Charles P. Schwinn
University of Southern California
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Skeletal Radiology | 1994
Bernard W. Hindman; Leanne L. Seeger; Philip Stanley; Deborah M. Forrester; Charles P. Schwinn; Shirley Z. Tan
The typical giant cell tumor (GCT) is a solitary neoplasm that occurs in the epiphysis or epimetaphysis of long bones. GCT is seen with a slightly increased frequency in females, and 70% of patients are between 20 and 40 years of age at the time of presentation. Multicentric giant cell tumor (MGCT; two or more centers) is an unusual variant of GCT. Patients with MGCT are likely to be younger than those with a solitary lesion. The multicentric variety is often of a higher stage at diagnosis and is more often associated with a pathological fracture than the unifocal tumor. We are reporting five new cases of MGCT, with a total of 21 tumors seen over a period of 25 years from 1967 to 1992.
Cancer | 1976
A. H. Williams; Charles P. Schwinn; John W. Parker
The ultrastructural features of 20 cases of osteosarcoma are discussed. Characteristically, the malignant cells (osteoblasts) contained large quantities of dilated, anastomosing rough endoplasmic reticulum, often forming large lakes. Mitochondria were sparse. Similar features are seen in osteoblasts in normal developing bone. Marked ultrastructural similarities of cells from chondrosar‐comatous, fibrosarcomatous and typical osteosarcomatous areas of these tumors strongly supports the concept that these neoplastic cells all arise from the same progenitor cell. Malignant giant cells were readily differentiated from benign osteoclasts. The most significant ultrastructural findings were the varying degrees of calcification in the intercellular areas (osteoid), ranging from an extensive dense deposition of hydroxyapatite crystals which obscured the underlying collagen fibers, to focal collections, or puffs, of slender needle‐shaped hydroxyapatite crystals deposited on or along collagen fibers. The earliest apparent evidence of calcification was the presence of small electron‐dense particles on or in collagen fibers.
Skeletal Radiology | 1987
Michael P. Marks; Susan Marks; Hervey D. Segall; Charles P. Schwinn; Deborah M. Forrester
Address reprint requests to: Hervey D. Sega11, M.D., Department of Radiology, Los Angeles County University of Southern California Medical Center, 1200 North State Street, Los Angeles, CA 90033, USA until she noted the mass, one-and-a-half years prior to presentation at this hospital. She initially sought medical help at that time in Saigon (she was of Vietnamese descent). No biopsy was obtained, but the patient was given a fifteen week course of radiation therapy. Her tumor did not respond to radiation, gradually enlarging in size. The amount of radiation could not be learned. On presentation to this hospital her laboratory values were unremarkable except for an alkaline phosphatase of 21 IU (normal range: 35-110 IU).
American Journal of Obstetrics and Gynecology | 1968
Edward Gomer Jones; Charles P. Schwinn; Weldon K. Bullock; Alex Varga; John E. Dunn; Herbert Friedman; John Weir
Abstract The results of 5 years of cytodetection of cancer of the cervix during pregnancy in the Prenatal Clinics of the city and county of Los Angeles are presented. Abnormal cytology rates or each month of pregnancy and post partum are compared. Rates for different racial groups are shown. The accuracy of fluorescent staining is compared to the Papanicolaou staining method. The percentage of false negatives by the cervical scrape method is discussed. The tissue diagnoses and treatment of 988 patients are reported. The report includes prevalence rates for dysplasia and in situ carcinoma, the fate of 475 patients with dysplasia, and the treatment of 274 patients with in situ carcinoma, 14 patients with microinvasive carcinoma, and 18 patients with invasive disease.
