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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Well documented examples of primary malignant giant cell tumor of bone (giant cell tumor and concurrent sarcoma arising de novo) are exceedingly rare in the literature. We report a case arising in the left ischium of a 44-yr-old man. He had no previous history of radiation therapy or multiple resections. Histologically, the tumor was a typical giant cell tumor of bone juxtaposed to a malignant fibrous histiocytoma (MFH). The juxtaposition of a high grade sarcoma (MFH) and a locally aggressive nonmalignant neoplasm such as giant cell tumor is analogous to several other tumors of bone and soft tissue in which a low grade malignant or locally aggressive tumor can be associated with MFH or fibrosarcoma de novo, namely chondrosarcoma, chordoma, liposarcoma, and well differentiated intraosseous and parosteal osteosarcoma. The presence of a high grade malignant component in each of the aforementioned neoplasms generally portends a more ominous prognosis, although this is not invariably true. Recognition of the phenomenon of "dedifferentiation" (or tumor progression) in some bone tumors and sarcomas is important to ensure appropriate treatment. Distinction from secondary malignant giant cell tumors which are usually radiation induced is also important, since the latter have a much worse prognosis than those with dedifferentiation occurring de novo.
Mod Pathol 1989 Sep
PMID:Primary malignant giant cell tumor of bone: "dedifferentiated" giant cell tumor. 255 83

Forty patients with refractory Hodgkin's disease (24 patients) or non-Hodgkin's lymphoma (16 patients) who were considered for high-dose therapy but not for autologous bone marrow transplantation (ABMT) due to BM metastases, previous pelvic irradiation, a history of marrow involvement by tumor or hypocellular marrow in conventional harvest sites received high-dose therapy and autologous peripheral blood (PB) hematopoietic stem cell transplantation. Disappearance of circulating neutrophils and development of RBC and platelet transfusion-dependence was followed, in the evaluable patients, by reappearance of 0.5 x 10(9)/L circulating granulocytes and sufficient platelets to obviate the need for platelet transfusions at a median of 25 days after transplantation. Twenty-three patients experienced a clinical complete remission (CR). The projected 2-year event-free survival was 24% for all 40 patients and 49% for the non-Hodgkin's lymphoma patients. The projected 18-month event-free survival for the Hodgkin's disease patients was 15%. PB stem cell transplantation provided an opportunity to administer high-dose salvage therapy to patients with refractory lymphoma who otherwise were not candidates for such therapy. For some of those patients, the high-dose therapy produced prolonged survival, free of tumor progression.
Blood 1989 Sep
PMID:High-dose therapy and autologous peripheral blood stem cell transplantation for patients with lymphoma. 256

At the outset of the meiotic pairing process in man, trial and error mismatching and misalignment, both within homologous pairs and between heterologues, can be observed cytologically. Pairing starts at early zygotene principally within subtelomeric regions where the synaptonemal complex initiates. In the present paper, evidence for the primary role in synaptic initiation of a GC rich minisatellite in the human XY pseudoautosomal segment is presented, and circumstantial evidence is provided to support the view that GC rich sequences (minisatellites and Alu repeats) function to promote pairing within autosomes. The known sequence hypervariability of proterminal human minisatellites, it is suggested, arises as a secondary consequence of unequal exchange after misalignment between tandem repeats at the outset of the pairing process. Unequal exchange within misaligned repeat sequences at early prophase of meiosis could make a major contribution to de novo germinal mutation (conversion, duplication, deficiency, inversion, translocation), with serious consequences in man for the production of hereditary disease. For somatic tissues, rare mispairing between G rich repeats followed by unequal exchange could be a key step in cancer progression. It might also explain somatic mosaicism in some non-neoplastic clinical conditions.
J Med Genet 1989 Sep
PMID:Asymmetry in chromosome pairing: a major factor in de novo mutation and the production of genetic disease in man. 268 83

Chemoprevention is a new area of research emphasis in cancer control. The rationale is based on the accumulation of laboratory and epidemiological data indicating that various agents may halt or reverse cancer progression in animals and may reduce risks in humans. For planning purposes, research leads are submitted to a strategic system of staging with defined criteria and decision points. A research lead that enters an intervention stage must evolve through a series of phases of testing and evaluation. Human intervention clinical trials have begun to test the hypothesis that certain agents can lower cancer incidence.
Prev Med 1989 Sep
PMID:Chemoprevention and modern cancer prevention. 269 55

Transforming growth factor beta (TGF beta) is an inhibitor of normal epithelial cell growth. To investigate the role of TGF beta in respiratory epithelial cell neoplasia, normal, preneoplastic, tumorigenic and tumor-derived rat tracheal epithelial (RTE) cells were plated in serum-free medium and grown in the presence of 0-300 pg TGF beta 1/ml. TGF beta 1 markedly inhibited the formation of colonies by primary RTE cells and some preneoplastic RTE cells. However, tumor-derived RTE cells were relatively resistant to TGF beta 1-induced growth inhibition. Resistance to TGF beta 1-induced growth inhibition, therefore, accompanies neoplastic progression of RTE cells.
Carcinogenesis 1989 Sep
PMID:Increased resistance to transforming growth factor beta accompanies neoplastic progression of rat tracheal epithelial cells. 276 54

