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Predictive value of grade for metastasis development in the main histologic types of adult soft tissue sarcomas: a study of 1240 patients from the French Federation of Cancer Centers Sarcoma Group.

BACKGROUND: Histologic grade is said to be the most important prognostic factor in adult soft tissue sarcomas (STS), but most grading systems have been tested in the overall sarcoma group and the predictive value of histologic grade needs to be assessed specifically for each of the histologic categories. METHODS: From 1980 to 1994, 1240 nonmetastatic patients were entered in the French STS database. The following parameters were studied: patient's age and gender, previous history, tumor location, size and depth, neurovascular or bone involvement (NBI), histologic type and subtype, and grade (the French Federation of Cancer Centers [FNCLCC] system). Median follow-up for the survivors was 88 months; only 5% of patients were lost to follow-up. The authors performed univariate and multivariate analyses for metastasis-free survival for the overall sarcoma group and for every main histologic type. RESULTS: In order of importance, parameters were respectively retained as independent predictors of metastasis as follows: grade, tumor size, NBI and tumor depth for the overall group, grade and NBI for malignant fibrous histiocytomas (n = 349), tumor size, histologic subtype and grade for liposarcomas (n = 188), NBI, grade and tumor size for leiomyosarcomas (n = 148), grade and NBI for synovial sarcomas (n = 125), grade for unclassified sarcomas (n = 140), and sarcomas of other types (n = 158). No parameter was significant for malignant schwannomas (n = 72) or for rhabdomyosarcomas (n = 60). CONCLUSION: In this study, histologic grade appeared as an independent predictor of metastasis development in the main histologic types of adult STS, with the exception of malignant schwannomas and rhabdomyosarcomas.

Adolescent↗

Bands involved in primary chromosome rearrangements in sarcomas are not constitutionally liable to breakage in sarcoma patients.

The localization of breakpoints in spontaneous chromosome aberrations, i.e., chromatid and chromosome gaps, breaks, and exchanges, has been studied in cultured skin fibroblasts from 34 untreated patients with musculoskeletal sarcoma and 38 controls. A total of 325 aberrations in the sarcoma group and 251 in the control group could be assigned to particular bands. The distribution was non-random (P less than 0.001) in both groups. Twenty-one bands in the sarcoma group and 20 in the control group appeared as hot spots, with 11 represented in both groups. Only three hot spots, all of which were present among both patients and controls, coincided with bands involved in primary sarcoma-associated chromosome rearrangements. The results indicate that the chromosome breakage pattern of non-malignant cells is similar in sarcoma patients and controls. Hence, the occurrence of primary structural rearrangements in sarcomas cannot be accounted for by any constitutional proneness to chromosome breakage at these bands.

Adult↗

Review of the distribution of Kaposi's sarcoma-associated herpesvirus (KSHV) in Africa in relation to the incidence of Kaposi's sarcoma.

In the years before human immunodeficiency virus (HIV) infection, the incidence of Kaposi's sarcoma varied markedly across the African continent, and it was a disease primarily affecting men. In contrast, the evidence reviewed here shows that the causal virus-Kaposi's sarcoma associated herpesvirus (KSHV)-is prevalent in many African countries, including places where Kaposi's sarcoma was almost unknown before HIV, and that it is as common in women as in men. Therefore, the geographical distribution of Kaposi's sarcoma in Africa before the spread of HIV and its predominance as a disease affecting men are not a simple reflection of the distribution of KSHV. Since the epidemic of HIV in Africa, Kaposi's sarcoma has become relatively more frequent in women, and the incidence has increased in countries where it was previously rare, but where KSHV is prevalent, as well as in countries where it was already common. These changes point to a role for other (as yet unknown) factors in the aetiology of Kaposi's sarcoma that may have the most effect in the absence of concurrent HIV infection.

Africa↗

Synovial sarcoma. A Scandinavian Sarcoma Group project.

