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“Rhabdoid” Wilms’ Tumor. An Ultrastructural Study
ONCOLOGY AND CHEMOTHERAPY
nephrectomy and excision of a solitary pulmonary metastasis is presented. Authors' abstract. 2 figures, 3 tables, 28 references
833
These authors have investigated the role of urine as a tumorenhancing agent in bladder carcinogenesis. A model of carcinogenesis was produced by feeding the rats a derivative of nitrosamine for 4 to 10 weeks. The bladder of a number of rats was then heterotopically transplanted into the rats to avoid any contact with the urinary stream. These bladders received repeated instillations of normal saline as opposed to normal rat urine. The authors reported a higher incidence of carcinoma in the bladders that were instilled with normal rat urine. They concluded that normal urine may contain tumor promoter(s). N. J. 1 figure, 2 tables, 13 references
result of widespread response of urothelium to carcinogenic stimuli and that a spectrum of lesions exists, ranging from premalignant urothelium to florid, cystoscopically visible bladder lesions. However, detailed descriptions of cellular features of developing urothelial carcinoma are lacking. The authors conducted an experimental study on Wistar rats to determine cytologic as well as histologic features of developing carcinoma in mammalian bladder. Ninety rats were used for this study, and they were divided into equal groups of treated and age-matched controls. Each treated animal ingested 1.8 gm. N-n-butyl-N-(4-hydroxybutyl) nitrosamine (BHBN), which is a known carcinogen that produces transitional cell carcinoma in the bladder ofWistar rats. There were 6 randomly selected animals (3 control and 3 treated) sacrificed at each of the following weeks after the start of the experiment: 5, 8, 10, 14, 16 and 20. Bladders were studied under light as well as electron microscopy. Microscopic changes in the treated urothelium were statistically different from those in the control specimens. The histologic changes could be grouped into 3 moderately overlapping phases. The earliest changes consisted of an increase in the number of cell layers, loss of polarity, and enlarged and indented nuclei. There was nuclear crowding in some areas. Most nuclei showed dusty chromatin. The intermediate phase was characterized by focal increase in the number of cell layers (papillary hyperplasias). The morphology of the cells comprising these papillations was similar to those in adjacent flat areas. The nuclear indentation and crowding became more prominent and so were the mitoses. The chromatin was finely granular and regular in distribution. In the late phase transitional cell carcinomas developed in the majority of the bladders. The flat urothelium adjacent to the tumors also exhibited significant changes. As the number of cells increased the nuclear size decreased. Mitoses, macronucleoli, nuclear crowding and nuclear notching were prominent features. The chromatin was coarsely granular and irregular in distribution. The superficial layer of urothelium usually was spared and did not show the aforementioned changes. Furthermore, the malignant cells were not distributed uniformly through the urothelium. This study supports the clinical observations that developing urothelial carcinoma passes through a continuum of cellular changes, starting with minimal morphologic changes and progressing to extreme atypicality. The cellular atypicalities among individual cells determine the biologic behavior of the tumor, even though such cells do not occupy the full thickness of the urothelium. Thus, invasive carcinoma can develop from a group of atypical cells that do not progress through a recognizable full thickness, in situ stage. The authors hope that their study may provide a basis for experimental investigations on urothelial carcinoma in the future. N. S. D. 5 figures, 2 tables, 21 references
The Cellular Features of Developing Carcinoma in Murine Urinary Bladder
Smoking and Cancers of Bladder and Pancreas: Risks and Temporal Trends
W. M. MURPHY AND C. C. IRVING, Departments of Pathology and Urology, University of Tennessee Center for Health Sciences and Veterans Administration Medical Center, Memphis, Tennessee
S. H. MooLGA VKAR AND R. G. STEVEN, Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, Pennsylvania
Cancer, 47: 514-522 (Feb. 1) 1981
The authors analyzed the mortality data for carcinoma of the pancreas and bladder in England and Wales to study the association between cigarette smoking and these cancers. Their
"Rhabdoid" Wilms' Tumor. An Ultrastructural Study C.
H. K.
F. GONZALES-CRUSSI, T. N. YONAN AND N. Department of Pathology, Mercy Hospital Medical Center, and Children's Memorial Hospital, Chicago, Illinois FUNG,
MARTINEZ,
Arch. Path. Lab. Med., 105: 521-523 (Oct.) 1981 The pathology section of the National Wilms Tumor Study characterized an uncommon renal neoplasm, tentatively classified as a sarcomato us variant of Wilms tumor under the names of rhabdomyosarcomatoid pattern and rhabdoid tumor. These designations were intended to emphasize the distinctive light microscopic appearance of the tumor cells, whose eosinophilic cytoplasm may be reminiscent of rhabdomyoblasts. Because this tumor variant portends an unfavorable outcome and may be associated with brain metastases and second independent tumors of the posterior fossa its recognition is important. The authors studied a 5-week-old newborn who had a rhabdoid Wilms tumor. Ultrastructural studies disclosed aggregates of cytoplasmic filaments that seemed to correspond with the eosinophilic cytoplasmic bodies seen by light microscopy but did not uncover evidence of rhabdomyoblastic differentiation. The histogenesis of this subtype was not established but the origin from the metanephric blastema could not be ruled out. WW. K. 3 figures, 18 references Enhancement by Urine of Urinary Bladder Carcinogenesis
R.
