Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient who developed diffuse normolipidemic plane xanthomas also presented with IgG lambda monoclonal gammopathy, hypernephroma, an unusual family cluster of leukemia (with two family members in two generations), and a unique, acquired C1-esterase inhibitor deficiency. A second patient presented with widespread normolipidemic papular xanthomas in which histiocytes containing Langerhans' granules were found. The lipid composition of the lesions of these two patients showed striking differences. Excesses of triglycerides and cholesterol ester were demonstated in plane xanthoma, whereas phospholipids were prominent in the popular xanthoma of histiocytosis X. We present and classify these two cases to emphasize the diagnostic value of chemical and ultrastructural studies of normolipidemic cutaneous xanthomatosis.
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PMID:Unusual normolipidemic cutaneous xanthomatosis: a comparison of two cases illustrating the differential diagnosis. 7 9

10-Chloro-5-(2-dimethylaminoethyl)-7H-indolo [2,3-c]-quinolin-6(5H)-one hydrochloride (CIQ) was shown to exert significant antitumor activity against the Ehrlich carcinoma and sarcoma 180 transplantable tumors in mice by the intraperitoneal (ip) or oral (po) routes and when incorporated into diet. A solid tumor induced in BALB/c mice by the subcutaneous (sc) implantation of nonproducer murine sarcoma virus-transformed BALB/3T3 cells was also inhibited by CIQ after ip or po treatment but there was no effect against leukemia L1210 ascites or a transplantable murine renal adenocarcinoma. When tested in rats, CIQ significantly reduced the growth of Flexner-Jobling carcinoma, Murphy-Sturm lymphosarcoma and Walker 256 carcinosarcoma when administered by the ip or po routes. Pretreatment, but not posttreatment, with CIQ slightly inhibited the humoral antibody response of mice to sheep red blood cells. CIQ therefore differs from immunosuppressive agents such as imuran, methotrexate, cytosine arabinoside, or 6-mercaptopurine which affect the antibody response of mice to sheep erythrocytes when administered after immunization.
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PMID:Activity of 10-chloro-5-(2-dimethylaminoethyl)-7H-indolo [2,3-c]-quinolin-6(5H)-one hydrochloride against experimental tumors in mice and rats. 57 26

Interferons are proteins with antiviral, antiproliferative, and immune-regulating activity. They are classified as alfa, beta, or gamma on the basis of antigenicity and biologic properties. Alfa interferons as single-agent therapy produce clinical improvement in approximately 90 percent of patients with hairy-cell leukemia, and up to 70 percent of patients with chronic myelogenous leukemia (CML) in early-stage disease. Prolonged suppression or elimination of the leukemic cell clone by interferon may ultimately increase survival of patients with CML. Interferon is not effective single-agent therapy for multiple myeloma, but improves response rate when combined with conventional agents. AIDS-associated Kaposi's sarcoma demonstrates a 40 percent objective response rate to interferon, with less risk of immune system suppression than conventional cytotoxics. Other applications of alfa interferon include malignant melanoma and renal cell carcinoma. Beta interferon is similar to the alfa subtype and may have utility in treatment of brain tumors. Gamma interferon is an important immune regulator with qualitative and quantitative differences in its efficacy and toxicity when compared with alfa interferon.
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PMID:Clinical use of biologic response modifiers in cancer treatment: an overview. Part I. The interferons. 169 95

Interferons are currently the most widely used biological response modifiers. They are of high clinical value in haematological malignancies (chronic myelogenous leukaemia, multiple myeloma, non-Hodgkin lymphoma), in solid tumours (malignant melanoma, hypernephroma, pancreas neoplasms, carcinoid tumours, Kaposi's sarcoma, glioma, in ovarium, cervix and bladder carcinoma, and in basalioma) and in infectious diseases (chronic hepatitis B, chronic non-A/non-B hepatitis, chronic delta hepatitis, AIDS, Papova virus and Rhinovirus infections, leishmaniasis, leprosy) and some other conditions. Although the mechanism of action of interferons has not been explained in every detail these agents are promising therapeutic means in a number of diseases.
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PMID:Role of interferon in clinical practice. 172 32