UNLABELLED: Synovial sarcoma accounts for 5-10% of all soft tissue sarcomas. More than 90% are found in the extremities or trunk wall. Characteristic for synovial sarcoma is the translocation t(X;18) (p11.2;q11.2). Cloning of the breakpoints of this translocation revealed fusion of two novel genes, SYT and SSX. The SYT gene, located on chromosome 18, is fused with one of three closely related genes; SSX1, SSX2 or SSX4 located on the X chromosome. The long term survival rates have continuously improved and have at best been reported to around 50%. However, since almost no population based studies on synovial sarcoma have been reported, these improvements may be due to differences in patient selection due to a changes in referral practice. This project was based on a consecutive series of synovial sarcoma patients from the Scandinavian Sarcoma Group Register acquired during a 9-year period. Only surgically treated patients without metastases at diagnosis were included in the prognostic analyses. The tumors were defined clinically, histopathologically, molecular and cytogenetically and these features were related to clinical course. EPIDEMIOLOGY: 34 of 104 patients developed metastases. The overall 5 and 7 years survival rates were 0.76 (95% CI 0.66-0.83) and 0.69 (0.58-0.78), respectively. Large tumor size and amputation were significantly associated with impaired metastasis free survival. In addition, patients with local recurrence had a higher risk for metastases following the local event. HISTOLOGY: All were high grade lesions, 74 Grade III and 30 IV. Kaplan-Meier estimates of metastasis-free survival at 5 years were 83% (95% CI 72-92%) for patients with Grade III tumors versus 31% (95% CI 13-51%) for Grade IV. Histologic grading conveyed more prognostic information than any single histologic factor. Immunostaining with anti-Ki-67 antibodies (MIB1) and p53 based on formalin-fixed paraffin-embedded material from 86 patients revealed that MIB-1 > or = 10% was associated with poorer metastasis-free survival but p53 was not. GENETICS: Type of fusion transcripts (SYT-SSX1 or SYT-SSX2) and Ki-67 were assessed in fresh frozen tissue from 33 patients. The 5-year metastasis-free survival for patients with SYT-SSX1 was 42% versus 89% for those with SYT-SSX2. The hazard ratio for metastasis associated with the SYT-SSX1 fusion transcripts was 7 (95% CI 1.5-36, log-rank p = 0.004). There was a significant association between SYT-SSX1 and high tumor proliferation rate. Comparative Genomic Hybridization revealed DNA sequence copy number changes in 35 of 69 tumor specimens. The frequency of aberrations/tumor were higher in monophasic tumors than in biphasic. Gains of chromosome 8 were associated with large tumors (> 5 cm). There was no obvious association between secondary aberrations and clinical outcome. CONCLUSIONS: Large tumor size, local recurrence, histologic Grade IV, MIB1 index > or = 10 and possibly SYT-SSX1 fusion transcript were associated with impaired clinical outcome.

Adolescent↗

Mutants of nonproducer cell lines transformed by murine sarcoma virus. II. Relationship of tumorigenicity to presence of viral markers and rescuable sarcoma genome.

Tumorigenic and nontumorigenic mutants induced by a single 5'-bromodeoxyuridine (BrdU) treatment of a nonproducer (NP) tumorigenic cell line were isolated and characterized. Among the cloned derivatives were examples of virus-free and sarcoma virus-producing cell lines. Oncogenicity did not correlate with production of virus or ease of rescue of the sarcoma genome. All lines, including nononcogenic derivatives, retained the sarcoma genome. Phenotypic reversion of some cell mutants was observed after in vivo inoculation or long term in vitro cultivation. The M-50T cell line, obtained from a tumor induced by M-50 cells, had a sarcoma genome rescuable by direct superinfection; this was only achieved with parental M-50 cells by a cell fusion rescue technique. The M-43-2T cell, obtained from a single small static tumor induced by otherwise nononcogenic M-43-2 cells, shed sarcoma virus and became tumorigenic. M-58-4-48 became tumorigenic after passage 48 of the M-58-4 line, which was originally nontumorigenic. These observations of phenotypic reversion demonstrate that the presence of the sarcoma gene in cells is an essential but not sufficient condition of tumorigenesis.

Animals↗

[Surgery of recurrent soft tissue sarcoma of the extremities and the trunk wall: a comparison to primary sarcoma].

PURPOSE: To evaluate the place of conservative surgery in locally recurrent soft tissue sarcoma of the extremities and the trunk wall. METHODS: Retrospective data base analysis. Comparison between 32 patients with recurrent sarcoma of the extremities and the trunk wall to 105 comparable patients with primary sarcoma treated from 1996 to 1999. Tumor characteristics, quality of surgery and outcome are analyzed. Mean follow-up are respectively 63 and 61 months. RESULTS: Rates of resections R0 are 56% vs 68%, amputations 13% vs 1%, local recurrences 29% vs 9% (p < 0.01) in recurrent and primary sarcoma, respectively. Two prognostic sub-groups are identified within patients with recurrent sarcoma: good (n = 25) and bad prognosis (n = 7) with resections R0 in 64% vs 29% of patients, five year survival of 76% vs 29%, respectively. The differences are due to tumor biology, anterior treatment, especially radiotherapy, and recurrence-free interval. A decision tree is developed, taking into account precedent radiotherapy and prognosis. CONCLUSION: In recurrent sarcoma, conservative treatment remains possible in a selected group of patients, combined to new means of treatment.

