Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 41,109 women diagnosed with breast cancer between 1935 and 1982 in Connecticut, 3,984 developed a second cancer, whereas 2,426 were expected [relative risk (RR) = 1.64; 95% CI = 1.6-1.7]. This increased risk persisted for 30 years and was highest in women under 55 years of age at the time of breast cancer diagnosis. Second primary breast cancers (RR = 3.0) accounted for almost one-half of all new neoplasms. However, if subsequent breast cancers were excluded, the risk for all other second cancers was only 1.15 (95% CI = 1.10-1.20), and no excess risk was seen among women over age 55 at initial breast cancer. Significant risks were found for cancers of the ovary (RR = 1.7) and uterine corpus (RR = 1.4), possibly linked with shared reproductive factors such as nulliparity or late age at menopause. Malignant melanoma (RR = 1.5), thyroid cancer (RR = 1.6), and colon cancer (RR = 1.2) were also significantly elevated; possible shared risk factors remain to be elucidated. Significant deficits of multiple myeloma and chronic lymphocytic leukemia were noted. Women who received initial radiotherapy compared with those who did not were at slightly higher risk of developing a second cancer, most notably acute nonlymphocytic leukemia, non-Hodgkin's lymphoma, and cancers of the esophagus, kidney, and connective tissue, although the nature of the associations was not always clear. Some of the soft tissue sarcomas were lymphangiosarcomas of the arm, a consequence of the lymphedema that may complicate radical mastectomy (Stewart-Treves syndrome). Women treated with radiation were at higher risk of developing a second breast neoplasm (RR = 3.9) than nonirradiated women (RR = 2.8). Further investigation should focus on the mechanisms underlying the relationships between breast, genital tract, and colon cancers, and on the effects of treatment modalities on the risk of subsequent neoplasms.
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PMID:Second cancer following cancer of the breast in Connecticut, 1935-82. 408 15

Since 1970, we have carried out cancer chemotherapy and immunotherapy in cooperation with Japanese scientists, particularly Prof. H. Umezawa, who has generously supplied bleomycin, peplomycin, acalcinomycin A (ACM), THP-adriamycin (THP), neothramycin and bestatin. Malignant tumors curable by pharmacotherapy are polycythemia vera (CR 100%), acute lymphoid leukemia (ALL) (CR 80%), Burkitt tumor (CR 80 or 50%), Hodgkin disease (CR 80%), chorioepithelioma (CR 80%), testicular cancer (CR 80%), ovary cancer of children (CR 80%), Wilms renal cancer (CR 60%), rhabdomyosarcoma (CR 75%), osteosarcoma (CR 60%), Ewing tumor (CR 60%), brain tumor of children (CR greater than 50%), testicular embryonal cancer of children (CR greater than 50%), acute myeloid leukemia (AML) (CR 50%), non-Hodgkin lymphoma (NHL) (CR 50%), ovary cancer of adults (CR 40%), small cell lung cancer (CR 20%) and breast cancer. Our experimental and/or clinical experience with ACM, THP, methoxy-9-ellipticine lactate, navelbine, 4-demethyl-epipodophyllotoxin-beta-d-ethyledene glucoside, bestatin and interferon is presented. ACM is effective against AML, ALL, NHL, Burkitt tumor, breast cancer. We have comparatively investigated cardiac and dermal toxicity of 12 kinds of anthracycline antibiotics and mitoxantrone, using golden hamsters. Of the drugs examined, ACM, THP, AD-32 and AD-143 cause much less cardiomyopathy and alopecia than the other agents. The results have been confirmed by electron microscopic studies. Bestatin is an immunorestorator, which recovers immunological functions decreased in aged animals. We hope that cancer chemotherapy and immunotherapy will progress in future and contribute to cure of neoplasms. Japanese scientists have been making a great contribution in the field of cancer pharmacotherapy, and we are eager to cooperate with Japanese scientists in cancer treatment studies.
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PMID:[Japanese-French cooperation in tumor pharmacotherapy: 1970-1990]. 619 71

In the mouse, retrovirus B and C are causal agents of mammary cancer and leukemia, respectively. In previous work it was demonstrated that sera of leukemia-lymphoma patients possess antibodies which react with antigenic determinants of Type C virus present on AKR-lymphoma and AKR-thymus targets. The object of this paper was to determine whether these antibodies also reacted with Type B viral antigens present on a virus-induced BALB-mammary carcinoma; at the same time a comparative study was carried out with sera of breast cancer patients. A total of 325 sera were obtained from 277 leukemia-lymphoma cases under protocol treatment: 232 acute lymphoid leukemia, 23 acute myeloid leukemia, 15 chronic myeloid leukemia and 55 Hodgkin lymphoma sera. A total of 240 sera were obtained from breast cancer patients at the time of diagnosis and 196 sera from normal blood donors served as controls. Using indirect immunofluorescence with labeled anti-human IgG and the murine targets, antibodies were encountered in a high percentage of cancer cases and were consistently absent in normal sera. The results confirm the presence of antibodies reacting with murine Type C virus in leukemia-lymphoma cases and indicate the presence of antibodies reacting to both Type B and C retroviruses in the sera of breast cancer patients.
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PMID:Antibodies presumably cross-reacting with mouse retrovirus type B and C in the sera of both leukemia-lymphoma and mammary cancer patients. 631 22

