The HER2 gene, amplified in 10 to 35% of invasive human breast carcinomas, has prognostic and therapeutic implications. Fluorescent in situ hybridization is one method currently used for assessing HER2 status, but fluorescent in situ hybridization involves the time-consuming step of manual signal enumeration. To address this issue , Vysis has developed an automated signal enumeration system , Vysis AutoVysion. A multicenter , blinded study was conducted on 39 formalin-fixed , paraffin-embedded invasive breast carcinoma specimens , including 20 HER2 nonamplified and 19 HER2 amplified (weakly to highly amplified) , provided in duplicate to each study site for analysis. Calculation of the HER2/CEP17 ratio and the hands-on time of both manual and automated enumeration approaches were compared. Overall agreement of HER2 classification results (positive and negative) was 92.5% ( The HER2 gene (ERBB2) is located on chromosome 17 (q11.2-q12) and encodes a 185-kd transmembrane glycoprotein with intracellular tyrosine kinase activity, which is closely related to the epidermal growth factor receptor.1-6 Overexpression of the HER2 oncogene seems to stimulate growth and cellular motility and has been implicated in several malignancies. 4,6,7 Approximately 10 to 35% of invasive human breast carcinomas are associated with HER2 protein overexpression.2,6,8 HER2 overexpression is considered an unfavorable prognostic factor and is associated with better response rates to trastuzumab (Herceptin) therapy and anthracycline-based chemotherapy regimens. 9 Most breast carcinomas that overexpress HER2 are invasive ductal adenocarcinomas (95.5%) and are high-grade tumors [histopathological grades 2 (28%) or 3 (69%)]. Overexpression of HER2 is rare in invasive lobular carcinoma (0.8%) and other specialized types of breast carcinomas. 8,10 Studies have shown that the most common mechanism (90 to 96%) of HER2 overexpression is gene amplification. 2,9,11,12 Widely used approaches to assess HER2 status include immunohistochemistry (IHC) to determine protein expression and fluorescent in situ hybridization (FISH) to determine HER2 gene copy number. 4,11,[13][14][15] Reportedly, FISH has shown greater interlaboratory concordance and has been found to be a better predictor of response to trastuzumab (Herceptin) therapy, as compared with IHC.
Rhabdomyosarcoma presenting as a systemic disease is rare. This report concerns a 12-year-old girl who came to medical attention for what was thought to be a hematologic malignancy. Diffuse lytic bone lesions and large primitive cells in the bone marrow exhibiting erythrophagocytosis supported this diagnosis. During the course of the disease, a soft tissue mass in the region of the left ankle was removed and was a typical alveolar rhabdomyosarcoma. Retrospective review of the marrow, including electron microscopy, demonstrated that the primitive marrow cells were probably rhabdomyoblasts as well. The clinical course was a rapid downhill one in which lytic bone lesions and hypercalcemia were prominent. Although rhabdomyosarcoma eventually may disseminate, initial widespread disease without a clinically apparent primary can be a diagnostic dilemma. This clinical presentation, in combination with the recognized aggressiveness of the alveolar histologic subtype, identifies a rare subgroup of patients with rapidly fatal disease.
Acute leukemia frequently has been described as a late complication of chemotherapy with alkylating agents in patients treated for multiple myeloma. However, the simultaneous occurrence of multiple myeloma and acute leukemia in the same patient, without previous exposure to chemotherapy, is a rare association. We describe a case of concomitant involvement by multiple myeloma and acute monocytic leukemia. To our knowledge, only 9 such cases have been reported in the literature to date. We discuss the criteria used in diagnosing the 2 separate diseases and the possible mechanisms responsible for this occurrence.
A 50-year-old male with a history of tonsillar and right axillary lymph node enlargement due to atypical lymphoid hyperplasia presented two years later with marked bilateral axillary and inguinal lymphadenopathy. The lymph node biopsy showed a composite lymphoma (follicular, mixed, small and large cell plus B-immunoblastic sarcoma) with associated focal Langerhans' cell granulomatosis (LCG) (Histiocytosis X). The diagnosis of composite lymphoma was supported by the immunohistochemical demonstration of two different monoclonal patterns in the follicular and diffuse areas. The typical Birbeck's granules were demonstrated ultrastructurally in LCG areas, which also stained with S-100 protein. LCG may coexist with malignant lymphoma, however, it appears to be confined to the neoplastic nodes with no tendency to systemic spread. It is important to recognize this association so that the impact of this apparently benign lesion (LCG) not be overestimated and that the subsequent management of the patient be directed according to the type of the coexisting malignant lymphoma.
Five large cell malignant neoplasms were studied by immunohistochemistry and electron microscopy. Ultrastructural examination demonstrated numerous circumferential microvilli in 3 cases and a more polarized distribution in 2 cases. The tumor cells in 2 cases demonstrated the surface glycoprotein T29/33, indicative of a hematopoietic neoplasm. Two cases (including one positive for T29/33) contained intracytoplasmic IgG-kappa. Anti-keratin staining using both polyclonal and monoclonal antibodies was negative. Two patients are alive and in remission after treatment for lymphoma. One died with tumor following a progressive course, and one has been lost to follow-up. A fifth patient died of tumor and at autopsy was found to have a disseminated pancreatic tumor. Microvilli around large malignant cells have been commonly associated with epithelial tumors; however, our findings indicate that, in the absence of intercellular junctions and tonofilaments, the possibility of malignant lymphoma should be considered and pursued immunohistochemistry.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.