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

A patient with acute myelogenous leukemia (AML) whose bone marrow cells had complicated chromosomal abnormalities, in addition to an 8--21 translocation and a missing Y chromosome, is reported. The complex additional abnormalities did not appear to have much influence on the clinical aspects of the disease, eg, cytology of the leukemic cells and the patient's response to chemotherapy, even though the patient did have a rectal tumor due to leukemic cell infiltration.
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PMID:A case of acute myelogenous leukemia with an 8--21 translocation, missing Y, and additional karyotypic abnormalities. 28 Nov 28

Spontaneous sister chromatid exchanges and banded karyotypes were studied in blood lymphocytes from 96 individuals: seven patients with chronic myelogenous leukemia, 15 normal controls, and five "cancer families" comprising 12 cancer patients, 40 tumor-free blood relatives and 22 spouses. The families had: malignant melanoma; Epstein-Barr virus-associated malignancies and a birth defect syndrome; non-Hodgkin lymphoma and diverse carcinomas; Hodgkin's lymphoma and adenocarcinomas; and acute myelogenous leukemia. In addition to the Philadelphia chromosome in chronic myelogenous leukemia patients, karyotypic abnormalities, especially breaks and fragments, were found in 29% of cancer family members, but were inconsistent and usually attributable to radiotherapy. Mean sister chromatid exchange values were normal in chronic myelogenous leukemia, but low (by t-test) in tumor patients and their blood relatives in cancer-prone families. In tumor patients, mean sister chromatid exchange levels fell as age increased. After adjusting for this age effect, no significant differences remained among groups. In patients at high risk of cancer (because they have chronic myelogenous leukemia or a strong family history of cancer), spontaneous sister chromatid exchange rates were not a marker of cancer risk.
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PMID:Sister chromatid exchanges and chromosomes in chronic myelogenous leukemia and cancer families. 28 71

Genetic effects of cancer in childhood were examined among offspring of patients enrolled in the tumor registries of the Sidney Farber Cancer Institute and the Kansas University Medical Center. For 146 patients, 84 women and 62 men, 293 pregnancies were reported after cessation of treatment of diverse neoplasms. The outcomes of 286 completed pregnancies were as follows: 242 live births (1 set of twins), 1 stillbirth, 25 spontaneous abortions, and 19 therapeutic abortions. Seven live-born infants died during the first 2 years of life, a frequency in accord with expectation. Two offspring have developed cancer. One girl and her father had bilateral hereditary retinoblastoma. A second girl developed acute myelocytic leukemia; her mother had received radiotherapy during childhood for a brain tumor. Compared with their cousins and with published figures for the general population, the study progeny had no excess of congenital anomalies or other diseases. Chromosome and immunoglobulin studies of a few offspring did not reveal damage from preconception exposure to cancer chemotherapy and radiotherapy. Findings indicated that large collaborative studies are needed to monitor the offspring of childhood cancer survivors for inherited traits associated with the parental tumors and for mutagenic effects of therapy, particularly intense multimodality treatments.
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PMID:Offspring of patients treated for cancer in childhood. 28 96

DNA complementary to Moloney murine leukemia viral RNA was annealed with DNA isolated from peripheral leukocytes of twelve patients with leukemia. Six to 10% of the complementary DNA annealed to the DNA of one patient with acute myelogenous leukemia. The level of annealing of the complementary DNA to the other leukemic DNA's did not differ significantly from that to normal human spleen DNA. This result is consistent with reports of occasional positive results from other laboratories, but the significance, especially in reference to a causal role for RNA tumor viruses in human leukemia, remains unclear.
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PMID:Detection of sequences in human leukemic cell DNA homologous with moloney mouse leukemia viral RNA. 28 36

One hundred and thirty-three patients, 94 with acute luekemia and 39 with solid tumors, received rubidazone, alone or in combination, at M. D. Anderson Hospital. The initial study, a phase I--II study carried out in 39 patients with acute leukemia, revealed substantial antileukemic activity with optimal results at a dose level of 450 mg/m2. Toxic manifestations included an acute reaction suggestive of histamine release with dose-limiting mucositis at a dose of 600 mg/m2. Forty-seven patients with acute leukemia were treated at phase II dose levels. Thirteen of 32 patients (42%) with acute myelogenous leukemia and seven of ten patients (70%) with acute lymphocytic leukemia achieved complete remission. Twenty-seven previously untreated patients with acute leukemia who were greater than 50 years old were treated with rubidazone in combination with cytosine arabinoside, vincristine, and prednisone. Fifteen patients (50%) achieved complete remission including 12 of 15 patients (73%) who were treated at a dose of 200 mg/m2 of rubidazone on Day 1 and a dose of 70 mg/m2/day X 7 days of cytosine arabinoside (continuous infusion). For patients with solid tumors, the dose-limiting toxic effect was myelosuppression at a dose of 200 mg/m2. Other toxicity at that dose level was minimal. The best responses were seen in patients with carcinoma of the period with two of four evaluable patients showing objective tumor regression. Of six previously untreated patients with thyroid carcinoma none responded, and in a phase II study of patients with breast cancer there were no partial remissions among 13 patients. Cardiac toxicity, manifested by congestive heart failure, occurred in seven patients at cumulative doses of 1050--2600 mg/m2 of rubidazone; all patients had had prior anthracycline therapy at low doses. Rubidazone has been shown to be an active antileukemic agent, but appears to be less active than Adriamycin in our studies of patients with solid tumors.
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PMID:Clinical studies with rubidazone. 28 57