Twenty patients with recurrent or persistent epithelial ovarian cancer failing conventional therapies were treated with a single intraperitoneal injection of iodine-131-labeled OC 125 monoclonal antibody. Rare acute side effects were nausea and mild diarrhea. At doses up to 120 mCi of iodine-131, median white blood cell and platelet count nadirs were 3.6k/microliters and 187k/microliters, respectively. Two patients acquired thyroid toxicities despite thyroid blockage with "cold" iodine. One patient had transient TSH elevation while remaining clinically euthyroid, and 1 patient developed activation of a thyroid nodule and clinical hyperthyroidism. Dose-limiting toxicity has not yet been observed. Twelve of 20 patients are alive 3 to 17 months following therapy. Tumor progression was noted in the majority of patients, although 3 patients had documented decreases in tumor burden of short duration. We conclude that, at the doses examined, iodine-131 OC 125 can be safely administered intraperitoneally.
Gynecol Oncol 1989 Sep
PMID:Intraperitoneal radiolabeled OC 125 in patients with advanced ovarian cancer. 276 26

In order to distinguish those chromosomal aberrations associated with tumorigenesis from those associated with tumor progression of malignant melanoma, chromosome analysis was performed on eight tumors derived from one patient. Three common marker chromosomes, a deletion of chromosome 1, a deletion of chromosome 9, and a translocation involving chromosomes 7 and 12, were identified in each tumor. The presence of common markers in these intrapatient tumors indicates the monoclonal origin of these tumors. Furthermore, the consistent and specific involvement of chromosome 9 in both interpatient and intrapatient studies suggests the crucial role that chromosome 9 plays during the development of human malignant melanoma. In addition to common markers, different overlapping markers including those involving chromosomes 2, 3, and 6, were also identified, suggesting that chromosomes 2, 3, and 6 are most likely associated with the progression, instead of the genesis, of the tumor. Finally, lesion-specific marker chromosomes were identified in each tumor indicating the nonrandom selection and modification of the metastatic process. The nature of chromosomal evolution among the eight tumors was clearly demonstrated by the retention and amplification of specific marker chromosomes, with the latter tumors containing more overlapping markers than the early tumors and the recurrence of identical markers in the different branches of evolution. One of the last three tumors obtained immediately before the death of the patient contained all the overlapping markers identified in other tumors, which may indicate that a plateau of chromosomal evolution of these tumors has been reached. These observations demonstrate a nonrandom or programmed chromosome evolution of human neoplasia that could be intrinsic to the aneuploid nature of neoplasia.
Cancer Genet Cytogenet 1989 Sep
PMID:Chromosomal evolution in the progression and metastasis of human malignant melanoma. A multiple lesion study. 277 22

We have studied changes in the (11C-methyl)-L-methionine (C-11 Met) uptake index in six glioma cases subsequent to radiotherapy, using positron emission tomography (PET) to evaluate the effects of radiotherapy on the amino acid metabolism of the tumor. The uptake index of the tumor represented as a percentage of the total count in the atrial blood recorded during a period of 45 min, showed an average of 0.037% and 0.039% prior to and within two months after the therapy, respectively. Out of three cases where a fall in the index was seen, two cases showed tumor regression in the size of the contrast enhanced lesion measured by CT; all three cases had a relatively long period of clinical and neurological amelioration. However, following a short period of clinical improvement, the other three patients with a rise in the index showed no change or tumor progression on CT. These findings indicate that changes in the C-11 Met uptake index can be a sensitive and precise indicator for evaluating the effect of radiotherapy on gliomas.
Gan No Rinsho 1989 Sep
PMID:[Changes in the (11C-methyl)-L-methionine uptake index in gliomas following radiotherapy]. 278 98

Twenty-four patients with recurrent malignant glioma were treated with intravenous BCNU (80 mg/m2/day X 3 days) alternating with AZQ (8 mg/m2/day X 5 days) every 6-8 weeks. Twenty patients received two or more courses of chemotherapy, ten anaplastic astrocytomas (AA), eight glioblastomas (GBM), and two malignant oligodendrogliomas (Oligo). All had prior surgery and irradiation; one had prior chemotherapy. Median age was 37.5 years. The median Zubrod performance status (PS) was 1. Three patients (15%) achieved response status, and 7 (35%) had stable disease with median times to tumor progression (MTP) of 56 wks and 35 wks. MTP for patients with progression was 11 weeks. No GBM was responsive to chemotherapy and none of the ten patients with stable or responsive disease were older than fifty years. Dose limiting toxicity was consisted of thrombocytopenia and leukopenia. Young patients with recurrent AA and good PS appear more likely to respond to alternating BCNU/AZQ chemotherapy. The overall response rate (response plus stable) of 50% was comparable to that of BCNU alone and the hematologic toxicity was cumulative.
J Neurooncol 1989 Sep
PMID:Intravenous BCNU and AZQ in patients with recurrent malignant gliomas. 279 18

We describe the neuropathologic findings at autopsy in six patients who developed a progressive encephalopathy complicating the treatment of malignant gliomas with combined intra-arterial 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and cerebral irradiation. Four brains were free of tumor and one contained a microscopic focus of residual glioma. In only one case was there evidence of tumor progression. A disseminated process characterized by miliary foci of necrosis with mineralizing axonopathy was present in all cases, restricted to the internal carotid distribution of the perfused hemisphere and involving primarily though not exclusively the white matter, which was diffusely and severely edematous. This was combined in 3 cases with a histologically dissimilar, massive necrotizing leukoencephalopathy indistinguishable from pure radionecrosis. Much of the toxicity of this therapy is mediated by vascular injury, but the disseminated necrotizing lesion probably reflects, at least in part, direct neural damage.
J Neurooncol 1989 Sep
PMID:Fatal necrotizing encephalopathy complicating treatment of malignant gliomas with intra-arterial BCNU and irradiation: a pathological study. 182 43


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