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Treatment of pelvic sarcomas in adolescents and young adults with intensive combined modality therapy.

Adolescent and young adult patients with pelvic sarcomas continue to have a poor prognosis with standard combination chemotherapy and local irradiation. In addition to a significant risk of local failure, these patients are at high risk for systemic relapse. Twenty-three consecutive patients with Ewing's sarcoma, alveolar rhabdomyosarcoma, undifferentiated sarcoma, or malignant peripheral neuroepithelioma originating in the pelvis were treated with short, intensive combined modality therapy. This approach integrates 5 cycles of VADRIAC chemotherapy (Vincristine, Adriamycin, Cyclophosphamide) with high dose irradiation to the primary lesion (55-60 Gy) and sites of gross metastatic disease (45-50 Gy). Following achievement of a complete response, intensification therapy consisting of total body irradiation (TBI) (8.0 Gy), high dose VADRIAC chemotherapy, and autologous bone marow transplantation is given. All therapy is completed within 6-7 months. No maintenance chemotherapy is given; no surgery is intended. Of the twenty-three patients with pelvic sarcomas treated on this combined modality protocol, 22 achieved a complete remission. Local control was achieved and maintained in all twenty-three patients. With a median follow-up of 21 months since initiation of treatment, there have been nine relapses (all systemic). Seven relapses occurred among the thirteen patients who presented with overt metastatic disease and the other two relapses were among the ten patients with localized disease at presentation. All seven metastatic patients who relapsed have died, whereas both of the relapsed localized patients remain alive. Acute and late toxicities have been acceptable using this aggressive combined modality approach. Induction chemotherapy had a significant impact on reduction of the typically large (greater than 10 cm diameter) soft tissue mass associated with these pelvic tumors, thus facilitating achievement of local control by high dose irradiation. Of 18 patients with measureable soft tissue tumor, all experienced a partial response (greater than 50% reduction in size) following the initial two cycles of chemotherapy given prior to local irradiation. In conclusion, this short, intensive chemoradiotherapeutic regimen is highly effective in controlling the primary lesion (100% local control) and inducing a complete response in a high proportion (96%) of these high risk pediatric and young adult patients with pelvic sarcomas. The role of TBI as "systemic" adjuvant therapy to control micrometastatic disease is discussed as still under investigation.

Adolescent↗

Current soft-tissue sarcoma classifications.

In order to analyse the impact of modern sarcoma classification criteria, pathological material from 281 extremity soft-tissue sarcomas (STS) was reviewed. The cases were originally diagnosed between 1972 and 1994, and the most frequent diagnoses then were malignant fibrous histiocytoma (MFH) (26%), liposarcoma (21%), fibrosarcoma (11%), and leiomyosarcoma (10%). After reclassification, the proportions had changed significantly, with the largest group now being leiomyosarcomas (20%), liposarcomas (17%), synovial sarcomas (14%), and sarcomas "not otherwise specified" (NOS) (11%). The original diagnosis was changed in 57% of the cases; in particular, the number of fibrosarcomas was reduced from 32 to 6, and MFHs from 72 to 2, with 22 renamed as myxofibrosarcomas; 20 (7%) were found not to be sarcomas. The main reasons for these results are the recent advances in immunohistochemistry (IHC) together with changes in nomenclature. The findings have obvious implications, in particular for retrospective research.

Fibrosarcoma↗

Integrated Clinicopathologic and Multiomic Profiling Reveals MEIS1-Rearranged Sarcoma as a Distinct Entity With 2 Prognostic Subgroups.

