Concurrent Chronic Lymphocytic Leukemia Cutis and Acute Myelogenous Leukemia Cutis in a Patient with Untreated CLL

2001 ◽  
Vol 23 (4) ◽  
pp. 334-340 ◽  
Author(s):  
Michael K. Miller ◽  
James A. Strauchen ◽  
Khanh T. Nichols ◽  
Robert G. Phelps
Author(s):  
Amer Yazdanparast ◽  
Gholamreza Fathpour ◽  
Shirin Saberianpour

Global cancer statistics will continue to grow in the coming years. Leukemia is the fifth leading cause of death in the world and the second one in Iran; therefore, it is very important to study the affected areas, including the cardiovascular system in this disease. In heart cancer, tumors whose primary origin is the heart are called primary tumors, which are very rare. Tumors that originate in other parts of the body and spread to the heart are called secondary tumors. Although heart cancer is still rare, most cancers found in the heart come from other parts of the body and are considered as secondary tumors. The symptoms of metastatic heart cancer vary and depend on the location and extent of the lesion. Cancer can also affect the heart in other ways. One of these ways is the effect of the treatments used, which is reported among acute lymphocytic leukemia, acute myelogenous leukemia, chronic lymphocytic leukemia, and chronic myelogenous leukemia due to the use of tyrosine kinase inhibitors as the main drug in reducing mortality among these patients. Pericardial involvement is reported to be the most common cardiovascular complication of drug use among different kinds of leukemias. In this article, we try to collect cardiovascular evidence related to acute lymphocytic leukemia, acute myelogenous leukemia, chronic lymphocytic leukemia, and chronic myelogenous leukemia, separately.


2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 6562-6562 ◽  
Author(s):  
E. M. Nelli ◽  
K. Leitzel ◽  
S. M. Ali ◽  
H. A. Al-Mondhiry ◽  
L. Demers ◽  
...  

6562 Background: Ras is a GDP/GTP binding G protein that acts as a molecular switch converting signals from the cell membrane to the nucleus to regulate cell proliferation, differentiation, and protein synthesis. Activation of ras oncogenes has been identified in a variety of cancers, including 30% of acute myelogenous leukemia patients. The purpose of our study was to evaluate serum ras levels and correlate with survival in hematologic cancer patients. Methods: A novel ras p21 ELISA (Oncogene Science/Bayer Diagnostics, Cambridge, MA) employing two monoclonal antibodies reactive with H, K, and N ras was utilized to quantify total ras levels in serum obtained from patients with various hematologic malignancies including acute myelogenous leukemia (AML), acute lymphocytic leukemia (ALL), chronic myelogenous leukemia (CML), and chronic lymphocytic leukemia (CLL). Results: The total leukemia patient group consisted of 52 patients. At the 75th percentile serum ras cutpoint (524 pg/ml) 11/52 patients were defined as elevated for serum ras. From this patient group, 38 patients had clinical followup available and were included in the Kaplan-Meier analysis of overall survival. Patients with elevated serum ras (>524 pg/ml) had significantly shorter overall survival compared to those without (median OS 205 vs. 677 days) (p= 0.04). In a multivariate analysis including serum ras level and type of leukemia, serum ras level remained a significant independent variable for shorter overall survival (p=0.004). Within leukemia subtypes 2/18 AML, 4/9 CML, 3/7 ALL, and 0/4 CLL patients had elevated serum ras levels. Conclusions: Leukemia patients with elevated serum ras levels had a significantly shorter overall survival. Serum ras should be evaluated as a potential biomarker in larger leukemia trials, especially for response to treatment with inhibitors of the ras signaling pathway. [Table: see text]


Cancer ◽  
1989 ◽  
Vol 63 (11) ◽  
pp. 2192-2200 ◽  
Author(s):  
Maria R. Baer ◽  
Maurice Barcos ◽  
Howard Farrell ◽  
Azra Raza ◽  
Harvey D. Preisler

Blood ◽  
1964 ◽  
Vol 23 (4) ◽  
pp. 526-544 ◽  
Author(s):  
DONALD W. KUNDEL ◽  
GEORGE BRECHER ◽  
GERALD P. BODEY ◽  
GEOFFREY M. BRITTIN

Abstract Reticulin fibrosis was found in 21 of 40 patients with acute lymphocytic leukemia when marrows were studied sequentially by Vim-Silverman needle biopsies. Reticulin fibrosis frequently occurred early in the development of the disease. Mild degrees were completely reversible with remission, severe degrees usually persisted, even through remissions. Fibrosis appeared to develop during relapse. Duration of the disease in itself had little influence on the degree of reticulin fibrosis, and collagen fibrosis seldom followed reticulin fibrosis even after many months’ duration. The prognosis of patients with reticulin fibrosis of their marrows was definitely poorer than for the group without increased reticulin. Reticulin fibrosis virtually always prevented successful marrow biopsies by the standard technic of needle aspiration. Bone necrosis occurred in 11 of 75 patients with acute lymphocytic leukemia, but in none of 53 patients with acute myelogenous leukemia studied by Vim-Silverman needle biopsies during life or at autopsy. Bone necrosis was the major cause of severe bone pain and it was always associated with reticulin fibrosis of the marrow. Bone infarcts were not associated with short survival in all cases, but in general the prognosis of patients with bone necrosis was even poorer than that of patients with reticulin fibrosis but without demonstrable infarction.


Blood ◽  
1983 ◽  
Vol 61 (5) ◽  
pp. 858-866 ◽  
Author(s):  
AJ Malcolm ◽  
PM Logan ◽  
RC Shipman ◽  
R Kurth ◽  
JG Levy

Abstract The properties of a rabbit antiserum (anti-AML) raised to a purified protein from membranes of human acute myelogenous leukemia (AML) cells is described. Bone marrow and peripheral blood leukocytes (PBL) from either normal individuals or patients with either myeloproliferative or other disorders were analyzed in a fluorescence-activated cell sorter (FACS IV) after labeling with anti-AML, normal rabbit serum (NRS), or antiserum raised to normal human membrane antigens. Of 40 cell samples from patients with acute myelogenous leukemia, 39 reacted strongly with the anti-AML antiserum. Similarly, all of 19 specimens from patients with chronic granulocytic leukemia reacted with the anti-AML. When 42 bone marrow or PBL samples from patients with a variety of lymphoproliferative disorders were examined, 2 specimens reacted with the antiserum, both from individuals with diagnoses of acute lymphocytic leukemia (ALL). None of the 14 normal bone marrow or PBL donor specimens tested reacted with the antiserum. It was also found that essentially all samples from patients in clinical remission from AML had high numbers of cells reactive with the anti-AML. When cells from such individuals were labeled and sorted on the FACS IV, it was found that cells fluorescing strongly with the anti-AML contained cells of both myeloid and lymphoid origin. The implications of these results are discussed.


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