39 research outputs found
Association of EWS-FLI1 Type 1 Fusion with Lower Proliferative Rate in Ewing’s Sarcoma
The Ewing's sarcoma (ES) family of tumors, including peripheral neuroectodermal
tumor (PNET), is defined genetically by specific chromosomal translocations
resulting in fusion of the EWS gene with a member of the ETS family of
transcription factors, either FLI1 (90-95%) or ERG (5-10%). A second level of
molecular genetic heterogeneity stems from the variation in the location of the
translocation breakpoints, resulting in the inclusion of different combinations
of exons from EWS and FLI1 (or ERG) in the fusion products. The most common type
of EWS-FLI1 fusion transcript, type 1, is associated with a favorable prognosis
and appears to encode a functionally weaker transactivator, compared to other
fusion types. We sought to determine whether the observed covariation of
structure, function, and clinical course correlates with tumor cell kinetic
parameters such as proliferative rate and apoptosis, and with expression of the
receptor for insulin-like growth factor I (IGF-1R). In a group of 86 ES/PNET with
defined EWS-ETS fusions (45 EWS-FLI1 type 1, 27 EWS-FLI1 non-type 1, 14 EWS-ERG),
we assessed proliferation rate by immunostaining for Ki-67 using MIB1 antibody (n
= 85), apoptosis by TUNEL assay (n = 66), and IGF-1R expression by immunostaining
with antibody 1H7 (n = 78). Ki-67 proliferative index was lower in tumors with
EWS-FLI1 type 1 than those with non-type 1 EWS-FLI1, whether analyzed as a
continuous (P = 0.049) or categorical (P = 0.047) variable. Logistic regression
analysis suggests that this association was secondary to the association of type
1 EWS-FLI1 and lower IGF-1R expression (P = 0.04). Comparing EWS-FLI1 to EWS-ERG
cases, Ki-67 proliferative index was higher in the latter (P = 0.01, Mann-Whitney
test; P = 0.02, Fisher's exact test), but there was no significant difference in
IGF-1R. TUNEL results showed no significant differences between groups. Our
results suggest that clinical and functional differences between alternative
forms of EWS-FLI1 are paralleled by differences in proliferative rate, possibly
mediated by differential regulation of the IGF-1R pathway
Predictors of survival in malignant tumors of the sternum
AbstractFrom 1930 to 1994, 54 patients with primary malignant tumors of the sternum were seen. Fifty patients were first seen with a mass, and one half of them also had pain in the sternal region. Two patients had no symptoms at presentation. Among 39 solid tumors were 26 chondrosarcomas, 10 osteosarcomas, 1 fibrosarcoma, 1 angiosarcoma, and 1 malignant fibrous histiocytoma. Of these, 25 were low-grade and 14 were high-grade tumors. Among 15 small cell tumors were 8 plasmacytomas, 6 malignant lymphomas, and 1 Ewing's sarcoma. Partial or subtotal sternectomy was done in 37 patients and total sternectomy in 3. Of the remaining 14 patients, 3 had local excision; 10 had external radiation or chemotherapy without operation, or both; and 1 had no treatment. All but one patient treated by wide resection ( N = 40) had some form of skeletal reconstruction of the chest wall defect. Thirty-one (78%) underwent repair with Marlex mesh, and in 25 this was combined with methyl methacrylate. The skin edges were closed per primum in 32 patients; 8 required muscle, omentum, or skin flaps. Resection in chondrosarcomas yielded a 5-year survival (Kaplan-Meier) of 80% (median follow-up, 17 years). The 5-year survival in osteosarcomas was 14%. Resection was curative in 64% of low-grade sarcomas but in only 7% of high-grade sarcomas. In small cell tumors, resection and radiation were helpful for local control; all failures were a result of distant metastases. We conclude that primary sarcomas of the sternum though uncommon are potentially curable by wide surgical excision. With rigid prostheses to repair the skeletal defects, the surgical complication rates are low. Overall survival after complete surgical resection is related to tumor histologic type and grade. (J THORAC CARDIOVASC SURG 1996;111:96-106
Prostatic sarcoma after treatment of rectal cancer
<p>Abstract</p> <p>Background</p> <p>The relationship between radiation exposure for treatment of cancer and occurrence of a second primary cancer at the irradiated site is well known. This phenomenon is however rare in prostate.</p> <p>Case presentation</p> <p>A 75-year-old farmer was treated for rectal cancer with preoperative 45 Gy of radiotherapy and abdominoperineal resection. Four years later he developed symptoms of bladder outlet obstruction and acute urinary retention. He underwent a transurethral resection of the prostate. Histological examination of the removed prostate tissue and immunohistochemistry revealed it to be a poorly differentiated sarcoma.</p> <p>Conclusion</p> <p>We believe this to be the first reported case of radiation-induced sarcoma following radiotherapy treatment for rectal cancer. Since radiotherapy plays a pivotal role in the contemporary treatment of rectal adenocarcinoma, it is relevant to be aware of the potential long-term carcinogenic complications of radiotherapy of the pelvis.</p
Pathological validation and significance of micrometastasis in sentinel nodes in primary breast cancer
In embracing a multidisciplinary approach to the management of patients with sentinel node biopsy in breast cancer, the pathologist task is to screen sentinel nodes for possible metastasis. The consequences of missing sentinel node micrometastasis can directly influence treatment strategies, and this screening therefore has to be performed with more attention than usual. There is presently great diversity in the histopathological work-up of sentinel nodes, with many centres employing additional techniques such as immunohistochemistry, reverse transcription polymerase chain reaction or flow cytometry in addition to routine haematoxylin and eosin staining. In this review, we address the pathological validation and significance of micrometastasis in sentinel node biopsy in primary breast cancer
BMQ
BMQ: Boston Medical Quarterly was published from 1950-1966 by the Boston University School of Medicine and the Massachusetts Memorial Hospitals