Breaking the cure barrier is a biologic and a conceptual problem that has already been accomplished for several tumors. It is helpful to consider neoplasms in mathematical terms as many-celled tumors (polycytomas: kilocytomas, megacytomas, gigacytomas, and teracytomas). A new chemotherapeutic taxonomy recognizes curable, subcurable, and precurable cancers each with definable characteristics. A simplified technique of recognizing early cures is described by calculating the probability that an interruption in an exponential failure slope occurred by chance. Examples of cures of acute myelocytic leukemia, of superior chemotherapy for Hodgkin's disease in young adults, and of superior adjuvant chemotherapy for breast cancer are given. The interaction of surgery with chemotherapy is illustrated in pure form in acute myelocytic leukemia and in ovarian cancer. Curative chemotherapy is closer at hand than is generally believed. Nomograms for cure prediction are presented as inducements to contemplate curative approaches to cancer therapy.
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PMID:Karnofsky Memorial Lecture. Breaking the cure barrier. 632 78

Etoposide (VP 16) is a semi-synthetic derivative of 4'- demethylepipodophyllotoxin , a naturally occurring compound synthesized by the North American May apple (Podophyllum peltatum ) and the Indian species Podophyllum emodi Wallich . Although podophyllotoxins are classical spindle poisons causing inhibition of mitosis by blocking mitrotubular assembly, etoposide inhibits cell cycle progression at a premitotic phase (late S and G2), probably via inhibition of DNA synthesis. There appears to be a selective antileukemic dose response relationship when compared to normal hematopoietic elements. Etoposide is effective when administered orally at about twice the recommended parenteral dosage. Schedule dependency in both animal models and clinical trials has been observed; multiple dosing over three to five consecutive days is superior to weekly single dose administration. Etoposide's dose-limiting toxicity is myelosuppression (leukopenia), which is quite predictable; alopecia and Gl toxicity (nausea, vomiting, stomatitis) occur in about 20-30% of patients given recommended dosages. Etoposide appears to be one of the most active drugs for small cell lung cancer, testicular carcinoma (the Food and Drug Administration approved indication), ANLL and malignant lymphoma. Etoposide also has demonstrated activity in refractory pediatric neoplasms, hepatocellular, esophageal, gastric and prostatic carcinoma, ovarian cancer, chronic and acute leukemias and non-small cell lung cancer, although additional single and combination drug studies are needed to substantiate these data. Its contribution in front-line combination chemotherapeutic regimens for these cancers will be better defined in the forthcoming years. Etoposide appears to have minimal activity in breast cancer and, based on current data, it is inactive against malignant melanoma, colorectal adenocarcinoma and cancer of the head and neck, although the dosage and schedules used in many of the Phase II studies may have been suboptimal.
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PMID:Etoposide: a semisynthetic epipodophyllotoxin. Chemistry, pharmacology, pharmacokinetics, adverse effects and use as an antineoplastic agent. 632 63

We have examined mononuclear cell preparations from patients with chronic myeloid leukemia [CML] for binding of and response to 1,25-dihydroxycholecalciferol [1,25-(OH)2D3]. Whole cells specifically took up [3H]-1,25-(OH)2D3 with high affinity (Kd 3.6 X 10(-11) M) and low capacity. Subcellular fractionation of labeled cells showed that binding was restricted to cytosols and nuclei. Sucrose gradient centrifugation of cells preincubated with [3H]-1,25-(OH)2D3 revealed a single 3.6S peak which was totally displaced with 100-fold excess nonradioactive hormone. However, we were unable to demonstrate specific binding of 1,25-(OH)2D3 by postlabeling standard cytosol preparations. In addition, cytosols prepared from a mixture of CML cells and 1,25-(OH)2D3 receptor-positive T47D (human breast cancer) cells had less than 10% of the binding measured in T47D cytosol alone. However, the levels of binding in T47D cytosols were not reduced if the receptors were occupied with [3H]-1,25-(OH)2D3 prior to the addition of the CML cytosols. Thus, CML cells appear to contain both the receptor for 1,25-(OH)2D3 and an unknown substance which prevents its detection following the preparation of cytosol. Cells from patients with CML in the chronic phase specifically bound more 1,25-(OH)2D3 [18.0 +/- 3.2 (S.E.) fmol/10(7) cells] than did those in acute myeloid transformation [7.2 +/- 1.5] or than did cells from patients with acute myeloid leukemia [2.6 +/- 0.8]. Only cells from the first group of patients responded to the addition of 1,25-(OH)2D3 by differentiating along the monocyte-macrophage pathway. We conclude that the differentiation-induction effect of 1,25-(OH)2D3 is likely to depend on adequate levels of receptor and that intact cells rather than cytosol preparations should be studied before cells of a particular tissue are designated as receptor negative.
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PMID:Specific uptake of 1,25-dihydroxycholecalciferol by human chronic myeloid leukemia cells. 633 55

