Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuroblastoma remains a common and deadly childhood tumor, resistant to both surgical and chemo/radiotherapeutic intervention in its advanced stages. The role of immunotherapy in such cancers has yet to be defined. In previous work, we found that the addition of interferon gamma (IFN-gamma) to 3-day in vitro tissue cultures of the murine neuroblastoma C1300, led not only to the tumor's increased cell surface expression of the immunologically important major histocompatibility complex (MHC) class I antigen, but also to an increased susceptibility of such modified tumor to subsequent lymphokine activated killer (LAK) cell lysis. In this study, we sought to determine the in vivo applicability of these findings. Initial dose-response studies helped define a regimen of rIFN-gamma's administration that upregulated MHC class I without activating host natural killer (NK) activity. A/J mice bearing 7-day-old subcutaneous C1300 were randomized to receive daily morning injections of either 0, 25,000, 50,000, or 100,000 U of rIFN-gamma intraperitoneally for 6 days. Animals were killed at days 3, 6, and 9 after initiation of rIFN-gamma therapy, and tumors were excised, digested, and stained for both MHC class I and II expression. At the time of sacrifice, splenocytes from each animal were tested for NK cytotoxicity toward YAC (an NK-sensitive lymphoma) and C1300. These studies defined 3 days of therapy with 25,000 U as a "priming" dose that increased expression of class I with minimal impact on NK activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low-dose interferon gamma renders neuroblastoma more susceptible to interleukin-2 immunotherapy. 190 48

Lag time (the interval between symptom onset and diagnosis) was described for 2665 children with lymphoma or a solid tumor who participated in Pediatric Oncology Group therapeutic protocols from 1982 until 1988. Median lag time ranged from 21 days for neuroblastoma to 72 days for Ewing sarcoma. Significant differences in lag time were found among diagnostic groups (p less than 0.001), even after adjustment for age, gender, and race. Age was significantly associated with lag time for all diagnoses (p less than 0.05) except Hodgkin disease. Girls had increased lag times for non-Hodgkin lymphoma (p = 0.02) but decreased lag times for Ewing sarcoma (p = 0.02). Differences in lag time related to race were significant only for children with osteosarcoma (p = 0.02), for which white children had longer lag times. Type of tumor and age were strongly associated with lag time. Within diagnostic groups, age, gender, and race failed to explain more than 16% of the variance in lag time, suggesting that other factors may play more prominent roles. Further study is necessary to identify these factors and to assess the relationship between lag time, stage of disease at diagnosis, and prognosis, especially before designing early-detection interventions for childhood cancer.
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PMID:Interval between symptom onset and diagnosis of pediatric solid tumors. 194 78

The group of rounded small-cell tumors include different neoplasias involving different therapies; we can name neuroblastoma, Ewing' sarcoma, embrionary rhabdomyosarcoma, lymphoma and other pathology such as Askin's tumor or small cell tumor of the thorax area. Based on microscopic and immunohistochemistry findings, it is suggested that it originates from the neural crest or pluri-potential cells from the neuroectodermy. This has a very aggressive behaviour and is usually resistant to oncologic therapies.
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PMID:[Undifferentiated small cell tumor of the thoracopulmonary region]. 195 81

Targeting of radioactivity to tumors using antitumor antibodies is evolving from a laboratory curiosity toward a practical diagnostic and therapeutic technique that promises widespread benefits for many common human cancers. The development of the hybridoma technique by Kohler and Milstein for producing monoclonal antibodies is probably the single most important contribution to the development of this field. A large array of monoclonal antibodies against many human tumors have been created and labeled with a variety of radioisotopes; 110 clinical trials have been identified from the literature between the interval of 1978 to the present. These studies are beginning to form the basis for certain conclusions regarding likely benefits for certain combinations of antitumor antibodies and isotopes in specific instances of clinical management in patients with malignant neoplasms. For example, in melanoma, lymphoma, neuroblastoma, and colorectal malignancies, radiolabeled antibodies have demonstrated occult tumors, which could not be disclosed with conventional methodologies. Radioimmunotherapy of malignant lymphoma is achieving durable remissions in patients who have failed conventional forms of therapy. For the most part, these advances have been achieved through intelligent application of known principles of immunochemistry, imaging physics, and tumor immunology. Progress has been slow but steady. In a few instances, the term "magic bullet" is warranted in describing the targeting of a particular radiolabeled antibody to a human tumor. I-131, 3-F8, an IgG3 against the GD2 antigen of neuroblastoma, which was introduced by Cheung, and In-111 T-101, against the CD5 antigen of T-cells, which was developed by Royston, stand out because of the consistency and high concentration of radioactive targeting to human tumors in clinical trials. If certain technical innovations fulfill their initial promise, the future will be bright for radioimmunologic methods of diagnosis and therapy. Genetic engineering will permit the development of "humanized" antibodies with biologic properties that favor tumor localization. New chemical approaches will broaden the range of isotopes available as diagnostic and therapeutic radiolabels. Application of modern imaging methodologies, such as positron emission tomography (PET), will detect more lesions of smaller size and permit quantitative imaging for dosimetry considerations. Greater speed and ease of use of computerized work stations will lead to the broader application of fusion imaging in which radioantibody images will be viewed simultaneously with TCT or MRI for better anatomic correlation of abnormal sites of antigen-reactive tumor deposits.
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PMID:Radioimmunology. Imaging and therapy. 199 Dec 86

