scholarly journals Insulin receptors on leukemia and lymphoma cells

Blood ◽  
1983 ◽  
Vol 62 (2) ◽  
pp. 251-255
Author(s):  
PM Chen ◽  
SH Kwan ◽  
TS Hwang ◽  
BN Chiang ◽  
CK Chou
Keyword(s):  
Binding Sites ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Lymphocytic Leukemia ◽  
Acute Monocytic Leukemia ◽  
Acute Myelocytic Leukemia ◽  
Chronic Myelocytic Leukemia ◽  
Monocytic Leukemia ◽  
Myelocytic Leukemia ◽  
Specific Insulin

Tumor cells obtained from leukemia and lymphoma patients were investigated for specific insulin receptors. Using radioactive 125I- labeled insulin, specific insulin binding sites were demonstrated on most acute lymphocytic leukemia (ALL) and acute myelocytic leukemia (AML) cells, including acute promyelocytic leukemia (APL), chronic myelocytic leukemia (CML), and acute monocytic leukemia (AMoL) cells. Insulin receptors were not found on chronic lymphocytic leukemia (CLL) and malignant lymphoma (ML) cells. Specific insulin binding sites were also found on monocytes and thymocytes after treatment with phytohemagglutinin (PHA-P), but not on inactivated tonsil cells, peripheral blood lymphocytes, or thymocytes. There was no inverse correlation between the content of insulin receptors and the basal level of circulating insulin. These data suggest that the insulin receptor may be a new marker of acute leukemia and chronic myelocytic leukemia.

scholarly journals Insulin receptors on leukemia and lymphoma cells

Blood ◽  
1983 ◽  
Vol 62 (2) ◽  
pp. 251-255 ◽  
Author(s):  
PM Chen ◽  
SH Kwan ◽  
TS Hwang ◽  
BN Chiang ◽  
CK Chou
Keyword(s):  
Binding Sites ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Lymphocytic Leukemia ◽  
Acute Monocytic Leukemia ◽  
Acute Myelocytic Leukemia ◽  
Chronic Myelocytic Leukemia ◽  
Monocytic Leukemia ◽  
Myelocytic Leukemia ◽  
Specific Insulin

Abstract Tumor cells obtained from leukemia and lymphoma patients were investigated for specific insulin receptors. Using radioactive 125I- labeled insulin, specific insulin binding sites were demonstrated on most acute lymphocytic leukemia (ALL) and acute myelocytic leukemia (AML) cells, including acute promyelocytic leukemia (APL), chronic myelocytic leukemia (CML), and acute monocytic leukemia (AMoL) cells. Insulin receptors were not found on chronic lymphocytic leukemia (CLL) and malignant lymphoma (ML) cells. Specific insulin binding sites were also found on monocytes and thymocytes after treatment with phytohemagglutinin (PHA-P), but not on inactivated tonsil cells, peripheral blood lymphocytes, or thymocytes. There was no inverse correlation between the content of insulin receptors and the basal level of circulating insulin. These data suggest that the insulin receptor may be a new marker of acute leukemia and chronic myelocytic leukemia.

scholarly journals Studies of a familial platelet disorder

Blood ◽  
1985 ◽  
Vol 65 (3) ◽  
pp. 557-563 ◽  
Author(s):  
SB Dowton ◽  
D Beardsley ◽  
D Jamison ◽  
S Blattner ◽  
FP Li
Keyword(s):  
Acute Monocytic Leukemia ◽  
Acute Myelocytic Leukemia ◽  
Bleeding Tendency ◽  
Monocytic Leukemia ◽  
Autosomal Dominant Disorder ◽  
Myelocytic Leukemia ◽  
Platelet Disorder ◽  
Familial Platelet Disorder ◽  
And Function ◽  
Congenital Neuroblastoma

At least 22 members of a large kindred have a bleeding tendency resulting from an autosomal dominant disorder of platelet production and function. Phenotypic manifestations include mild to moderate thrombocytopenia, bleeding time prolongation, and abnormal platelet aggregation. Platelet survival time is normal. The platelet disorder in this family appears to differ from known hereditary thrombocytopenic or thrombocytopathic syndromes and may represent a new genetic disease. Six family members reportedly developed hematologic neoplasms: acute monocytic leukemia nine years after treatment for congenital neuroblastoma; lymphosarcoma at age 10 years; myeloid leukemia at age 23 years; acute myelocytic leukemia at age 62 years; leukemia of unknown type at age 48 years; and lymphocytic lymphoma at age 52 years.