Sarcomas with MEIS1 fusions represent a rare, recently recognized group of mesenchymal neoplasms with a predilection for genitourinary and gynecologic sites. A subset exhibits skeletal muscle differentiation resembling spindle cell rhabdomyosarcoma. Existing literature is limited to case reports and small series, with scant comprehensive clinicopathologic, molecular, and outcome data. In this study, we analyzed a multi-institutional cohort of 20 MEIS1-rearranged sarcomas using integrated clinicopathologic review, genomic profiling, and DNA methylation analysis. The tumors occurred in 17 females and 3 males (median age, 41 years; range, 6-58 years), arising mainly in the uterus/vagina (n = 12), vulva/perineum (n = 4), bone (n = 2), and kidney (n = 2), with a median size of 9 cm (range, 2.5-20 cm). Histology showed mostly bland spindle cells in fascicles/storiform patterns, alternating cellularity, fibromyxoid stroma, prominent vascularity, and adipose metaplasia (45%). A subset of cases featured high-grade morphology with epithelioid cells and increased mitotic activity. Skeletal muscle markers were variably positive in 9 cases. Fusions involved MEIS1 with NCOA2 (16/20), NCOA1 (3/20), or FOXO1 (1/20). Recurrent additional genomic alterations included CTNNB1 mutations (31.6%) and MDM2 amplification (15%). DNA methylation profiling showed that MEIS1-rearranged sarcomas formed a unifying cluster comprising 2 subgroups, regardless of rhabdomyosarcomatous phenotype, clearly separated from other mesenchymal neoplasms, including various rhabdomyosarcoma subtypes and uterine sarcomas. The 2 DNA methylation (Meth) subgroups correlated with differences in genome-wide copy number variation (CNV) status (Meth-CNV high vs Meth-CNV low), with Meth-CNV high tumors characterized by high mitotic rate, frequent tumor necrosis, recurrent co-occurring CTNNB1 and MDM2 alterations, and recurrent chromosomal arm-level changes. Most importantly, this subgroup exhibited significantly worse overall survival (P = .027) and disease-free survival (median, 5 vs 99 months; P = .017). This study establishes MEIS1-rearranged sarcoma as a distinct entity with generally indolent but potentially aggressive behavior. The 2 methylation/CNV subgroups provide potential utility for prognostic stratification and highlight actionable molecular targets in high-risk cases.

Humans↗

Uterine sarcomas express KIT protein but lack mutation(s) in exon 11 or 17 of c-KIT.

OBJECTIVE: Several tumors express the protein product of the protooncogene c-KIT. Some of these respond to imatinib mesylate, a tyrosine kinase inhibitor. The tumors that respond frequently have mutation(s) in exon 11 of c-KIT that encodes for the regulatory juxtamembrane helix. Some tumors that express KIT protein have mutation(s) in exon 17 of c-KIT; however, these do not respond to imatinib mesylate. This investigation was performed to determine the expression of KIT protein and mutational status of exons 11 and 17 of c-KIT in uterine sarcomas. METHODS: Twenty-five uterine sarcomas treated from 1990 to 2002 were evaluated. These included 14 malignant mullerian mixed tumors (MMMT), 7 leiomyosarcomas (LMS), 2 endometrial stromal sarcomas (ESS), and 2 high-grade heterologous sarcomas (HGHS). Formalin-fixed, paraffin-embedded tissue sections were immunostained with anti-KIT antibody (Santa Cruz Biotechnology, Santa Cruz, CA) with a semiquantitative assessment. Normal myometrium when present in the section was used as an internal negative control. Areas of tumor were microdissected followed by DNA extraction, polymerase chain reaction (PCR) amplification of exons 11 and 17, single-strand conformational polymorphism (SSCP), and DNA sequencing to detect the presence of mutation(s). RESULTS: All 25 tumors expressed KIT protein at varying levels as assessed by immunohistochemistry. The staining was diffuse and of moderate to strong intensity in 22 tumors. In three tumors (one of each type except MMMT) the staining intensity was weak. In MMMT the epithelial and sarcomatous foci stained similarly. No mutation(s) in exons 11 or 17 of c-KIT were identified in 24/25 tumors. One LMS had deletion of both exons 11 and 17. CONCLUSIONS: Although uterine sarcomas express KIT protein, they lack KIT-activating mutation(s) in exon 11 or 17 of c-KIT. Therefore, these tumors are unlikely to respond to imatinib mesylate.

Adult↗

Parenchymatous pulmonary endometriosis - metastases of a low-grade endometrial stromal sarcoma?

Based on the data of a case of parenchymatous endometriosis of the lung in which three and a half years later a low-grade endometrial stromal sarcoma of the uterus was diagnosed the origin of this disease is discussed. The follow up of this patient gave the impression that the pulmonary nodules were early metastases of low-grade endometrial stromal sarcoma, which was initially not detected in the routine gynecologic examination. Furthermore, as histological and immunohistochemical examinations are not sufficient to distinguish reliable between endometriosis of the lung and pulmonary metastases from low-grade endometrial stromal sarcoma. In literature, in none of the few cases of parenchymatous pulmonary endometriosis a hysterectomy was performed to exclude a low-grade endometrial stromal sarcoma. Thus, parenchymatous pulmonary endometriosis nodules might be metastases and their occurrence should cause the treating physician to consider a distant metastatic spread from low-grade endometrial stromal sarcoma.