Magnetic resonance imaging (MRI) is a sensitive method for the diagnosis of bone marrow abnormalities, but its usefulness in detecting active disseminated cancer in this tissue in treated patients has not been determined. We therefore examined 14 children who had been treated for disseminated bone marrow involvement by neuroblastoma (n = 6), lymphoma (n = 3), Ewing's sarcoma (n = 3), osteosarcoma (n = 1), and leukemia (n = 1). MRI studies were performed at 21 marrow sites to evaluate residual or recurrent tumor and were correlated with histologic material from the same site. T1- and T2-weighted sequences were employed in 21 and 14 studies, respectively; short tau inversion recovery (STIR) in 18; and static gadolinium diethylene triamine pentaacetic acid (Gd-DPTA)-enhanced. T1-weighted sequences in 13. All MRI studies showed an altered bone marrow signal. Technetium 99m methylene diphosphonate (99mTc-MDP) bone scintigraphy was also performed (19 studies). On histologic examination, 7 marrow specimens contained tumor, and 14 did not. Of the 7 tumor-positive lesions, all T1-weighted, 4 of 6 T2-weighted, and all 6 STIR sequences showed abnormal signal; all 5 Gd-DTPA-enhanced. T1-weighted sequences showed enhancement of the lesion. However, abnormal signals were also observed on all T1-weighted, 6 of 8 T2-weighted, 11 of 12 STIR, and 5 of 8 Gd-DTPA-enhanced, T1-weighted images of the tumor-negative sites. In this clinical setting, MRI did not consistently differentiate changes associated with treatment from malignant disease.
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PMID:Magnetic resonance imaging of disseminated bone marrow disease in patients treated for malignancy. 202 Aug 67

Molecular characterization of neuroendocrine (Merkel cell) carcinoma of the skin. Review of the literature and report of three cases. Although neuroendocrine carcinoma of the skin (NECS) is comparatively a rare clinical-histological entity, numerous morphological and ultrastructural studies have been carried out since the tumor was identificated by Toker (1972). Recently immunocytochemistry has allowed a better molecular characterization (immunophenotype) of this tumor and a more exact diagnosis. The main problem for the pathologist is the differential diagnosis between NECS and skin neoplasms--both primitive and metastatic--which require a more aggressive treatment. Often the classical morphological criteria do not distinguish NECS from non-Hodgkin's lymphoma, amelanotic melanomas, cutaneous metastases of lung small cell carcinoma or of neuroblastoma. The co-expression of cytokeratins and neurofilaments constantly found in NECS, is surely the best differential criterion from non-neuroendocrine carcinomas. Furthermore, the typical paranuclear location of both the intermediate filaments in NECS is a distinctive peculiarity as opposed to lung microcytoma, where cytokeratins and neurofilaments, when present, show widespread perinuclear positivity. Chromogranin A is found only in a small percentage of tumor cells, whilst synthesis of calcitonin, somatostatin, gastrin, ACTH, is very rare. Finally, the lack of common leukocyte antigen (CLA), S-100 protein and vimentin in NECS rules out the diagnoses of lymphoma, melanoma and sarcoma respectively.
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PMID:[Molecular characterization of cutaneous neuroendocrine (Merkel cell) carcinoma. Review of the literature and presentation of a caseload]. 209 Oct 10

Studies were made on the appearance of second malignant tumors (SMT) in children followed in a pediatric hospital at metropolitan Santiago, Chile, between years 1968 and 1987. A retrospective analysis identified SMT in 7 of 430 patients who survived a childhood cancer (incidence 1.62%). An 8th patient was added, whose first neoplasm was treated in another hospital. The initial diagnosis in the affected children were medulloblastoma, neuroblastoma, Wilm's tumor retinoblastoma, Ewing's sarcoma, Hodgkin's disease and, in two cases, acute lymphocytic leukemias. The age range was 6 months to 11 years. Treatment was done by surgery in 5/8, chemotherapy in 7/8 and radiotherapy in all patients. The latent period between the diagnosis of the first cancer and the diagnosis of the SMT was 3.5 to 12 years (median 8.5 years). Osteosarcomas were the most frequent SMT (5/8). The other SMT were a rhabdomyosarcoma, a non Hodgkin lymphoma and an astrocytoma. The majority of SMT were located in the area of prior radiotherapy (6/8). In the other two cases, one had an osteosarcoma, after a bilateral retinoblastoma, which grew outside the previously treated area, and the last one consisted of a lymphoma which was identified 9 years after an acute lymphocytic leukemia. Only 3/8 SMT patients are alive after 14.21 and 34 months follow up. The other children died between 11 and 20 months after diagnosis of SMT. Notwithstanding these kinds of outcome, benefits of therapy for patients with primary tumors greatly outweight the later risk of cancer induction in a small proportion of them.
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PMID:[Second cancer in pediatric patients]. 213 86