Nineteen patients are reported who developed acute myeloblastic leukemia following treatment for a variety of solid tumors, including seminoma (four cases), melanoma (one case), and cancer of the ovary (six cases), colon or rectum (three cases), bladder (two cases), cervix, endometrium, and larynx (one case each). There were nine men and ten women, with a median age of 49.8 years (range 29 to 75). The mean interval between the diagnosis of solid tumors and acute leukemia is 5.8 years. In two patients the two diseases occurred simultaneously or within six months of each other. One patient was treated only surgically. Eight patients were treated with radiotherapy, five with chemotherapy, and five received both chemotherapy and radiotherapy. Pancytopenia was commonly noted prior to the onset of leukemia with chromosomal abnormalities observed in four cases in which a karyotype was performed. Three patients achieved complete hematological remission following antileukemic therapy. One hundred and six additional patients with non-hematopoietic neoplasms and acute leukemia are reviewed. Although acute leukemia may occur in a higher than expected frequency in patients with solid tumors because of a possible increased risk of a second neoplasm, it seems more likely that the acute leukemia is related to the radiotherapy and/or chemotherapy administered to treat the first neoplasm.
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PMID:Acute myeloblastic leukemia following treatment for non-hematopoietic cancers: report of 19 cases and review of the literature. 29 52

This paper briefly reviews some mechanisms of tumor immunity and the principles of cancer immunotherapy. Cellular and humoral immunity can both influence tumor cells. Most of the cells belonging to the immune system can act on neoplastic cells. T cells can kill them, macrophages inhibit their growth, and K cells through their Fc receptor also destroy antibody-coated tumor cells. Cancer patients have usually depressed cellular immune functions. The goal of immunotherapy is to amplify the immune reactions in order to destroy the tumor cells. The modalities of immunotherapy are described. They may become important as adjuvant therapy. Immunotherapy has already been successfully in skin cancers, lung cancer and acute myeloblastic leukemia.
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PMID:Cancer immunotherapy. 30 38

An intracerebral space occupying lesion was found in a 20-year-old woman with acute myelogenous leukemia (AML) when she was in complete hematological remission. Computerized tomography of the brain demonstrated the tumor in the roof of the third ventricle and its subsequent resolution after cranial irradiation and intraventricular cytosine-arabinoside. This form of central nervous system complication in AML has not been previously reported.
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PMID:Intracerebral tumor and diffuse central nervous system infiltration complicating acute myelogenous leukemia. 31 27

The clinical and pathologic findings in six patients with myelogenous leukemia presenting initially as multiple granulocytic tumors of the skin were reviewed. The skin of the trunk was most commonly involved with multiple, confluent erythematous plaques and soft, tender, non-ulcerated, violaceous nodules. Two patients had been treated for malignant lymphoma eight and nine years prior to the onset of skin lesions (Hodgkin's disease and nodular lymphocytic lymphoma, respectively), and cutaneous granulocytic leukemia developed in sites of irradiated skin. The skin biopsies in all cases were originally misinterpreted by the pathologist as malignant lymphoma and the correct diagnosis of granulocytic leukemia was not established in any of the cases until overt extracutaneous involvement was detected. The interval in the six patients from skin biopsy to definite involvement of blood and bone marrow by acute granulocytic leukemia ranged from three weeks to six months with a mean interval of 3.8 months. The mean duration of survival from the diagnosis of extracutaneous dissemination was 12.7 months (range of three months to two and one-half years). Poorly differentiated myelogenous leukemia was demonstrated at postmortem examination in all cases. Cytochemical stains of formalin-fixed, paraffin-embedded tissues confirmed the granulocytic origin of the neoplasm: leukemic cells in skin biopsies, bone marrow aspirates, and autopsy specimens contained abundant naphthol AS-D chloracetate esterase. The findings indicate that granulocytic leukemia may rarely present with skin tumors as the original manifestation of the disease. Recognition of the distinctive clinical, histopathologic, and enzyme histochemical features of the lesion provide a basis for distinguishing granulocytic sarcoma of the skin from mycosis fungoides and other cutaneous malignant lymphomas.
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PMID:Multiple granulocytic tumors of the skin: report of six cases of myelogenous leukemia with initial manifestations in the skin. 32 49

Granulocytic sarcoma, or chloroma, is a tumor composed of immature cells of the myeloid series, which usually occurs as a secondary manifestation of acute myelocytic leukemia. Unique problems in interpretation of these lesions arise when the leukemic picture is absent in peripheral blood and bone marrow. In these cases, granulocytic sarcoma is usually misinterpreted as "reticulum cell sarcoma". Two cases of this neoplasm involving the small intestine and stomach, are reported. Signs of leukemia appeared terminally. The value of cytochemical stains in the differential diagnosis and the possible benefits of early recognition and treatment are emphasized.
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PMID:Preleukemic granulocytic sarcomas of the gastrointestinal tract. Report of two cases. 33 75


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