Endometrial Neoplasms↗

Uterine sarcoma: twenty-seven years of experience.

PURPOSE: A correlation of treatment for uterine sarcoma with outcome, prognostic importance of pathology, and clinical parameters. PATIENTS AND METHODS: One hundred forty-one patients (median age: 56 years, range: 19-85 years) with a histologically verified uterine sarcoma were identified from a database compiled at the Royal Marsden Hospital and the University of Florence between 1974 and 2001. Seventy-two patients had leiomyosarcoma, 42 had mixed müllerian tumors, 22 had endometrial stromal sarcoma, 1 hemangiopericytoma, 1 rhabdomyosarcoma, and 3 patients had unspecified sarcoma. According to FIGO classification, Stage I, II, III, and IV tumors were identified in 71, 13, 31, and 26 patients, respectively. RESULTS: At the time of analysis, 73.7% of patients were dead, and 26.3% were alive with a median survival of 2 years from initial diagnosis. Univariate analysis for cause-specific survival demonstrated statistical significance for histology (p = 0.02), grade (p = 0.003), stage (p = 0.007), and age (p = 0.02). Multivariate analysis demonstrated significant prognostic values for stage (p = 0.02) and histology (p = 0.05) only. Postoperative radiotherapy with a total dose higher than 50 Gy seems to be significant (p = 0.001) in reducing local recurrence. CONCLUSIONS: Our data favor treatment for Stages I, II, and III of uterine sarcoma with radical surgery plus radical dose irradiation comprising both external beam radiotherapy and brachytherapy.

Adult↗

p53 expression and its relationship to DNA alterations in bone and soft tissue sarcomas.

The p53 gene is one of the best studied tumour suppressor genes. Recently we performed mutation analysis on the p53 gene in a large number of bone and soft tissue sarcomas, and found that approximately one-third of the sarcomas have some type of DNA alteration at the p53 locus (Toguchida et al., 1992). However, the expression of the p53 protein resulting from these alterations still remains to be clarified. In this study, p53 expression in the sarcoma tissues was analysed immunohistochemically using antibody PAb421 (Oncogene Science) and its relationship to DNA alterations was examined. Of 113 tumours, 29 (25.7%) showed positive staining for the p53 protein. These included 19 of 67 osteosarcomas, five of 20 chondrosarcomas, four of 11 malignant fibrous histiocytomas (MFHs) and one Ewing's sarcoma. In chondrosarcomas, most of the p53-positive tumours belonged to highly malignant and atypical tumour types (dedifferentiated or mesenchymal type), suggesting a role for p53 mutation in the progression of cartilaginous tumours. All the cases with a missense mutation showed strongly positive staining, while no immunoreactivity was observed in the remaining three-quarters with DNA alterations including gross rearrangement, frame-shift mutation, nonsense mutation or mutation at splicing site except in one case. These results demonstrated the dominance of the p53 mutations with null protein expression in bone and soft tissue sarcomas, showing a unique characteristic of these types of tumours compared with other malignancies such as colon carcinomas.

Base Sequence↗

p53: functions, mutations and sarcomas.

The p53 gene is the most commonly altered gene in a multitude of human cancers. The alterations can be acquired somatically or transmitted through the germ-line. Bone and soft tissue sarcomas are frequently found to have acquired abnormalities in the p53 and mdm-2 genes. In soft tissue sarcoma, the amplification of the mdm-2 gene and the binding of its oncogene product to wild-type p53 protein functionally inactivates normal p53-regulated growth. Inherited mutations of the p53 gene are associated with the rare Li-Fraumeni familial cancer syndrome. Various tumor types arise in these families, with sarcomas of the bone and soft tissues and carcinoma of the breast being the most frequently observed. Transgenic mice with highly expressed mutated p53 have a higher incidence of tumors, including predominantly osteosarcomas and soft tissue sarcomas. In close similarity with the Li-Fraumeni syndrome, homozygously p53-null mice (transgenic mice carrying two non-functional p53 allele) are developmentally normal however they are susceptible to spontaneous tumor formation. This article reviews briefly the structure, function, and dysfunction of the p53 tumor-suppressor gene with particular focus on its role in the development of bone and soft tissue sarcoma.