Extremities↗

Radiation-associated sarcoma: a review of 23 patients with postradiation sarcoma over a 50-year period.

Between 1934 and 1983, 23 patients with well-documented diagnosis of radiation-associated sarcoma (RAS) were seen at the University of Michigan Medical Center. The median latent period from irradiation to diagnosis of RAS was 13 years with a minimum latent period of 3 and a maximum of 34 years. All sarcomas originated in previously normal tissues within the irradiated field. Pathology slides available in all patients were reviewed by the same pathologist for the purpose of the study, and the diagnosis of sarcoma was confirmed histologically. There were five bone sarcomas and 18 soft tissue sarcomas. Thirteen patients developed radiation-associated sarcoma following megavoltage treatment with a minimum total radiation dose of 25 Gy in 2 1/2 weeks. The other 10 patients received orthovoltage and/or brachytherapy irradiation alone or combined with external beam radiation. In this group, the radiation doses ranged from 25 Gy to 72 Gy except for one patient who received 8 Gy delivered by orthovoltage irradiation as treatment of knee arthritis. Four patients were originally treated for benign conditions. All the other patients (n = 19) received radiation therapy for a variety of primary malignancies including carcinoma of the cervix (n = 4), brain gliomas (n = 13), Wilm's tumors (n = 2) and retinoblastomas (n = 2), among others.

Adolescent↗

Autoradiographic in vitro study of the cell kinetics of osteogenic sarcomas and Ewing's sarcomas in children.

Proliferation kinetic parameters of 9 osteogenic sarcomas (6 primary tumours, 3 lung metastases) and 3 Ewing's sarcomas were determined using an autoradiographic in vitro method (single and double labelling with 3H- and 14C-thymidine, and 3H-uridine). Osteogenic sarcomas and Ewing's sarcomas, respectively, showed clearly individual pattern of proliferation. The following values were obtained: The average 3H-thymidine labelling indices of 13.8/8.7%, the DNA synthesis times of 12.2/14.4 hours, mitosis times of 1.1/1.9 hours, and mean cell cycle times of 58.0/78.2 hours. The potential tumour doubling times determined with the inclusion of the growth fraction averaged 4.8/5.0 days. Using 3H-uridine labelling of tumours, autoradiography allowed the determination of the growth fraction fair accuracy. It is between 0.26 and 0.71 for osteogenic sarcomas, the average being 0.49. In vitro results were compared with the volume doubling times of metastases of osteogenic and Ewing's sarcomas, reported in the literature which had been determined from series of lung radiographs. The importance of cell kinetic studies of human tumours therapy is demonstrated by a "cell kinetic therapy index".

Autoradiography↗

Biphenotypic sarcomas with myogenic and neural differentiation express the Ewing's sarcoma EWS/FLI1 fusion gene.

Accurate diagnosis of primitive childhood sarcomas continues to be a formidable problem because these malignancies generally demonstrate very little morphological evidence of their tissue of origin. One of these tumor classes, the Ewing's sarcoma family of peripheral primitive neuroectodermal tumors (pPNETs), are thought to have a neural histogenesis based on evidence of neuroectodermal differentiation. Greater than 95% of pPNETs carry t(11;22) or t(21;22) chromosomal translocations which fuse the EWS gene from chromosome 22q12 in-frame with either FLI1 from chromosome 11q24 or ERG from chromosome 21q22. The pPNETs are considered to be histogenetically distinct from rhabdomyosarcomas, myogenic tumors lacking these EWS gene fusions and hypothesized to derive from immature skeletal muscle precursors. In the present study, we describe a unique set of childhood soft tissue sarcomas that show both neural and myogenic differentiation. These biphenotypic tumors express myogenic regulatory factors and muscle-specific antigens and also show neuroectodermal differentiation with ultrastructural evidence of neurosecretory granules and expression of neural-associated genes. Northern analysis and reverse transcriptase PCR reveal expression of EWS/FLI1 gene fusions in all biphenotypic sarcomas analyzed. Chimeric EWS/FLI1 transcripts and fusion proteins in these tumors are identical to those described for pPNETs. Our results provide evidence for a class of biphenotypic childhood sarcomas with myogenic and neural differentiation and suggest that these tumors may be related to the Ewing's sarcoma family of pPNETs.