The authors present two cases of patients with breast cancer with lymph node extension and who both had surgery. As a pancytopenia with hypercellular bone marrow was discovered at the same time in the first patient, she received no complementary treatment; 4 months later, she presented with an acute lymphocytic leukemia (ALL) for which a remission was easily induced, but she died of a pulmonary infection. The second patient received local radiotherapy (50 grays) and adjuvant chemotherapy (Alkeran for 26 months). Forty-seven months after the diagnosis of breast cancer and 16 months after the end of the treatment, an acute nonlymphoblastic leukemia (ANLL; M6) was diagnosed after 8 months of a preleukemic state. Treatment did not produce any results and death occurred on the 17th day. Cytogenetic studies on the bone marrow cells of both patients were performed. In the first patient in the ALL phase normal cells coexisted with a 47 chromosome clone, the extra chromosome being a D (+ 13?). In the second patient, several karyotype abnormalities were already present in the preleukemic state and also during the acute leukemic phase. No normal mitoses were found; hypodiploidy was present as well as major abnormalities such as markers, rings, and, among others, the systematic loss of a #5 and a #7. The first patient seems to have presented with a de novo ALL, associated with the malignant tumor; whereas, the second patient showed all the characteristics of an induced ANLL. The clinical, hematologic, and cytogenetic characteristics of these two patients are analyzed and compared to those of other cases in the literature.
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PMID:Hematologic and cytogenetic study of two cases of acute leukemia associated with breast cancer. 657 9

During the past 15 years, the records of 2,020 patients who received chemotherapy on the surgical oncology, chemotherapy service at the Pennsylvania Hospital were reviewed. Thirty-five patients had pathologically confirmed second independent malignant tumors (not recurrences). The second cancers that developed were varied. The patients who developed these second malignancies ranged in age from 35 to 77 years (24 females, 11 males). The time interval involved was two to 102 months. Nine patients in this group of second malignancies received prior radiation therapy. The following is a list of the second cancers. There were 8 colons, 5 ovaries, 5 lungs, 6 acute myelogenous leukemias, 1 esophagus, 2 bladders, 2 epidermoid carcinomas of the skin, 2 melanomas, 1 chronic lymphatic leukemia, 1 breast cancer, 1 non-Hodgkin's malignant lymphoma, and 1 stomach cancer. The majority of second malignant tumors were amenable to some form of therapy, ie, surgery, radiation or chemotherapy. However, all of the acute myelogenous leukemias were totally refractory to any therapeutic modalities and rapidly expired. The majority of second cancers developed in patients receiving adjuvant chemotherapy. This is a patient population with a much longer expected survival time, particularly when compared to patients receiving chemotherapy for advanced disease. Twenty-five of the 34 second cancers developed in patients who received adjuvant chemotherapy for breast (14) or colorectal (11) cancers. The etiology of the second malignancies is very difficult to determine. However, alkylating agents appeared to be the possible etiologic agent involved in the development of acute myelogenous leukemia.
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PMID:Second malignancies diagnosed in patients receiving chemotherapy at the Pennsylvania Hospital. 657 22

Interferons (IFNs) are a family of polypeptides originally identified as antiviral substances. Subsequently, other properties of interferons were recognized, including inhibition of cell proliferation, and effects on the immune response and on expression of surface antigens. In this paper we present evidence that interferons, even the highly purified cloned IFNs, can stimulate clonogenic tumor growth in vitro. Of 225 human tumor (HT) samples tested with IFN in a clonogenic assay (HTCA), 30 (13.3%) showed growth stimulation (greater than 2 S.E. above control). The phenomenon was observed most frequently with acute myeloid leukemia (6/22 samples, 27.3%), and renal (2/10, 20%) and breast cancer (4/21, 19%), but significantly less frequent in melanomas (2/34, 5.9%). As an independent assessment of proliferation, tritiated thymidine uptake by tumor cells was measured autoradiographically in 21 patients with multiple myeloma. A significant increase of the thymidine labeling index was seen in 4 (19%) of the samples. Since this growth stimulatory effect was also observed with cell lines which lack any contaminating immunoreactive cells, there is strong evidence that interferons can directly stimulate the proliferation of clonogenic tumor cells in vitro. Growth stimulation by interferons occurred preferentially with lower dosages. It is important to be cognizant of potential clinical implications of tumor growth stimulation by interferons.
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PMID:Tumor growth stimulation in vitro by interferons. 658 Jan 72

Hickman-Broviac catheters are often used when long-term venous access is required. Although generally safe, catheter-related thrombosis and infection are two of the most frequent and clinically important complications associated with their use. A 47-year-old woman with breast cancer had a Hickman catheter placed for chemotherapy; subsequently, the superior vena caval syndrome developed due to a large thrombus surrounding the catheter tip. A very low dose of streptokinase successfully lysed this clot within 12 hours. A 60-year-old woman with acute myelogenous leukemia had a Hickman catheter placed to facilitate induction and maintenance chemotherapy. Two episodes of catheter-related Staphylococcus epidermidis sepsis later developed, the first of which cleared without removal of the cannula.
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PMID:Thrombotic and infectious complications of Hickman-Broviac catheters. 658 78


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