Animals↗

CYTOCHEMICAL LOCALIZATION OF ADENOSINE TRIPHOSPHATASE IN THE MITOTIC APPARATUS OF HELA AND SARCOMA 180 TISSUE CULTURE CELLS.

ATPase was localized in distinct regions of the mitotic apparatus of HeLa and Sarcoma 180 tissue culture cells. ATPase was demonstrated in the metaphase spindle of HeLa and Sarcoma 180 cells fixed in cold buffered 2 per cent formalin (pH 6.5 to 6.8) containing 2 x 10(-3)M CaCl(2). A high concentration of ATPase was frequently observed at the poles of the spindle. ATPase was also demonstrated in the interzonal region of both cell types during anaphase. The narrowing of the band of ATPase activity localized in the interzonal region during telophase indicates that ATPase activity is associated with the central spindle. In polar views of Sarcoma 180 cells fixed in cold, unbuffered, 2 per cent formalin, ATPase was frequently localized in granules in the region of the inner circumference of the ring of chromosomes formed at metaphase. ATPase in the mitotic apparatus of HeLa and Sarcoma 180 cells was shown not to be due to non-specific alkaline phosphatase. Mitotic apparatus ATPase in Sarcoma 180 cells was suppressed by an -SH inhibitor.

Adenosine Triphosphatases↗

Recovery of avian sarcoma virus from tumors induced by transformation-defective mutants.

Transformation-defective (td) mutants of the Schmidt-Ruppin strain of Rous sarcoma virus (RSV), which contains deletions in the gene responsible for transformation (src gene), are unable to transform chicken embryo fibroblasts in vitro. Injection of some of these td mutants into newborn chickens resulted in the formation of sarcomas from which sarcoma virus was unfailingly recovered. The possibility that transforming RSV was present in the td virus preparations was excluded by further purification of the td viruses. Morphology of the foci induced by the newly recovered sarcoma virus was distinct from that of foci induced by the parental Schmidt Ruppin strain of RSV. It is suggested that the new sarcoma virus was generated as a result of the genetic interaction between the genomes of td virus and chicken cells.

Animals↗

Incidence and mechanisms of infiltration of sarcomas in the shoulder.

The intraarticular infiltration of sarcomas around the shoulder was analyzed. Of 58 sarcomas located around the shoulder, which were treated between 1993 and 1998, 15 osteosarcomas, 12 chondrosarcomas, and one Ewing's sarcoma that abutted the shoulder were selected. Radiologic images of 28 tumors were analyzed and compared with pathologic examinations. In 17 of 28 sarcomas (15 in the proximal humerus and two in the scapula), joint infiltration was suspected radiologically because of the existence of a tumor mass probably inside the joint or disruption of the joint surface and protrusion of the tumor. Seven of 17 tumors with radiologically positive and zero of 11 tumors with radiologically negative findings showed histologically positive findings for tumor inside the joint. Four of 11 osteosarcomas and three of four chondrosarcomas of the proximal humerus showed histologic findings of joint infiltration. Pericapsular extension was seen in two patients, direct articular spread with a pathologic fracture was seen in two patients, direct articular spread was seen in one patient, direct articular spread with pericapsular extension was seen in one patient, and pericapsular extension with a pathologic fracture was seen in one patient. The current study showed that pericapsular or direct articular infiltration into the glenohumeral joint is a phenomenon in sarcoma around the shoulder. Exact assessment of tumor existence inside the joint can be difficult in osteosarcoma and chondrosarcoma, so abnormal radiologic findings should be regarded as proof of existence of tumor, and extraarticular wide resection should be planned.

Adolescent↗

Diagnosis of synovial sarcoma with the reverse transcriptase-polymerase chain reaction: analyses of 84 soft tissue and bone tumors.