Nineteen cases with malignant tumors in the nasal cavities have been treated at the department of otolaryngology, Yokoharma City University, during the 10 years from 1978 to 1987. 1. Cases were 8 males and 11 females, and their ages ranged from 27 to 84 years (Mean age: 64.6). 2. In the histological classification, 9 cases were the epithelial malignant tumors (squamous cell carcinoma 5; adenoid cystic carcinoma 2; transitional cell carcinoma 1; malignant pleomorphic adenoma 1), 9 cases were non-epithelial malignant tumors (malignant melanoma 6; malignant lymphoma 2; olfactory neuroblastoma 1), and one case was unclassified malignant tumor. 3. Cases with epithelial malignant tumors showed better prognosis after treatment of surgical and radiation therapy. But those of non-epithelial malignant tumor were worse. 4. A very rare case with malignant pleomorphic adenoma, originated at the lateral nasal wall was reported and its clinical features and treatment were discussed. This tumor has not been reported up to the present in Japan.
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PMID:[Clinical studies of malignant tumors in the nasal cavity]. 217 85

We describe a series of 28 fine needle aspiration biopsies (FNAB) of soft tissue from 22 patients. Four patients had two separate FNABs, and one had three aspiration procedures. The patient population was limited to children and young adults (age range, 2 months to 29 years; mean, 16 years) who were known to have diverse forms of cancer, and who subsequently developed a mass in the peripheral soft tissues (including breast). The interval between the time of diagnosis of the primary malignant neoplasm and FNAB ranged from 1 day to 17 years (mean, 39 months). All FNAB diagnoses were confirmed by subsequent surgical open biopsy or clinical follow-up greater than 1 year. No complications occurred from the procedure. The cytomorphology is presented in selected cases and correlated with the patient's original tissue histopathology. Twenty aspirates were diagnosed as cytologically malignant, one as suspicious for malignancy. Seven were considered benign. None were unsatisfactory. One false-positive and no false-negative cytologic diagnoses were obtained. The overall accuracy of FNAB diagnoses was 96%, while sensitivity was 100% and specificity 88%. Sites of aspiration included soft tissues of the head and neck (seven cases), trunk (eight cases), breast (four cases), and extremities (nine cases). Malignant cytologic diagnoses included sarcoma (thirteen), seminoma (two), lymphoma/leukemia (two), melanoma (one), undifferentiated neoplasm (one), and neuroblastoma (one). Electron microscopy of aspirated cells was used to confirm the diagnosis in two cases. Fine needle aspiration biopsy of soft tissue masses from children and young adults with cancer demonstrates a high diagnostic accuracy, and its use is justified in this population.
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PMID:Metachronous soft-tissue masses in children and young adults with cancer: correlation of histology and aspiration cytology. 219 Sep 11

Experience has shown that markers created in research laboratories can be adapted to everyday surgical pathology practice for malignant melanomas. These studies are feasible and readily conducted on frozen tissue as is routinely done in typing of lymphoma. The demonstration of heterogeneity using this monoclonal antibody panel, and other antibodies yet to come, may be important for prognostication. Tumor cell heterogeneity of surface antigens reflects disruption of the tumor cell's patterned gene expression. This should be regarded as an indication of different clones of cells (subsets) with a tumor, whether primary or secondary. It is entirely possible that autologous immune cells can kill or at least restrict the growth of subsets of melanoma cells having certain surface antigenic phenotypes while they are incompetent to handle other subsets. This would enable a particular phenotype within a primary melanoma to survive and escape the immunologic regression known to occur in 3 to 6 percent of these tumors. Such patients may present years later with metastases in the brain, liver, gastrointestinal (GI) tract, or lymph nodes. There are also implications in chemotherapy and chemoimmunotherapy for melanoma in this regard. It could be theorized that these agents may dispose of or restrict the growth of some phenotypes, leaving others in a resistant state. Perhaps the MDR gene is activated. Alternatively a tumor suppressor gene(s) could be absent or inactivated, as in neuroblastoma and carcinoma of the breast and lung. Markers present at the cell membrane surfaces and in the membranes themselves constitute an important field for study in the understanding of tumorigenesis. Many of these markers are present in embryos as early as the 4-to-8-cell stage and in blastocysts. Embryonic antigens in the intercell mass of blastocysts are stage-specific embryonic antigens. They are signals for organ development and the differentiation of cells. At various stages of this development, these markers disappear, especially upon differentiation into tissue types and specific organs. These cell signals are therefore organogenesis markers. Detecting a given antigen is not simple because it may be present but not immunohistochemically detectable because glycosylation, acetylation, phosphorylation, or sulfation have not taken place, or have resulted in a structural conformation not recognized by monoclonal antibodies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunohistochemical phenotyping of malignant melanoma. A procedure whose time has come in pathology practice. 220 65


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