Adolescent↗

Kaposi's sarcoma-associated herpesvirus in Kaposi's sarcoma occurring in immunosuppressed renal transplant recipients.

Kaposi's sarcoma-associated herpesvirus (KSHV) has been implicated in the genesis of Kaposi's sarcoma and other tumors occurring in immunosuppressed individuals. Using amplification by the polymerase chain reaction and nucleotide sequencing of extracted DNA, we have detected the KS330(233) sequence of KSHV DNA in Kaposi's sarcoma tissue from 4 immunosuppressed renal transplant recipients. The sequences shared a greater than 98% homology with those described in KSHV DNA from Kaposi's sarcoma in patients with acquired immunodeficiency syndrome. In another 2 renal transplant recipients KSHV DNA could not be detected in scar tissue at the site of previous Kaposi's sarcoma that had resolved after immunosuppression was discontinued and haemodialysis recommenced. These findings support the hypothesis that KSHV may be the infectious agent concerned in the genesis of Kaposi's sarcoma.

Acquired Immunodeficiency Syndrome↗

Uterine Sarcomas With Recurrent KDM2B Gene Fusions: Three Cases of a Possible Novel Subtype of High-Grade Endometrial Stromal Sarcoma.

The advent of widespread genomic testing of uterine mesenchymal tumors has led to novel insights into the biology of these diverse tumors, and many genomically defined entities have been described in recent years. During a larger study of endometrial stromal sarcomas and unclassified uterine sarcomas, we identified 3 tumors harboring KDM2B gene fusions. Patients were 32, 61, and 67 years old, and all initially underwent incomplete sampling via laparoscopic myomectomy (n = 1), laparoscopic biopsy (n = 1), or hysteroscopic myomectomy (n = 1). One patient's tumor was densely adherent to the pelvic sidewall; she was treated with chemotherapy and died of widely metastatic disease at 29 weeks. Another underwent a subsequent recent hysterectomy with the tumor confined to the uterus and minimal follow-up to date. The final patient refused further treatment and was alive at 28 weeks, although the status of the disease progression was unknown. On microscopic examination, 2 tumors showed infiltrative borders, whereas interface with the myometrium was not present in the third. The tumors were variably cellular with alternating hypercellular and hypocellular zones in a myxoid to loosely collagenous stroma. The hypercellular areas contained round to ovoid cells in diffuse (n = 3) and sex cord-like arrangements, including cords (n = 3), nests (n = 2), and tubules (n = 1); 2 also contained occasional spindled cells arranged in vague fascicles. These cells showed moderate atypia with open chromatin, numerous mitoses (8, 24, and 25 per 10 high-power fields), and frequent apoptosis. The hypocellular areas contained sparse, ovoid-to-spindled cells with minimal atypia. All tumors were diffusely positive for cyclin D1, whereas BCL6 corepressor was diffusely positive in 1 and negative in 2; desmin and caldesmon were negative in all 3 neoplasms. All harbored KDM2B gene fusions; partner genes included EPC1, EP400, and CITED1. MDM2 amplification was also noted in 2. Clustering analysis based on RNA expression profiling revealed tight clustering of all 3 tumors within the broad group of high-grade endometrial stromal sarcomas. Based on the overall clinicopathologic and genomic features, we suggest that these tumors may represent a novel subtype of uterine sarcoma and may be best classified as high-grade endometrial stromal sarcoma, although additional confirmatory studies are needed.

Humans↗

Sarcoma viruses containing the mos oncogene induce lesions resembling Kaposi's sarcoma.

Kaposi's sarcoma is most accurately described as a multifocal angioproliferative lesion primarily involving the skin, although some studies indicated concomitant and/or exclusive visceral involvement. The mechanism(s) involved in Kaposi's sarcoma development, especially AIDS multiorgan distributed form, is not completely understood. Recent reports have identified a murine retrovirus, MoMuSV-349 that induces multiorgan disseminated angiosarcomatous tumors which resemble Kaposi's sarcoma when virus is inoculated intraperitoneally in newborn BALB/c mice. Performed time point experiment on mice infected with MoMuSV-349 indicated a two stages development of Kaposi's sarcoma-like tumors; sarcomatous and angiosarcomatous. Preliminary studies have demonstrated the pathogenesis of the disease process and the role of angiogenic growth factors released by the spindled cells in the stage development of mouse tumors. It is hypothesized that growth factors such as fibroblast growth factors released by the spindled cells stimulate the proliferation of endothelial cells and neovascularization which is an essential component of Kaposi's sarcoma-like tumors. Understanding the mechanism(s) of endothelial cells proliferation and neovascularization as a response to viral insult and microenvironmental changes will raise the possibilities of developing new therapeutic approaches to block this process.