A monoclonal antibody (Ki-M6) against the CD 68 antigen, which labels cells of the monocyte/macrophage system, was tested on Bouin-fixed, paraffin-embedded samples of normal, reactive and neoplastic tissues by an avidin-biotin-peroxidase complex method, with the aim of establishing its value in diagnostic pathology. In normal human tissues, Ki-M6 reactivity was confined to the so-called resident macrophages populating normal organs under physiological conditions. Moreover, restricted reactivity against cells of macrophage lineage was observed in reactive and inflammatory lesions. Granulocytes, monocyte/macrophage-related immune accessory cells, and other analysed normal tissue structures did not reveal any reactivity. Ki-M6 was strongly reactive with the cases of benign (4/4) and malignant (15/15) fibrous histiocytomas, in addition to the true histiocytic lymphomas (3/3). Cases of granular cell tumour (2/3) showed strong reactivity with Ki-M6, whereas only few immunoreactive cells, with weak staining, were seen in the other Ki-M6-positive neoplasms [neurofibroma (3/3), benign schwannoma (1/2), ganglioneuroma (1/1), malignant schwannoma (5/9), melanoma (9/28), dermatofibrosarcoma protuberans (1/1), myelomonocytic leukaemia (3/3)]. Among the epithelial malignancies tested (47 cases), Ki-M6 was positive only in renal cell carcinoma (11/14). Malignant lymphomas of the Hodgkin (56 cases) and non-Hodgkin type (67 cases) were uniformly non-reactive. From these data, Ki-M6 appears to be an excellent marker of monocyte/macrophage-related cells and appears to be a reliable indicator for fibrous histiocytomas and true histiocytic malignancies. The availability of this additional antibody capable of staining routinely processed tissue is of practical interest.
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PMID:Immunohistochemical characterization of Ki-M6 monoclonal antibody in Bouin-fixed, paraffin-embedded sections of normal and neoplastic human tissues. 185 Aug 96

This paper describes the cellular and tissue distribution of P-glycoprotein (P-GP) (mdr1 gene product), the role of P-GP in vivo and immunodiagnosis of multi-drug-resistant cancers. We mainly used MRK 16 monoclonal antibody (MAb) reactive with P-GP. P-GP was found to be expressed very strongly in the adrenal cortex of adults and strongly in the renal tubules of the kidney, capillary blood vessels of the brain, and also in placenta. Interestingly, P-GP was not distributed in fetal and neonatal adrenals, and thus may be closely related to adrenal maturation. A high level of P-GP expression was also seen in all cases of functional hormone-producing adrenal tumor, one case of insulinoma, two cases of untreated colonic cancer, one case each of untreated lung cancer, gastric cancer and breast cancer, six cases of renal cell carcinoma and 17 cases of bladder cancer. Using flow cytometry and immunocytochemistry, we investigated the reactivity of MRK 16 MAb with peripheral human mononuclear cells (mainly blastic cells and lymphocytes) from 31 patients with leukemia or malignant lymphoma. Reactivity with MRK 16 MAb was observed in five cases. Some cases reflected the prior administration of adriamycin, vincristine and VP-16, which are known to induce P-GP expression. P-GP-MRK 16-protein A-Sepharose complex derived from human adrenal possessed marked ATPase activity. These data suggest that P-GP may play a physiological role in the human adrenal. Finally, diagnostic criteria of multi-drug-resistant cancers are presented.
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PMID:Expression and functions of P-glycoprotein (mdr1 gene product) in normal and malignant tissues. 197 61

