative specimens). The current study revealed that some of the genetic changes that commonly occur with invasive urothelial carcinoma were frequently found in the adjacent stroma and suggested that the stroma of urothelial carcinoma may play an important role in bladder carcinogenesis. Cancer 2003. © 2003 American Cancer Society.

Sex cord–stromal tumors account for < 5% of all adult testicular tumors, and 10% are malignant. Due to the limited reported experience, there is no agreement on the best management, especially in patients who have tumors with malignant pathologic features or who present with metastatic disease. The authors attempt to evaluate the role of retroperitoneal lymph node dissection (RPLND) in the management of patients with these malignant sex cord–stromal tumors. Reviewing the Indiana University testis cancer registry revealed 17 patients who underwent RPLND for sex cord–stromal tumors. Pathology was reviewed for features suggestive of malignancy. The data examined included clinical and pathologic stage, surgical procedure, additional therapy received, and outcome. Pathology included Leydig tumors in six patients, Sertoli tumors in four patients, sex cord–stromal tumors in five patients, a granulosa cell tumor in one patient, and a poorly differentiated non–germ cell tumor in one patient. Nine patients had histologic features suggestive of malignancy. Clinical stage at surgery was Stage I in nine patients and Stage IIA–IIIA in eight patients. Patients underwent modified or bilateral RPLND. Nine patients had pathologic Stage I tumors, and the remaining eight patients and had pathologic Stage IIB–IIIA tumors. Follow-up ranged from 8 months to 11 years. Of the eight patients with Stage II–III disease, six patients eventually died of metastatic disease despite additional radiotherapy and/or chemotherapy. Sex cord–stromal tumors have a potentially aggressive malignant behavior that is difficult to predict based on clinical and pathologic features. Although the therapeutic role of RPLND in patients with small-volume metastatic retroperitoneal tumors is unclear, RPLND remains an option to be performed immediately after orchiectomy, especially in patients who have tumors with malignant features and/or small-volume metastatic disease. Cancer 2003;98:753–7. © 2003 American Cancer Society.

Human bladder carcinoma is thought to arise from a field change that affects the entire urothelium. Whether independently transformed urothelial cell populations exist in the same patient is uncertain. We studied the clonality of urinary bladder carcinoma in 18 female patients who underwent cystectomy for urothelial carcinoma. None had multiple tumors. Tumor samples were obtained from different areas of the same tumor. Sixty-seven tumor samples were analyzed. Tumor genomic DNA was microdissected and extracted from formalin-fixed, paraffin-embedded slides. The clonality of urothelial tumors was evaluated on the basis of a polymorphism of the X chromosome-linked human androgen receptor gene (HUMARA) locus. The technique is dependent on digestion of DNA with the methylation-sensitive restriction enzyme HhaI, polymerase chain reaction (PCR) amplification of HUMARA locus, and detection of methylation of this locus. With this method, only the methylated HUMARA allele is selectively amplified by PCR. Eleven of 18 patients were informative. Nonrandom inactivation of the X chromosome was found in 9 of the 11 informative patients (82%). Seven patients showed different patterns of nonrandom X chromosome inactivation for tumor samples obtained from different regions of the same tumor. Two patients showed the same pattern of nonrandom X chromosome inactivation in all samples. Some muscle-invasive urothelial carcinomas may arise from independently transformed progenitor urothelial cells, supporting the “field effect” theory for bladder carcinogenesis. Cancer 2002;94:104–10. © 2002 American Cancer Society.