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Background: The T1 and T2 classifications of the International Union Against Cancer TNM classification system for renal cell carcinoma are based on primary tumor size, and in various editions of the classification, the cut points between T1 and T2 have been amended to provide clinical utility. In the current edition, the T1/T2 cut point is less than or equal to and greater than 7 cm. and more recently a subdivision of the T1 classification (less than or equal to and < 4 cm) has been proposed to identify patients suitable for partial nephrectomy. This study investigates the prognostic significance of tumor size in a series of organ-confined clear cell renal cell carcinomas., Methods: One hundred thirty cases of organ-confined clear cell renal cell carcinomas, with a minimum of 5 years' follow-up, were identified from the New South Wales Cancer Registry. Tumor size was compared with survival using the method of Kaplan and Meier for TNM size categories, and proportional hazards regression was used for assessing size as a continuous variable. Proportional hazards regression also was used for multivariable comparisons of size and other prognostic parameters (Fuhrman grade, AgNOR score, and Ki-67 index) against survival., Results: Of 116 cases for which tumor dimension was recorded, 25 patients had died of cancer-related causes. Primary tumor size ranged from 12 to 140 mm (mean, 57.3 mm). The association between survival and size was significant irrespective of the TNM classification and was also significant when size was modeled continuously (P = 0.000125, hazard of death increased by 3.51 times for each doubling of tumor size). On univariate analysis, Fuhrman grade (P = 0.04) and AgNOR score (P = 0.015) were associated with survival; however, on multivariate analysis only tumor size retained significance., Conclusions: Although the cut point of T1 and T2 TNM categories and the proposed T1 subdivision cut point correlate with survival, our finding that size is a continuous variable indicates that as a prognostic parameter for clear cell renal cell carcinoma, primary tumor size is relative rather than indicative., (Copyright 2002 American Cancer Society. DOI 10.1002/cncr.10255)

Background: Whether phenacetin-containing analgesics cause renal pelvic tumors by virtue of the weak mutagenicity of phenacetin, or indirectly through local effects of analgesic-induced renal papillary scarring, is debated. Because phenacetin consumption ceased in New South Wales, Australia in 1975, cases of renal pelvic carcinoma seen 14-15 years later (many of which were associated with long-standing analgesic-induced renal papillary pathology) provided an opportunity to examine the temporal relation between phenacetin exposure and those histologic characteristics of the tumors and adjacent renal tissue that may implicate analgesics in their etiology., Methods: The authors conducted a "blinded" histopathologic review of tumors of the renal pelvis and adjacent noncancerous renal tissue from 100 cases for which epidemiologic data regarding risk factor exposure (specifically phenacetin-containing analgesics, tobacco, infection, and kidney stones) had been obtained in a population-based case-control study from New South Wales in 1989 and 1990., Results: A history of consumption of phenacetin-containing analgesics was associated strongly with the presence and severity of diffuse renal papillary scarring, and less strongly with papillary calcification. The histologic grade of the renal pelvic tumors tended to rise significantly with consumption of phenacetin-containing analgesics in a dose-dependent fashion and with the degree of papillary scarring, but was not related to smoking. In multivariate analysis it was the degree of papillary scarring (to a greater extent than the amount of phenacetin consumption) that was associated significantly and strongly with a higher histologic grade. Only diffuse papillary calcification was associated significantly with squamous change in the renal pelvic tumors., Conclusions: Based on the results of the current study, the authors conclude that 1) in phenacetin-related tumors of the renal pelvis, the presence and severity of analgesic-induced renal papillary scarring correlates with tumor progression and 2) papillary calcification is a risk factor for squamous change in renal pelvic urothelioma., (Copyright 1999 American Cancer Society.)

Background: Women with breast carcinoma diagnosed before age 40 years have a greater prevalence of germline BRCA1 and BRCA2 mutations than women with breast carcinoma diagnosed at older ages. Several recognizable histologic characteristics have been identified in breast carcinoma from studies of BRCA1/2 mutation carriers who belong to multiple-case families. The authors attempted to determine whether breast carcinoma occurring before age 40 years in BRCA1 or BRCA2 mutation carriers who were not selected for family history could be distinguished histologically from one another and from breast carcinoma in women of a similar age without a germline BRCA1 or BRCA2 mutation., Methods: The study undertook a histologic assessment of breast carcinomas diagnosed before age 40 years identified from a population-based study., Results: Breast carcinoma in BRCA1 mutation carriers was associated with a distinct histologic appearance; these tumors were high grade, and had exceptionally high mean mitotic counts, a syncytial growth pattern, pushing margins, and confluent necrosis. Atypical medullary carcinoma was overrepresented in BRCA1 mutation carriers. All low grade tumors and tumors with low mitotic rates belonged to the group without BRCA1 or BRCA2 mutations. Pleomorphic lobular carcinomas and extensive intraduct carcinomas were more common in BRCA2 mutation carriers., Conclusions: Breast carcinoma occurring in women with a germline BRCA1 or BRCA2 mutation have recognizable histologic phenotypes, which may be useful in identifying individuals more likely to carry germline mutations. Histologic examination of breast carcinoma should become an important part of the evaluation of women seeking genetic testing for germline mutations in these breast carcinoma susceptibility genes.