The chimeric transcript SYT-SSX is generated as a result of reciprocal translocation t(X;18), which is the primary cytogenetic abnormality found in, and appears to be specific for, synovial sarcoma. We performed a reverse transcriptase-polymerase chain reaction (RT-PCR) for SYT-SSX transcripts in a series of 84 tumors (61 soft tissue tumors and 23 bone tumors), including a variety of histologic types, to assess its usefulness in molecular diagnosis. Ten synovial sarcomas, three tumors initially unclassified, and one malignant peripheral nerve sheath tumor contained the chimeric transcripts. A review of the original slides and additional examination showed that a diagnosis of synovial sarcoma was appropriate for these cases. Additionally, in situ hybridization with an SSX1 probe indicated that the chimeric transcripts exist not only in the cells of special components but also in cells showing a variety of histologic patterns. Therefore, RT-PCR can be considered a useful molecular biological technique that can provide objective evidence for diagnosis of synovial sarcoma. Northern blot analysis with an SSX1 probe also detected chimeric SYT-SSX transcripts in the synovial sarcoma cases. The additional smaller bands, however, were also detected in six peripheral primitive neuroectodermal tumors (pPNETs) and one embryonal rhabdomyosarcoma. In five of these pPNETs, other bands ranging in size from 2.0 to 2.2 kb were also found, and it seems possible that these bands might represent novel karyotypic aberrations and/or splicing variants of SSX.

Adult↗

Staining for factor VIII related antigen and Ulex europaeus agglutinin I (UEA-I) in 230 tumours. An assessment of their specificity for angiosarcoma and Kaposi's sarcoma.

In this study we examined the staining reactivity of commercially available antisera to factor VIII related antigen (F VIII RAg) and Ulex europaeus agglutinin I (UEA-I) on sections from 230 formalin fixed paraffin embedded tumours. These included 196 sarcomas, 20 carcinomas and 14 angiomas. All angiomas showed positive staining for F VIII RAg; all carcinomas showed negative staining; the vasoformative areas of all angiosarcomas stained positively but only four of six angiosarcomas showed positive staining of their solid areas; of seven Kaposi's sarcomas, all showed positive staining of vessels and six showed positive staining of the spindle cell component. In the remaining 181 non-vascular sarcomas there was a false positive result in four tumours (2.2%), three of which had a history of irradiation. Pre-radiotherapy biopsies of these three tumours stained negatively with anti-F VIII RAg. UEA-I was demonstrated in all the angiomas studied, in all angiosarcomas (including the solid components) and in well-formed vessels of all Kaposi's sarcomas, but only in the spindle cell component of 3/6. However, there was an unacceptably high rate of false positive staining amongst the carcinomas and non-vascular sarcomas. In conclusion, F VIII RAg is a specific but not a sensitive marker of angiosarcomas; UEA-I is a sensitive but not a specific marker of angiosarcomas.

Adolescent↗

Nucleotide sequence analysis of the long terminal repeat of integrated simian sarcoma virus: evolutionary relationship with other mammalian retroviral long terminal repeats.

Nucleotide sequence analysis of the long terminal repeat (LTR) of the integrated simian sarcoma virus showed that the simian sarcoma virus LTR comprised 504 nucleotides with an inverted repeat of seven bases at its 5' and 3' termini. At the site of simian sarcoma virus integration, cellular flanking sequences adjacent to the proviral LTR contained a direct repeat of four bases. A 13-base sequence after the 5' LTR was found to be complementary to prolyl tRNA, suggesting that tRNAPro may serve as the primer for reverse transcription of simian sarcoma virus RNA. The U5 and R regions, derived respectively from the 5' end and terminally redundant sequences of the viral RNA, were found to have similar organization and sequence homology close to that of Moloney murine sarcoma virus or Moloney murine leukemia virus. These results indicate that regions within LTRs with known functionally important sequences have been most well conserved during retrovirus evolution.

Biological Evolution↗

Cervical and peritoneal fluid cytology of uterine sarcomas.

OBJECTIVE: To study the cytologic features of uterine sarcoma. STUDY DESIGN: The pathology records of 102 patients with uterine sarcoma were reviewed. Four patients, including one case of leiomyosarcoma (LMS), one high grade stromal sarcoma (HGSS) and two malignant mixed müllerian tumor (MMMT), had abnormal cervical and/or peritoneal cytologic findings. Three abnormal cervical smears and two abnormal peritoneal fluids from these patients, including immunohistochemically stained sections of cell block, were reviewed. RESULTS: The diagnostic cells appeared in clusters or in isolation. They had enlarged and hyperchromatic nuclei. Occasional mitotic figures were seen. The cells were considered suspicious for malignancy in cervical smears of HGSS and in the peritoneal fluid of LMS. Adenocarcinoma cells were identified in both the cervical smear and peritoneal fluid of one patient with MMMT. Atypical cells were found in another patient with MMMT. CONCLUSION: Positive cervical or peritoneal cytology is uncommonly detected in association with uterine sarcomas. Even when abnormal cells are found, it may be difficult to give a definitive diagnosis of uterine sarcoma based directly on the cytomorphologic characteristics of cervical or peritoneal smears. However, such a possibility should be kept in mind by the cytopathologist to avoid missing the diagnosis.