Synergistic effect of recombinant IFN-gamma (IFN-gamma) and OK-432, a streptococcal preparation, using chromium release assay was studied in vitro on killer cell induction. The target cells utilized for assay were a human leukemia cell line K562, a human renal carcinoma cell line KU-2, autologous normal kidney tissues and autologous renal cell carcinomas. Culture supernatant of peripheral blood lymphocytes (PBL) and OK-432 (designated as OK conditioned medium or OK-CM) demonstrated enhanced cytotoxicity of fresh PBL against these target cells. Killer cell activity against autologous cancer cells could be also induced from PBL of renal cell carcinoma patients. Pretreatment of PBL with IFN-gamma revealed synergistic effect of OK-CM on killer cell induction. OK-CM derived from patients was shown to contain IL-2 activity as well as high titer of interferon. Neutralizing monoclonal antibody against IFN-gamma and IL-2 receptor demonstrated reduction of cytotoxicity. These results suggested potential benefit of sequential use of IFN-gamma and OK-432 for the treatment of metastatic renal cell carcinoma.
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PMID:Combination therapy for renal cell carcinoma using IFN-gamma and OK-432: in vitro study. 211 48

Six out of 204 patients with Hodgkin's disease developed second malignant tumours 25, 30, 61, 65, 68 and 130 months following their treatment. The length of follow-up ranged between 24-233 months with a mean value of 95.8 months. Half of the tumours appeared within the volume irradiated. Five patients received radio- and polychemotherapy, only but one radiotherapy alone. The location of tumours found was as follows: 1 melanoma of the skin, 1 adenocarcinoma of the nasopharynx, 1 cancer of the rectum, 1 renal cell cancer as well as two cancers of the lung. Four patients are living following treatment of their secondary tumour. Until now no case of acute leukaemia could be observed.
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PMID:[Development of a secondary malignant tumor in patients with Hodgkin's disease]. 218 43

Biological modification in cancer therapy involves many different strategies and substances. Bacterial products with established usefulness include BCG, C. parvum and L-Asparaginase. Immunotherapy with such agents has not, however, found general application, although revived interest in 'Coley's mixed toxins' (used earlier this century) paralleled the development of their presumed effector molecules, tumour necrosis factor and lymphotoxin. Many other Cytokines, both natural or recombinant, are now produced on a vast scale following the recent biotechnology revolution. Of these, Alpha Interferons have already proved useful in hairy cell leukaemia, carcinoid tumours, renal cell cancer, Kaposi's sarcoma, chronic granulocytic leukaemia and certain lymphomas, whilst their use as adjuvants or in combination is currently being investigated. More recently, Interleukin-2, which stimulates the clonal expansion of activated T-cells, has shown promise both as a single agent, and when used with lymphokine activated killer (LAK) cells or tumour infiltrating lymphocytes (TILS). A different approach involves the Colony Stimulating Factors such as G-CSF and GM-CSF which reduce the degree and duration of treatment-related myelosuppression, thereby allowing more intensive cytotoxic or radiation therapy, as well as facilitating early recovery following bone marrow transplantation. Monoclonal antibodies have not proved as specific for malignant cells as was originally hoped, but certain tumours, such as lymphoma, are now realistic targets for therapy. Increasingly sophisticated effector mechanisms (e.g. conjugated pro-drugs) and genetically engineered "humanised" monoclonal antibody hybrids present the brightest hopes for the future. Biotherapy, the "fourth modality of cancer treatment" has already assumed its place alongside surgery, radiotherapy and cytotoxic chemotherapy, and will grow in importance as our understanding of the molecular biology of cancer increases in the coming decades.
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PMID:Biological modifiers and their role in cancer therapy. 218 42

The influence of in vivo application of recombinant interferon-alpha 2c (IFN-alpha 2c) and recombinant interferon-gamma (IFN-gamma) on beta-2 microglobulin levels was studied in eight patients with chronic myelogenous leukaemia or advanced renal cell carcinoma. Data indicated enhanced beta-2 microglobulin biosynthesis in close temporary association with injection of both types of interferons. The influence of in vivo stimulation by allogenic leukocytes and the influence of renal allografts or cytomegalovirus infection on serum beta-2 microglobulin and IFN-gamma levels were also studied. Increased beta-2 microglobulin concentrations were observed again in each of these clinical situations and were closely associated with enhanced endogenous interferon production. From these in vivo data and the in vitro data presented in the preceding publication, (1) we conclude that endogenous interferon levels are crucial for the regulation of beta-2 microglobulin release in vivo.
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PMID:Cytokines in the control of beta-2 microglobulin release. II. In vivo studies with recombinant interferons and antigens. 245 79


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