scholarly journals Studies of a familial platelet disorder

Blood ◽  
1985 ◽  
Vol 65 (3) ◽  
pp. 557-563 ◽  
Author(s):  
SB Dowton ◽  
D Beardsley ◽  
D Jamison ◽  
S Blattner ◽  
FP Li
Keyword(s):  
Acute Monocytic Leukemia ◽  
Acute Myelocytic Leukemia ◽  
Bleeding Tendency ◽  
Monocytic Leukemia ◽  
Autosomal Dominant Disorder ◽  
Myelocytic Leukemia ◽  
Platelet Disorder ◽  
Familial Platelet Disorder ◽  
And Function ◽  
Congenital Neuroblastoma

Abstract At least 22 members of a large kindred have a bleeding tendency resulting from an autosomal dominant disorder of platelet production and function. Phenotypic manifestations include mild to moderate thrombocytopenia, bleeding time prolongation, and abnormal platelet aggregation. Platelet survival time is normal. The platelet disorder in this family appears to differ from known hereditary thrombocytopenic or thrombocytopathic syndromes and may represent a new genetic disease. Six family members reportedly developed hematologic neoplasms: acute monocytic leukemia nine years after treatment for congenital neuroblastoma; lymphosarcoma at age 10 years; myeloid leukemia at age 23 years; acute myelocytic leukemia at age 62 years; leukemia of unknown type at age 48 years; and lymphocytic lymphoma at age 52 years.

scholarly journals Granulocytic Sarcoma (Chloroma)

Blood ◽  
1970 ◽  
Vol 35 (3) ◽  
pp. 361-369 ◽  
Author(s):  
PETER H. WIERNIK ◽  
ARTHUR A. SERPICK
Keyword(s):  
Chest Wall ◽  
Granulocytic Sarcoma ◽  
Acute Monocytic Leukemia ◽  
Reticulum Cell ◽  
Acute Myelocytic Leukemia ◽  
Reticulum Cell Sarcoma ◽  
Partial Regression ◽  
Monocytic Leukemia ◽  
Myelocytic Leukemia ◽  
Leukemia Diagnosis

Abstract Four patients with granulocytic sarcoma are described. Granulocytic sarcoma of the cheek occurred in one patient 10 months before the diagnosis of acute myelocytic leukemia could be made. Another patient had multiple bone and dural granulocytic sarcomas 17 months before she developed acute myelocytic leukemia. One patient had a breast granulocytic sarcoma and acute myelocytic leukemia diagnosis simultaneously, and a fourth patient developed a chest wall granulocytic sarcoma 11-½ months after the diagnosis of acute monocytic leukemia. The cheek and chest wall granulocytic sarcomas responded completely to antileukemic chemotherapy but subsequently recurred. Radiotherapy effected a permanent complete remission of the chest wall sarcoma, and partial regression of the bone granulocytic sarcomas in another case. The possibility that acute myelocytic leukemic, granulocytic sarcoma and reticulum cell sarcoma are variations of the same disease is suggested and discussed.

scholarly journals Arabinosyl Cytosine: A Useful Agent in the Treatment of Acute Leukemia in Adults

Blood ◽  
1968 ◽  
Vol 32 (4) ◽  
pp. 507-523 ◽  
Author(s):  
ROSE RUTH ELLISON ◽  
JAMES F. HOLLAND ◽  
MARISE WEIL ◽  
CLAUDE JACQUILLAT ◽  
MICHEL BOIRON ◽  
...  
Keyword(s):  
Remission Rate ◽  
Hemoglobin Level ◽  
Lymphocytic Leukemia ◽  
Acute Myelocytic Leukemia ◽  
Pyrimidine Nucleoside ◽  
Myelocytic Leukemia ◽  
Daily Dose ◽  
Significant Superiority ◽  
Infusion Duration ◽  
Arabinosyl Cytosine

