Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A probe identifying CBL2, the human cellular homolog of the murine oncogene v-cbl and murine cellular protooncogene Cbl-2, and panels of rodent X human somatic cell hybrids were used to study the relationship of this protooncogene to translocations associated with acute leukemia, lymphoma, and Ewing sarcoma. CBL2 was mapped to 11q23 and found to translocate from chromosome 11 to 4 in an acute leukemia cell line possessing a t(4;11)(q21;q23) and from chromosome 11 to 14 in a B-cell lymphoma with a t(11;14)(q23;q32). In an Ewing sarcoma cell line with a t(11;22)(q23;q12), however, CBL2 remained on chromosome 11. Additional studies of other genes in the region of 11q23 allowed the following ordering of these genes and breakpoints: 11cen--q23--NCAM--CD3(E-D-G)--[t(11;14), t(4;11)]--(THY1, CBL2, ETS1)--t(11;22)--11qter. The gross structure of the CBL2 sequences examined was not altered by either of the flanking breakpoints. Given that the 5' and 3' ends of the CBL2 gene are not known and are probably not evaluated by the v-cbl probe, these results do not rule out the possibility of CBL2 involvement in the pathogenesis of a subset of acute leukemias possessing a t(4;11), B-cell lymphomas possessing a t(11;14), or Ewing sarcomas possessing a t(11;22).
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PMID:Relationship of the human protooncogene CBL2 on 11q23 to the t(4;11), t(11;22), and t(11;14) breakpoints. 201 28

Ifosfamide/mesna was given to 97 patients who had malignant solid tumors diagnosed before they were 21 years of age. Patients received 1.6 g/m2 ifosfamide daily x 5, given i.v. over 15 min, followed by 400 mg/m2 i.v. mesna at 15 min and 4 and 6 h after ifosfamide. Responses were noted in patients with osteosarcoma, Ewing's sarcoma, rhabdomyosarcoma and other soft-tissue sarcomas, rhabdoid tumor, neuroblastoma, Wilms' tumor, primitive neuroectodermal tumor, retinoblastoma, germ-cell tumors, and B-cell lymphoma. Toxicity included mild to moderate nausea and vomiting, transient, reversible myelosuppression, transient elevations of serum blood urea nitrogen (BUN) and creatinine and liver enzymes, infections, and self-limiting neurotoxicity characterized by changes in mental status, motor dysfunction, cranial nerve palsy, cerebellar dysfunction, and seizures. Neurotoxic symptoms were generally seen in patients who had previously received cisplatin. Ifosfamide is an important alkylating agent that should be combined with other agents in phase II and III trials. Alternate dose schedules should also be investigated.
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PMID:Ifosfamide in pediatric malignant solid tumors. 250 57

Autologous bone marrow transplantation is used for children with cancers which are only partially responsive to bone marrow toxic doses of cancer chemotherapy and irradiation. The use of megatherapy and autologous bone marrow transplantation instead of conventional doses for children has yielded substantial benefits in B-cell lymphoma, relapse of leukaemia, disseminated neuroblastoma and germ cell tumors. In the case of Wilms' tumor, rhabdomyosarcoma, osteosarcoma and Ewing's sarcoma with a partial initial response or a relapse, autologous bone marrow transplantation has been used to a limited extent. Based on the best results from conventional therapy and autologous bone marrow transplantation, respectively, the present need for autologous bone marrow transplantation in Denmark is estimated to be 24 transplantations a year.
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PMID:[Autologous bone marrow transplantation in children]. 831 84

Thirty-one seminars have been held in the 16 years since 1981. A principal interest from the beginning was the genetics of cancer, well before this subject became widely popular. This interest arose in part because of marked binational differences in type-specific cancer rates, such as the very low rates among Japanese for Hodgkin's disease in the young, testicular cancer, Ewing's sarcoma, superficial spreading melanoma, chronic lymphocytic leukemia, and Wilms' tumor (half the U.S. frequency). Three seminars were devoted to the seeming reciprocal relationship between B-cell lymphoma (low in Japan) and certain autoimmune diseases (high in Japan), which is perhaps similar in origin to the male/female differences in the rates for these diseases. A seminar on Li-Fraumeni syndrome led to the recognition of cases among Japanese pedigrees brought to the meeting, and generated a study of its occurrence in Japanese families with adrenocortical carcinoma in a child. Another seminar revealed a marked clustering of rare cancers in Werner's (premature aging) syndrome in Japan, and led to a binational study and analysis of case-reports worldwide. Three seminars on pathology heightened appreciation of the importance of subclassifying cancer by subsite and subtype for racial and other comparisons. Four seminars on biostatistics in cancer research generated a substantial exchange of specialists and trainees in this field.
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PMID:The U.S.-Japan Cooperative Cancer Research Program: some highlights of seminars, interdisciplinary program area, 1981-1996. 861 22

Bladder cancer-associated protein (BLCAP) is a novel candidate tumor suppressor gene identified from human bladder carcinoma and highly associated with the invasion of bladder cancer. We previously reported that it also plays a key role in the tumorigenesis and metastasis of human osteosarcoma. In the present study, we constructed a recombinant encoding BLCAP cDNA. Overexpression of BLCAP resulted in growth inhibition and induced apoptosis of human TC-135 Ewing's sarcoma cells in vitro. We further investigated the caspase-3/7 activity and expressions of the fusion transcription factor Ewing's sarcoma protein-friend leukemia virus integration 1 (EWS-FLI1) and the apoptosis regulator B-cell lymphoma 2 (BCL-2). Cell apoptosis was accompanied by the down-regulated expression of EWS-FLI1 and BCL-2. Our present results suggest that BLCAP may play a role not only in regulating cell proliferation but also in coordinating apoptosis through the down-regulation of BCL-2 and EWS-FLI1 in human Ewing's sarcoma cells.
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PMID:BLCAP induces apoptosis in human Ewing's sarcoma cells. 2184 21