Acquired Immunodeficiency Syndrome↗

Nuclear beta-catenin correlates with cyclin D1 expression in spindle and pleomorphic sarcomas but not in synovial sarcoma.

Nuclear beta-catenin staining in soft tissue sarcomas (STSs) has been shown to correlate with tumor progression as assessed by proliferative activity or poor prognosis. Frequent activation of Wnt signaling pathway has been also shown in synovial sarcoma (SS), suggesting a specific role of this pathway in SS. We examined roles of nuclear beta-catenin staining within soft tissue sarcomas. Immunohistochemical detection of nuclear beta-catenin accumulation correlated with cyclin D1 overexpression in spindle cell and pleomorphic sarcomas (P = .037), and the expression of these proteins evenly distributed throughout each section. In some cases, strong beta-catenin nuclear staining was observed in highly pleomorphic and mitotic cells. Furthermore, tumors with nuclear beta-catenin accumulation showed statistically significant increasing cyclin D1 mRNA expression level compared with those without (P = .023). Cyclin D1 mRNA expression levels were statistically higher in tumors with cyclin D1 overexpression than in tumors without (P = .037), suggesting that cyclin D1 overexpression is due to transcriptional activation. However, these correlations could not be detected in SS. In biphasic SS, beta-catenin nuclear staining was observed in spindle cells, whereas cyclin D1 nuclear staining was seen in glandular areas where beta-catenin kept membranous expression. Mutations in exon 3 of the beta-catenin gene and in the mutation cluster region of adenomatous polyposis coli gene were absent in this series of cases. Thus, cyclin D1 could be considered as one of the targets of the nuclear beta-catenin in spindle cell and pleomorphic sarcomas. A possible association between beta-catenin accumulation and spindle cell morphogenesis may exist in SS.

Cell Nucleus↗

Brachytherapy in the combined modality treatment of pediatric malignancies. Principles and preliminary experience with treatment of soft tissue sarcoma (recurrence) and Ewing's sarcoma.

Radiotherapy is an integral part in the treatment of soft tissue and Ewing's sarcoma in children. By brachytherapy a high dose can be delivered in a restricted volume with sparing of normal tissues surrounding the target. Taking into account this principle potential benefit brachytherapy may play some role in the local treatment especially in children. However, only limited experience with pediatric brachytherapy has been reported apart from a few centers, which have gained their experience with Low-Dose-Rate (LDR)-brachytherapy. Since 1991 - 12 patients with soft tissue sarcoma and 6 patients with Ewing's sarcoma were treated with High-Dose-Rate (HDR) and Pulse-Dose-Rate (PDR)-brachytherapy at the departments of radiotherapy in Münster, Kiel and Vienna. The combined modality treatment was performed according to the CWS-86/91, EICESS-92 and CESS/CWS-REZ-91 protocols. In 8 patients with soft tissue sarcoma brachytherapy was part of the recurrence treatment regime, in 4 patients brachytherapy was part of the primary treatment alone or in combination with external beam therapy. In HDR-treatment a dose of 15 to 43 Gy was delivered in 3 to 16 fractions, in PDR-treatment 13 to 36 Gy in fractions of 1 Gy/hour. Follow-up is 3-39 months (median 14 months). 7 patients show no evidence of disease, 9 patients are locally controlled and 3 patients progressed locoregionally. In 6 patients with Ewing's sarcoma brachytherapy was performed intraoperatively as a boost treatment after external beam therapy (50-55 Gy), if no wide resection could be achieved within first line-treatment. A dose of 10-12 Gy was applied in one fraction in a limited volume (20-50 ccm) at the time of surgery. Follow-up is 13-26 months (median 21 months). There is no evidence of disease in all patients, perioperative and subacute morbidity was not increased. These encouraging preliminary results with HDR/PDR-brachytherapy must be further evaluated prospectively and systematically within an interdisciplinary approach by some specialized collaborating centers, which not only have the equipment (HDR/PDR/(LDR)-brachytherapy) but also can meet the complex demands to accumulate the necessary experience.