Abstract Arabinosyl cytosine (ara-C), a synthetic pyrimidine nucleoside related to the normal metabolites cytidine and deoxycytidine, has been found capable of producing marrow remission at tolerable doses in acute myelocytic and acute lymphocytic leukemia in adults. There were 16 per cent remissions complete in all aspects, 3 per cent complete except for hemoglobin level, and 6 per cent partial remissions among 180 adults with acute myelocytic leukemia treated with any one of 8 variants of infusion duration or daily dose of ara-C. Twenty-four per cent of 37 adults with acute lymphocytic or unclassified leukemia had complete or partial remissions. The comparison of 1, 4, 12 and 24 hours infusion of ara-C (to total dose tolerated) does not show significant superiority for any one group. The complete remission rate with 1 or 12 hour infusions, however, is 25 per cent (superior to that obtained with 6-mercaptopurine) and the recommended schedule of treatment for ara-C based on these data is, therefore, daily infusions of 100 or 50 mg./m.2 in one hour for approximately 3 to 6 weeks followed by maintenance therapy of once weekly subcutaneous injection of 30 mg./m.2 of ara-C. Platelet transfusions should be available when ara-C is used.

scholarly journals Gambaran Laboratorium Leukemia Kronik di Bagian Penyakit Dalam RSUP Dr. M. Djamil Padang

2013 ◽  
Vol 2 (3) ◽  
pp. 141
Author(s):  
Muthia Rendra ◽  
Rismawati Yaswir ◽  
Akmal M Hanif
Keyword(s):  
Internal Medicine ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Lymphocytic Leukemia ◽  
Chronic Myelocytic Leukemia ◽  
Laboratory Findings ◽  
Medicine Department ◽  
Chronic Leukemia ◽  
Myelocytic Leukemia ◽  
Moderate Anemia

AbstrakLeukemia merupakan penyakit keganasan sel darah yang berasal dari sumsum tulang ditandai oleh proliferasi sel-sel darah putih, dengan manifestasi adanya sel-sel abnormal dalam darah tepi. Pada tahun 2006, leukemia berada pada urutan ke-5 dari keseluruhan penderita kanker di Indonesia. Leukemia kronik merupakan leukemia yang paling sering terjadi pada dewasa dan lanjut usia. Secara umum leukemia kronik diklasifikasikan atas Leukemia Granulositik Kronik (LGK) dan Leukemia Limfositik Kronik (LLK). Leukemia kronik yang perjalanannya lambat dan diiringi oleh gejala yang tidak khas, maka penelitian ini bertujuan untuk mengetahui gambaran laboratorium leukemia kronik di bagian Peyakit Dalam RSUP DR. M. Djamil Padang. Jenis penelitian ini adalah deskriptif retrospektif. Instrumen yang digunakan pada penelitian ini adalah data sekunder yang diperoleh dari Instalasi Rekam Medik RSUP Dr. M. Djamil Padang berupa data pasien leukemia kronik yang dirawat di Bagian Penyakit Dalam RSUP Dr. M. Djamil Padang sejak 1 Januari 2010 – 31 Desember 2012. Hasil penelitian ini menunjukkan bahwa dari 16 kasus leukemia granulositik kronik terdapat 37,5% pasien mengalami anemia sedang, 100% leukositosis, jumlah trombosit dapat menurun, normal, dan meningkat dengan presentase masing-masing 25%, 25%, dan 50%. Gambaran eritrosit sebagian besar normositik anisositosis. Separuh pemeriksaan darah tepi menunjukkan peningkatan persentasi mielosit, 31,25% menunjukkan peningkatan persentasi metamielosit dan eosinofil, serta sebagian besar menunjukkan presentasi blast. Sedangkan gambaran sumsum tulang hiperseluler, penekanan eritropoetik, mielopoetik hiperaktif, dan trombopoetik dalam batas normal. Leukemia limfositik kronik yang terdiri dari 1 kasus menunjukkan gambaran laboratorium berupa anemia sedang, leukositosis, trombositopenia, gambaran eritrosit nomokrom anisositosis, peningkatan jumlah leukosit, peningkatan jumlah limfosit, presentasi smudge cell, dan ditemukan presentasi blast pada darah tepi, tetapi selularitas tidak dapat dinilai.Kata kunci: leukemia kronik, darah tepi, BMPAbstractLeukemia is a malignant disease of blood cells derived from the bone marrow characterized by the proliferation of white blood cells, with the manifestation of the abnormal cells in the peripheral blood. In 2006, leukemia was ranked 5th of all cancer patients in Indonesia. Chronic leukemia is the most common leukemia in adult and the elderly. In general, chronic leukemia classified on chronic myelocytic leukemia (CML) and chronic lymphocytic leukemia (CLL). The onset of chronic leukemia is insidious and accompanied by symptoms that are not typical, this research aims to describe the laboratory findings of chronic leukemia patients treated at Internal Medicine Department of Dr. M. Djamil Hospital Padang.This research is a retrospective descriptive research. The instruments used in this research are the secondary data derived from the Medical Record Departement Dr. M. Djamil Hospital Padang in the form of leukemia chronic patients’ data who were treated in Internal Medicine Department of Dr. M. Djamil Hospital Padang since January 1st 2010 – December 31st 2012. The results of this research showed that of 16 cases of chronic myelocytic leukemia contained 37.5% of the patients had moderate anemia, leukocytosis 100%, platelet count can be decreased, normal, and increased the percentage of each 25%, 25%, and 50%. The morphology of erythrocytes mostly normocytic anisocytosis. Half of peripheral blood examination showed an increase in the percentage of myelocyte, 31.25% showed an increase in the percentage metamyelocyte and eosinophils, as well as most of the shows presentation blast. The bone marrow are hypercellular, compressing erythropoietic, myelopoietic hyperactivity and thrombopoietic mostly normal in number. Chronic lymphocytic leukemia consisting of 1 case shows the laboratory findings are moderate anemia, leukocytosis, thrombocytopenia, the morphology of erythrocyte is normochromic anisocytosis, leukocytes increase in number, increase in the number of lymphocytes, presentations smudge cells, and blast presentation is found in the peripheral blood, but the cellularity not be assessed.Keywords: chronic leukemia, peripheral blood, BMP

