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 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rhabdomyosarcoma manifested as a systemic disease is very rare and cases showing diffuse metastasis in the bone marrow are most unusual. Recently we encountered two cases of rhabdomyosarcoma with diffuse bone marrow metastasis which were clinically manifested as acute leukemia. The first patient was a 15-year-old female, who was admitted in 1982 with pancytopenia and many large primitive cells in bone marrow aspirates, hematological malignancy being diagnosed. Thereafter the bilateral breasts showed rapid swelling and a biopsy specimen revealed the histological features of typical alveolar rhabdomyosarcoma. The primary site of the neoplasm remained undetermined during the course. At autopsy, it was disclosed that the neoplasm originated from the left thigh and showed generalized metastasis. The second patient was a 38-year-old man, who was admitted in 1986 because of a nasal polyp obstructing the nasal cavity, and persistent nasal bleeding. Peripheral blood samples showed leukoerythroblastosis and thrombocytopenia, and large primitive cells were found in bone marrow aspirates, so that hematological malignancy was initially diagnosed. A biopsy specimen of the nasal polyp showed proliferation of large round cells and electron microscopy demonstrated the ultrastructural features of rhabdomyosarcoma.
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PMID:Rhabdomyosarcoma with bone marrow metastasis simulating acute leukemia. Report of two cases. 321 18

A common feature of follicular lymphoma, the most prevalent haematological malignancy in humans, is a chromosome translocation (t(14;18] that has coupled the immunoglobulin heavy chain locus to a chromosome 18 gene denoted bcl-2. By analogy with the translocated c-myc oncogene in other B-lymphoid tumours bcl-2 is a candidate oncogene, but no biological effects of bcl-2 have yet been reported. To test whether bcl-2 influences the growth of haematopoietic cells, either alone or together with a deregulated c-myc gene, we have introduced a human bcl-2 complementary DNA using a retroviral vector into bone marrow cells from either normal or E mu-myc transgenic mice, in which B-lineage cells constitutively express the c-myc gene. Bcl-2 cooperated with c-myc to promote proliferation of B-cell precursors, some of which became tumorigenic. To determine how bcl-2 expression impinges on growth factor requirements, the gene was introduced into a lymphoid and a myeloid cell line that require interleukin 3 (IL-3). In the absence of IL-3, bcl-2 promoted the survival of the infected cells but they persisted in a G0 state, rather than proliferating. These results argue that bcl-2 provided a distinct survival signal to the cell and may contribute to neoplasia by allowing a clone to persist until other oncogenes, such as c-myc, become activated.
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PMID:Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells. 326 2

Etoposide (VP-16-213) has been used in the treatment of many solid tumors and hematologic malignancies. When used in high doses and in conjunction with autologous bone marrow transplantation, this agent has activity against several treatment-resistant cancers including malignant glioma. In six of eight patients (75%) who we treated for recurrent or resistant glioma, sudden severe neurologic deterioration occurred. This developed a median of 9 days after initiation of high-dose etoposide therapy. Significant clinical manifestations have included confusion, papilledema, somnolence, exacerbation of motor deficits, and sharp increase in seizure activity. These abnormalities resolved rapidly after initiation of high-dose intravenous dexamethasone therapy. In all patients, computerized tomographic (CT) brain scans demonstrated stability in tumor size and peritumor edema when compared with pretransplant scans. This complication appears to represent a significant new toxicity of high-dose etoposide therapy for malignant glioma.
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PMID:Acute neurologic dysfunction after high-dose etoposide therapy for malignant glioma. 328 26

Antibodies against cell-surface determinants present on limited types of normal cells, such as differentiation antigens, offer an approach to detecting and characterizing tumor cells that is well-suited to fluorescence flow cytometry. This paper reviews the technology involved and its application in the study of hematologic malignancies, especially in the detection and characterization of tumor cells in leukemias and lymphomas.
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PMID:Fluorescence flow cytometry and immunology applied to cancer. 330 Jun 84

Hypereosinophilic syndrome (HES) is a disease process of unknown pathogenesis. Although some cases are believed to be primary hematologic malignancies, this issue remains unsolved. We present a case of HES in whom we have observed a clone of cytogenetically abnormal cells in the bone marrow in parallel with a clinical picture of a hematologic disorder characterized by progressive proliferation and organ infiltration by eosinophils. The cytogenetic abnormality 46,XY,t(7;12)(q11;p11) is previously unreported. Our case, plus other evidence present in the literature, supports the concept that HES is a hematologic malignant neoplasia.
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PMID:Evidence for the clonal nature of hypereosinophilic syndrome. 335 92

Abnormalities of chromosome 1 have been reported in a number of solid tumors and hematologic malignancies, indicating that this is a frequent event in neoplasia. Here we report our observations on aberrations of chromosome 1 in malignancies of the uterine cervix. Tumor material obtained from 148 patients with invasive carcinoma of the cervix and two cases of carcinoma in situ (CIS) was analyzed on direct preparations by G-banding. The results showed abnormalities of chromosome 1 to be one of the most common karyotypic changes, with 95% of the patients showing rearrangements of this chromosome. These changes were never seen as the sole abnormality but were always found in association with other chromosomal aberrations. Numerical rearrangements were present in 54% of the cases, with losses of unaltered chromosome 1 predominating. Consistent marker chromosomes included deletions of chromosome 1 at bands q32, p34, q42, p32, and p22, isochromosomes of both the "p" and "q" arms and translocations, particularly on the long arm. Specific regions on both arms of chromosome 1 (1p11-p13 and 1q21-q32) were preferentially overrepresented in changes involving this chromosome. Certain breakpoints were nonrandomly involved in the structural changes, particularly band 1q32 breaks occurring at this site in 88 instances. The presence of chromosome 1 aberrations in the two cases of CIS suggests that rearrangements of this chromosome are not always a secondary change contributing to the progression of the cancer, but also may represent an early cytogenetic event as in neuroblastoma, some leukemias, and myeloproliferative disorders.
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PMID:Chromosome 1 abnormalities in cervical carcinoma. 341 74