Adolescent↗

Analysis of clinicopathologic prognostic factors for 157 uterine sarcomas and evaluation of a grading score validated for soft tissue sarcoma.

BACKGROUND: Uterine sarcomas (US) are rare and carry a poor prognosis characterized by high rates of local recurrence and metastasis. The aim of this study was to test, for what the authors believe was the first time with US, the prognostic impact of the histologic grade validated by the French Federation of Anticancer Centers (FNCLCC) for soft tissue sarcomas (STS). The grade is the sum of the scores allocated for three major histologic criteria: tumor differentiation, mitotic count, and tumor necrosis. Other histologic and clinical factors were tested as well. METHODS: The study included 157 patients in whom 78 leiomyosarcomas (LMS), 52 malignant mixed müllerian tumors (MMMT), and 27 endometrial stroma sarcomas (ESS) were documented. RESULTS: The median follow-up was 54 months (range, 6-230 months). The median OS and EFS were 33 and 13 months, respectively. The FNCLCC grade validated in soft tissue sarcomas was not a prognostic factor for survival or relapse for any of the US histologic subtypes. For LMS, stage and mitotic count were the only factors that had an influence on survival and relapse. For MMMT, stage and age were the only prognostic factors, and none of the histologic criteria impacted on the outcome. For ESS, the grade defined by Norris and Taylor was an important prognostic factor, particularly for survival. CONCLUSIONS: The FNCLCC grading score could not be used as a prognostic indicator for uterine sarcomas. The diagnosis of US is in itself an unfavorable prognostic factor, except when the diagnosis is low grade ESS.

Adult↗

Postirradiation sarcoma of the head and neck: a report of three late sarcomas following therapeutic irradiation for primary malignancies of the paranasal sinus, nasal cavity, and larynx.

Sarcoma of the head and neck region following irradiation for primary malignancy other than retinoblastoma has rarely been reported. Three cases of postirradiation sarcoma arising in the head and neck region following definitive radiotherapy for primary malignancies of the nasal cavity, paranasal sinuses, and larynx are presented. The intervals from initial radiation to diagnosis of sarcoma were 10 years, 10 1/2 years, and 12 1/2 years, respectively. The dosage ranged from 6000--6400 rads using conventional fractionation (1750--1811 ret) on a 60Cobalt teletherapy unit. Methotrexate (25 mg I. V. every three days for seven doses) was utilized during the initial course of radiation in two of the three patients. The cases conform well to established criteria for the diagnosis of radiation-induced sarcoma. Postirradiation sarcoma of the head and neck region is a remote hazard that must be weighed against the benefits of curative radiation therapy, particularly when treating in the presence of bone disease or when treating retinoblastoma or benign lesions.

Adult↗

The interaction of Kaposi's sarcoma with monoclonal antibodies to human sarcoma and connective tissue differentiation antigens.

Four monoclonal antibodies (McAbs) previously generated against human soft tissue sarcomas and reacting with connective tissue differentiation antigens were evaluated for their interaction with tissues obtained from patients with classic Kaposi's sarcoma. Biopsy was performed on active neoplastic lesions from the skin of 26 patients, frozen sections were prepared, and the binding of the McAbs was tested using the indirect immunofluorescence assay. Clinically uninvolved skin from the same patients as well as skin and muscle from eight non-cancer patients were treated similarly and served as controls. McAbs IXG11, 23H7, IIIE5, and 15G5 interacted strongly with the Kaposi's sarcoma lesions and weakly with the uninvolved skin in 22 of 26 (84%), 23 of 26 (88%), 12 of 14 (85%), and 1 of 6 (16%) of the patients, respectively. IXG11, 23H7, and IIIE5 interacted weakly with the skin of seven of eight non-cancer patients. McAb 15G5 was found to bind strongly to tumor lesions, to the respective uninvolved skin in four of five Kaposi's sarcoma patients, and also to skin and connective tissues of muscle from non-cancer patients. The mode of interaction was morphologically different for each McAb. It is suggested that McAbs IXG11, 23H7 and IIIE5 identify markers whose expression is markedly increased in Kaposi's sarcoma lesions as compared with uninvolved skin of the same patients. These markers may serve as immunologic probes for the investigation of this neoplastic process.

Adult↗