The six-transmembrane epithelial antigen of prostate (STEAP) protein was identified in advanced prostate cancer and is up-regulated in multiple cancer cell lines, including prostate, bladder, colon, ovarian, and Ewing sarcoma. STEAP1 was described as a suitable antigen for T-cell-based or antibody-based immunotherapy. We have investigated the expression of STEAP1 in 40 human tumor types - brain, epithelial, lymphoid - and in their normal tissue counterparts using publicly available gene expression data, including the Oncomine Cancer Microarray database. STEAP1 was found significantly overexpressed in 11 cancers. In addition, high STEAP1 expression was associated with poor overall survival in colorectal cancer, diffuse large B cell lymphoma, acute myeloid leukemia and multiple myeloma. Taken together, these data suggest that STEAP1 is a potential therapeutic target for T-cell based immunotherapy or antibody therapy in a large panel of cancers.
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PMID:STEAP1 is overexpressed in cancers: a promising therapeutic target. 2314 26

We report the case of a patient in whom the diagnosis of Ewing sarcoma arising from a soft tissue was made after successful treatment of diffuse large B-cell lymphoma. A 65-year-old woman presented with a rapidly growing mass in her left scapular region 8 years after successful chemotherapy with the cyclophosphamide, hydroxydaunomycin hydrochloride, vincristine, prednisolone regimen for diffuse large B-cell lymphoma. Computed tomographic examination and magnetic resonance imaging of the thorax revealed an intramuscular tumour measuring 40 mm in size in the left scapular region. Histopathological examination of an open biopsy specimen revealed a small round cell tumour that showed positive staining for CD99. Fluorescence in situ hybridization showed a split signal by a break-apart probe for the EWS gene in chromosome 22q12. Reverse transcriptase-polymerase chain reaction confirmed the expression of EWS-FLI1 fusion transcripts. Based on these findings, the patient was diagnosed as having secondary Ewing sarcoma. Despite adjuvant chemotherapy, however, she died of pulmonary metastases 2 years after the diagnosis of Ewing sarcoma. Therapy-related haematological malignancies with balanced translocations have been reported previously. A mechanism similar to that underlying the development of secondary malignancy might explain the occurrence of this solid cancer.
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PMID:Ewing sarcoma arising after treatment of diffuse large B-cell lymphoma. 2347 35

The term "small round blue cell" is frequently used as a cursory radiologic pathological correlation of aggressive tumors throughout the body. We present a pictorial essay of common and uncommon subtypes of small round blue cell tumors in the chest illustrating the characteristic radiologic findings of each lesion. In addition, we review the pathologic findings of each tumor subtype with characteristic hematoxylin- and eosin-stained photomicrographs and immunohistochemical and molecular studies. Represented tumors include small cell carcinoma, Ewing sarcoma, extranodal marginal zone B-cell lymphoma, embryonal rhabdomyosarcoma, desmoplastic small round cell tumor, and posttransplant lymphoproliferative disorder. Understanding and ability to recognize these lesions are essential to broaden the radiologist's differential diagnosis and help guide patient care.
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PMID:Thoracic Presentations of Small Round Blue Cell Tumors. 2740 3

The diagnosis between chronic osteomyelitis, Ewing sarcoma and lymphoma often is being confusing in many occasions. As the latter two conditions are malignant, early diagnosis and interventions are crucial. We present a 28 year old male with features of chronic osteomyelitis of right tibia 2 years back then changed through Ewing sarcoma to B-cell lymphoma in the histological diagnosis. This case report highlights the difficulties that arise in diagnosing primary bone lymphomas which may masquerade as chronic osteomyelitis and hence the need for immunohistochemistry in chronic recurrent osteomyelitis.
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PMID:Immunohistochemistry in Primary B-cell Lymphoma of Tibia Masquerading as Chronic Osteomyelitis. 2879 Apr 79

MicroRNAs (miRNAs) are small, single-stranded, non-coding RNA molecules involved in cancer initiation and progression. The present study aimed to determine the effect of miRNA-30d (miR-30d) on the growth, malignant phenotype, and apoptosis of Ewing's sarcoma (ES) SK-ES-1 cells, and to elucidate the underlying molecular mechanism and signaling pathway involved. Cell proliferation, invasion, migration, morphological changes, cell cycle distribution and apoptosis were investigated. Furthermore, the expression of matrix metalloproteinase (MMP)-2, MMP-9, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase-3 and poly (ADP-ribose) polymerase (PARP) were examined, as was the activity of the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3K)/Akt pathways. It was found that the overexpression of miR-30d repressed the proliferation, migration and invasion, and promoted morphological changes, S-phase arrest and apoptosis of SK-ES-1 cells. Additionally, it was observed that increased miR-30d levels inhibited the expression of MMP-2 and MMP-9, and inhibited the activity of the MEK/ERK and PI3K/Akt pathways, but elevated the ratio of Bax/Bcl-2 and the cleavage of caspase-3 and PARP. Taken together, the results demonstrated that miR-30d suppressed the biological progression of SK-ES-1 cells by targeting MMP-2 and MMP9, the Bax/Bcl-2 and caspase-3 cascade, and the MEK/ERK and PI3K/Akt signaling pathways. Therefore, miR-30d is a promising target in the treatment of ES. However, further investigations are urgently required to investigate the underlying molecular mechanisms of the effects of miR-30d on ES for a comprehensive understanding of the tumorigenesis and progression of this cancer.
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PMID:miR-30d inhibits cell biological progression of Ewing's sarcoma by suppressing the MEK/ERK and PI3K/Akt pathways in vitro. 2954 Dec 8


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