Adenocarcinoma↗

Allograft reconstruction of the acetabulum after resection of stage-IIB sarcoma. Intermediate-term results.

Seventeen consecutive patients were managed with an allograft reconstruction of the pelvis (including the acetabulum) following resection of a stage-IIB bone sarcoma during a twelve-year period. The initial diagnosis was chondrosarcoma in nine patients, osteosarcoma in six, Ewing sarcoma in one, and leiomyosarcoma in one. All patients who had osteosarcoma or Ewing sarcoma received chemotherapy preoperatively and postoperatively. Fifteen patients were managed with an allograft-total hip prosthesis composite. Two patients initially were managed with an osteoarticular allograft without a prosthesis, but one had a subsequent revision to an allograft-implant composite. Four patients died with an intact allograft reconstruction. Eight patients survived with an intact allograft reconstruction, and they were followed for at least four years (mean, seven years; maximum, fourteen years). All but one was able to walk in the community with one or two canes at the time of the latest follow-up. There was a high rate of local recurrence, which occurred in three of the seventeen patients, and of infection, which developed in two patients. The five patients had a subsequent hindquarter amputation or removal of the allograft. The mean functional score (and standard deviation), according to the rating system of the Musculoskeletal Tumor Society, was 65 +/- 21.16 per cent (median, 70 per cent; range, 13 to 87 per cent) for the thirteen patients who were thus evaluated. Preservation of the limb and reconstruction with an allograft may be considered as an alternative to hindquarter amputation in carefully selected patients who have a bone sarcoma involving the acetabulum. However, patients who have a high-grade bone sarcoma must be warned that there is a substantial risk of local recurrence or infection. In the present series, more than half of the patients either died or had failure of the reconstruction.

Acetabulum↗

Primary renal synovial sarcoma confirmed by cytogenetic analysis: a lesion distinct from sarcomatoid renal cell carcinoma.

Primary synovial sarcoma rarely originates in the renal parenchyma. When this occurs, origin of this unusual tumor type has been the subject of debate in the literature, with a suggestion that previously reported cases may be more correctly described as renal cell carcinoma with sarcomatoid dedifferentiation. Synovial sarcoma and sarcomatoid renal cell carcinoma may be indistinguishable on pure histologic and immunohistochemical grounds, but these tumors contain distinctly different sets of chromosomal abnormalities. Most previous cases of primary renal synovial sarcoma were confirmed by molecular biology techniques, which detected the SYT-SSX gene fusion transcript typical of this tumor, but no details of the other chromosomal anomalies have been published. We report a case of primary renal synovial sarcoma confirmed by standard cytogenetic analysis, showing the characteristic t(X; 18)(p11.2:q11.2) translocation and other chromosomal aberrations that are typical of synovial sarcoma as opposed to sarcomatoid renal cell carcinoma.

Carcinoma, Renal Cell↗

Uterine sarcomas in South African black women: a clinicopathologic study with ethnic considerations.

BACKGROUND: There is considerable evidence for a higher incidence of uterine sarcomas in blacks when compared to whites. However, whether this higher incidence is related to differences in clinicopathologic presentation is not known. PATIENTS AND METHODS: We reviewed slides and clinical charts of 81 patients with a primary diagnosis of uterine sarcoma referred between 1991 and 1999 to Kalafong Academic and Pretoria Academic Hospital. After review, 49 cases remained for study. RESULTS: Uterine sarcomas were distributed between leiomyosarcoma (LMS) (39%), carcinosarcoma (CS) (49%) and endometrial stromal sarcoma (ESS) (12%). LMS and ESS tend to present at an earlier age when compared to CS (respectively p < 0.008 and 0.02). Of women with LMS more women are premenopausal when compared to CS (p < 0.009). Lower abdominal pain is more common in LMS (p < 0.009), whereas bleeding is more common in women suffering from CS (p < 0.01). Lymphovascular space involvement and cervical involvement are more common in CS when compared to LMS. In CS, the carcinoma component has most of the metastatic potential. CONCLUSION: Among black South African women different clinicopathologic features for uterine LMS, CS and ESS are observed. We also present genetic and/or hormonal factors possibly contributing to the pathophysiology of uterine sarcomas in blacks.

Age Factors↗