The Seattle Marrow Transplant Team treated about 130 patients (age 4-68 yr) for hematologic cancer with supralethal chemoradiotherapy and bone marrow transplantation (BMT) from the normal genetically identical twin. The procedure was well tolerated. The principal problem was tumor resistance. Nevertheless, BMT for acute leukemia in relapse still cured about 20% of the patients. Moreover, BMT performed while in complete remission cured about 50% of patients with acute lymphocytic leukemia or acute nonlymphocytic leukemia. Sixteen patients received transplantation in the chronic phase of Ph1+ chronic granulocytic leukemia (CGL). All showed disappearance of all Ph1+ cells. Two died of pneumonitis. Of the 14 who are alive, 3 continue to have CGL 37-76 months after BMT and 11 remain in complete hematologic and cytogenetic remission without any Ph1+ metaphases at 31-108 months (median = 68) after BMT. Thus the Ph1-positive clone can be ablated and blast crisis prevented. BMT in the accelerated or blastic phase was far less effective. Syngeneic BMT also benefited or cured patients with lymphoma, hairy-cell leukemia, and multiple myeloma. Therefore, BMT should be considered for every patient who has a hematologic cancer and an identical twin.
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PMID:Identical-twin (syngeneic) marrow transplantation for hematologic cancers. 352 68

There are a variety of water and electrolyte disorders in patients with cancer. These disorders occur during the growth of tumors, generally as a consequence of inadequate intake and absorption of electrolytes, renal failure secondary to tumor or rapid tumor destruction and production of metabolically active substances by the tumor. In this paper, the electrolyte abnormalities associated with cancer were reviewed. Hyponatremia is one of the most common clinical electrolyte abnormalities in advanced cancer. Some patients may have hyponatremia, in spite of increased total body sodium and absence of a defect in water diuresis. This status is designated as "sick cell syndrome" or "essential hyponatremia". In addition, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in association with various tumors has been described. This syndrome is principally due to water retention, but can also be due to continuous urinary loss of sodium, and hypo-osmolality. Hypercalcemia is associated with coexistent primary hyperparathyroidism, prostaglandin (PGE2) or osteoclast-activating factor. It now seems likely that ectopic PTH is rarely the cause of hypercalcemia in nonparathyroid cancer. There are no data supporting the ectopic production of vitamin D-like substance as an important factor in the hypercalcemia of cancer. There are three general categories in which patients with hypercalcemia and cancer may be placed: those with bone metastases, those without bone metastases of solid tumors and those with hematologic malignancies. Hypokalemia is associated with ectopic ACTH- and insulin--producing tumors, and is often found in patients with mucin-secreting, potassium-losing adenocarcinoma of the colon.
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PMID:[Electrolyte abnormalities associated with cancer: a review]. 352 93

The clinical development of the alpha interferons has now progressed through initial Phase I and II trials into extensive controlled clinical trial designs. Alpha interferon has been a prototype of other biological agents that are now in clinical development. These agents operate through fundamentally different mechanisms of action than conventional chemotherapy and have produced a unique profile of side effects as well as response patterns. Time to response is generally longer than with chemotherapy, and dose-response and schedule-dependency questions continue to be explored for most tumor types. Although response rates have been low against most solid tumors when alpha interferon is used as a single agent, it has demonstrated a surprisingly wide range of efficacy in hematologic malignancies. These include tumors of presumed B-cell, T-cell, and myeloid lineages. In some diseases, e.g., hairy cell leukemia and chronic myelogenous leukemia, alpha interferon is broadly effective; it appears to considerably reduce or occasionally eliminate the malignant clone while normalizing the peripheral blood counts in most patients. In other diseases, alpha interferon appears destined to play a major role as part of combination therapy or in maintenance or consolidation therapy. In other disease settings, alpha interferon's role continues to be explored as part of combination therapy, adjuvant therapy, or as local-regional therapy. The full potential of alpha interferon as an antineoplastic agent will not be determined for many years. In this paper, the results from the first 5 years of widespread clinical testing are reviewed.
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PMID:Clinical overview of alpha interferon. Studies and future directions. 354 85

Hematologic malignancies, such as acute leukemia and malignant lymphoma. Respond well to cancer chemotherapy. Therefore, it is important to monitor the state of response to chemotherapy as well as to determine the complete disappearance of the tumor and to predict early detection of recurrence in routine clinical work by estimation of tumor marker levels. Although changes in the levels of paraprotein in multiple myeloma have been utilized for monitoring the responsiveness to chemotherapy, since the amounts of paraprotein are directly proportional to the number of myeloma cells, in other hematologic malignancies there are no tumor markers for monitoring the clinical course, for detecting the presence of minimal residual disease, or for predicting disease recurrence. In the future it is expected that developments in biotechnology create a large number of reagents including 'oncogene'-related markers or 'oncogene' products for application to the diagnosis and treatment of cancer patients.
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PMID:[Significance of tumor markers in the treatment of cancer: hematologic malignancy]. 367 91


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