Cancer | 1991
Raymond A. Kempf; Lowell Irwin; Lawrence R. Menendez; Parakrama Chandrasoma; Susan Groshen; Wilbur Melbye; Tillman M. Moore; Michael J. Pentecost; Michael F. Quinn; Michael D. Sapozink; Charles P. Schwinn; Andrew Sherrod; Mary L. Stewart; Walter Wolf; Franco M. Muggia
Preoperative therapy has been tested as part of limb salvage therapy for localized bone and soft tissue sarcoma of the extremities. The activity of cisplatin (CDDP) by intraarterial (IA) infusion was evaluated in 40 cases of which 36 were evaluable for response. All patients had high‐grade sarcomas. All but 3 patients received 3 or 4 courses (24 patients received 4 courses) of CDDP at a dosage of 120 to 150 mg/m2 given over 6 hours every 2 weeks by IA infusion. Patients younger than 18 years of age received the higher dose of CDDP. Treatment was well tolerated with combination antiemetics. One patient experienced severe hearing loss with the first cycle of the higher CDDP dose. Pathologic evaluation of resected osteosarcoma showed a favorable response (90% or greater necrosis) in 8 of 20 evaluable cases and in 3 of 4 patients with malignant fibrous histiocytoma (MFH) of bone (without osteoid). In soft tissue sarcomas, minimal (50% to 89%) necrosis was seen in two of nine cases and none had 90% or greater necrosis. Patients received postoperative chemotherapy based on pathologic response, but the value of this postoperative adjuvant therapy requires further follow‐up and is uncertain in this small study. IA CDDP can often cause significant tumor necrosis in patients with bone sarcomas, whereas soft tissue sarcomas are less sensitive to this therapy.
American Journal of Obstetrics and Gynecology | 1964
Edward Gomer Jones; Charles P. Schwinn; Weldon K. Bullock; Alex Varga; John E. Dunn; Philip Buell
Abstract 1. 1. An in vivo study has been started of patients with in situ carcinoma and dysplasia found during pregnancy to discern whether these lesions can be reversed by chemical substances. 2. 2. The first clinical trial with a trichomonacide given orally, a broad-spectrum antibiotic used vaginally, and a long-acting progesterone given intermuscularly (in sequential order) failed to produce regression in 50 per cent of cases within the time limit described. There was a suggestive change in some of the dysplasias. 3. 3. This group of cases demonstrates that the lesions found during pregnancy are similar to those found at other times and the majority persist if not treated or removed.
Cancer | 1987
Helen E. Gruber; G. June Marshall; Tillman M. Moore; Charles P. Schwinn; Mary E. Kirchen; Shaul G. Massry
Correct prediction of tumor behavior and interpretation of local factors in the tumor microenvironment rely in part upon accurate determination of tissue changes after tumor invasion. The authors examined local bone changes in primary malignant fibrous histiocytoma (MFH) of bone in a 59‐year‐old woman. Three noninvolved and three tumor‐involved sites were evaluated by quantitative determinations of bone structural and dynamic features. Compared to noninvolved sites, tumor‐involved bone was characterized by significantly increased osteoblast index (89.4 ± 15.6 [mean ± SEM] versus 7.3 ± 6.0, P = 0.008), percent osteoid area (12.1 ± 2.7 versus 1.2 ± 0.5, P = 0.02), percent of trabecular surface covered by osteoid (70.0 ± 6.0 versus 14.5 ± 4.8, P = 0.002), and percent osteoid lined by osteoblasts (36.4 ± 3.6 versus 3.7 ± 3.0, P = 0.002). Bone 7.8 mm distant from invading tumor cells showed features characteristic of noninvolved sites, whereas bone completely surrounded by tumor showed markedly decreased osteoblast features. Osteoblast function also was affected by tumor; the amount of matrix laid down per day bore a significant positive correlation with the osteoblast index. These data indicate the following: (1) distinctive bone morphologic changes occur in situ during invasion by MFH; (2) changes affect aspects of bone formation but not resorption during invasion; (3) both osteoblast number and osteoblast activity are significantly altered; and (4) changes are local in nature and probably reflect the osteoblast response to local tumor factor(s) and are dependent upon the extent of tumor invasion. Cancer 59:755‐760, 1987.
American Journal of Clinical Pathology | 1979
Patrick W. Chambers; Charles P. Schwinn
Cancer | 1964
Robert J. McKenna; Charles P. Schwinn; K. Y. Soong; Norman L. Higinbotham
Cancer | 1968
F. M. Finck; Charles P. Schwinn; L. E. Keasbey