0YASU, Y. HIRAO AND K. IZUMI, Department of Pathology, Northwestern University Medical School, Chicago, Illinois
Cancer Res., 41: 478-481 (Feb.) 1981
Available evidence from clinical material as well as from animal models suggests that bladder carcinoma develops as a
J. Natl. Cancer Inst., 67: 15-23 (July) 1981
nephrectomy and excision of a solitary pulmonary metastasis is presented. Authors' abstract. 2 figures, 3 tables, 28 references
833
These authors have investigated the role of urine as a tumorenhancing agent in bladder carcinogenesis. A model of carcinogenesis was produced by feeding the rats a derivative of nitrosamine for 4 to 10 weeks. The bladder of a number of rats was then heterotopically transplanted into the rats to avoid any contact with the urinary stream. These bladders received repeated instillations of normal saline as opposed to normal rat urine. The authors reported a higher incidence of carcinoma in the bladders that were instilled with normal rat urine. They concluded that normal urine may contain tumor promoter(s). N. J. 1 figure, 2 tables, 13 references
result of widespread response of urothelium to carcinogenic stimuli and that a spectrum of lesions exists, ranging from premalignant urothelium to florid, cystoscopically visible bladder lesions. However, detailed descriptions of cellular features of developing urothelial carcinoma are lacking. The authors conducted an experimental study on Wistar rats to determine cytologic as well as histologic features of developing carcinoma in mammalian bladder. Ninety rats were used for this study, and they were divided into equal groups of treated and age-matched controls. Each treated animal ingested 1.8 gm. N-n-butyl-N-(4-hydroxybutyl) nitrosamine (BHBN), which is a known carcinogen that produces transitional cell carcinoma in the bladder ofWistar rats. There were 6 randomly selected animals (3 control and 3 treated) sacrificed at each of the following weeks after the start of the experiment: 5, 8, 10, 14, 16 and 20. Bladders were studied under light as well as electron microscopy. Microscopic changes in the treated urothelium were statistically different from those in the control specimens. The histologic changes could be grouped into 3 moderately overlapping phases. The earliest changes consisted of an increase in the number of cell layers, loss of polarity, and enlarged and indented nuclei. There was nuclear crowding in some areas. Most nuclei showed dusty chromatin. The intermediate phase was characterized by focal increase in the number of cell layers (papillary hyperplasias). The morphology of the cells comprising these papillations was similar to those in adjacent flat areas. The nuclear indentation and crowding became more prominent and so were the mitoses. The chromatin was finely granular and regular in distribution. In the late phase transitional cell carcinomas developed in the majority of the bladders. The flat urothelium adjacent to the tumors also exhibited significant changes. As the number of cells increased the nuclear size decreased. Mitoses, macronucleoli, nuclear crowding and nuclear notching were prominent features. The chromatin was coarsely granular and irregular in distribution. The superficial layer of urothelium usually was spared and did not show the aforementioned changes. Furthermore, the malignant cells were not distributed uniformly through the urothelium. This study supports the clinical observations that developing urothelial carcinoma passes through a continuum of cellular changes, starting with minimal morphologic changes and progressing to extreme atypicality. The cellular atypicalities among individual cells determine the biologic behavior of the tumor, even though such cells do not occupy the full thickness of the urothelium. Thus, invasive carcinoma can develop from a group of atypical cells that do not progress through a recognizable full thickness, in situ stage. The authors hope that their study may provide a basis for experimental investigations on urothelial carcinoma in the future. N. S. D. 5 figures, 2 tables, 21 references
The Cellular Features of Developing Carcinoma in Murine Urinary Bladder
Smoking and Cancers of Bladder and Pancreas: Risks and Temporal Trends
W. M. MURPHY AND C. C. IRVING, Departments of Pathology and Urology, University of Tennessee Center for Health Sciences and Veterans Administration Medical Center, Memphis, Tennessee
S. H. MooLGA VKAR AND R. G. STEVEN, Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, Pennsylvania
Cancer, 47: 514-522 (Feb. 1) 1981
The authors analyzed the mortality data for carcinoma of the pancreas and bladder in England and Wales to study the association between cigarette smoking and these cancers. Their
"Rhabdoid" Wilms' Tumor. An Ultrastructural Study C.
H. K.
F. GONZALES-CRUSSI, T. N. YONAN AND N. Department of Pathology, Mercy Hospital Medical Center, and Children's Memorial Hospital, Chicago, Illinois FUNG,
MARTINEZ,
Arch. Path. Lab. Med., 105: 521-523 (Oct.) 1981 The pathology section of the National Wilms Tumor Study characterized an uncommon renal neoplasm, tentatively classified as a sarcomato us variant of Wilms tumor under the names of rhabdomyosarcomatoid pattern and rhabdoid tumor. These designations were intended to emphasize the distinctive light microscopic appearance of the tumor cells, whose eosinophilic cytoplasm may be reminiscent of rhabdomyoblasts. Because this tumor variant portends an unfavorable outcome and may be associated with brain metastases and second independent tumors of the posterior fossa its recognition is important. The authors studied a 5-week-old newborn who had a rhabdoid Wilms tumor. Ultrastructural studies disclosed aggregates of cytoplasmic filaments that seemed to correspond with the eosinophilic cytoplasmic bodies seen by light microscopy but did not uncover evidence of rhabdomyoblastic differentiation. The histogenesis of this subtype was not established but the origin from the metanephric blastema could not be ruled out. WW. K. 3 figures, 18 references Enhancement by Urine of Urinary Bladder Carcinogenesis
R.
0YASU, Y. HIRAO AND K. IZUMI, Department of Pathology, Northwestern University Medical School, Chicago, Illinois
Cancer Res., 41: 478-481 (Feb.) 1981
Available evidence from clinical material as well as from animal models suggests that bladder carcinoma develops as a
J. Natl. Cancer Inst., 67: 15-23 (July) 1981