Insulin receptors on Xenopus laevis oocytes: effects of injection of ob/ob mouse liver mRNA

1991 ◽  
Vol 100 (1) ◽  
pp. 167-171
Author(s):  
D.A. Diss ◽  
B.D. Greenstein
Keyword(s):  
Xenopus Laevis ◽  
Binding Sites ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Cell Types ◽  
Follicle Cells ◽  
Vitelline Membrane ◽  
Xenopus Laevis Oocytes ◽  
Endogenous Insulin ◽  
Order Of Magnitude

We describe here conditions for the detection of insulin binding sites on Xenopus laevis oocytes. The binding of 125I-labelled insulin displayed sigmoidal behaviour, which is characteristic of the binding relationship between insulin and its receptor. Resolution of the resulting curvilinear Scatchard plot into two components revealed KD values of 8.86 × 10(−10) +/− 1.9 × 10(−10) and 5.32 × 10(−9) +/− 2.4 × 10(−9) M and n values of 9.7 × 10(7) +/− 0.4 × 10(7) and 3.3 × 10(8) +/− 0.5 × 10(8) binding sites per oocyte, respectively. The possibility cannot be excluded, however, that receptors for IGF-1 were also being detected. Also described are conditions for the rapid and efficient removal of all tissues surrounding the oocyte, including the vitelline membrane. We could not detect any specific 125I-labelled insulin binding to oocytes that had their follicle cells or vitelline membrane removed and this was not due to the enzymic treatment used in the process. Microinjection of oocytes without follicular layers did not result in the appearance of any detectable insulin binding sites, which were, however, observed if oocytes were first stripped of the vitelline membrane. We suggest that oocytes may possess endogenous insulin receptors on their surface in numbers of the same order of magnitude as those present on somatic cells. The removal of tissues surrounding the oocyte should facilitate studies aimed at determining functional interactions of the various cell types during oocyte development and for studying insulin receptors on the oocyte-follicular cell complex.

Insulin Binding Sites Induced in the Tetrahymena by Rat Liver Receptor Antibody

1984 ◽  
Vol 39 (1-2) ◽  
pp. 183-185 ◽  
Author(s):  
G. Csaba ◽  
P. Kovács ◽  
Ágnes Inczefi-Gonda
Keyword(s):  
Rat Liver ◽  
Concanavalin A ◽  
Binding Sites ◽  
Binding Capacity ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Receptor Antibody ◽  
Receptor Antibodies

Abstract Tetrahvmena cells treated with purified rabbit anti­ bodies to rat hepatocellular membrane exhibited a consider­ able increase in binding capacity on reexposure to the antibody 24 h later. Insulin binding was similarly enhanced by preexposure to the antibody, and vice versa, preex­ posure to insulin enhanced the later binding of rat liver receptor antibodies. This suggests that (1) the Tetrahymena and the rat possess similar insulin receptors, and (2) the receptor antibody is also able to induce imprinting for itself as well as for insulin. Concanavalin-A, noted for binding overlap with insulin, failed to induce imprinting either for insulin or for antibodies to receptors, whereas the latter did induce imprinting for Concanavalin-A.

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