scholarly journals A pericentric inversion of chromosome 16 is associated with dysplastic marrow eosinophils in acute myelomonocytic leukemia

Blood ◽  
1984 ◽  
Vol 63 (4) ◽  
pp. 800-802 ◽  
Author(s):  
R Tantravahi ◽  
M Schwenn ◽  
C Henkle ◽  
M Nell ◽  
PR Leavitt ◽  
...  
Keyword(s):  
Pericentric Inversion ◽  
Surface Marker ◽  
Leukemic Cells ◽  
Acute Nonlymphocytic Leukemia ◽  
Chromosome 16 ◽  
Cytogenetic Studies ◽  
Fab Classification ◽  
Acute Myelomonocytic Leukemia ◽  
Surface Marker Analysis ◽  
Myelomonocytic Leukemia

Abstract Cytogenetic studies were performed in 18 consecutive children with acute nonlymphocytic leukemia (ANLL) between 1981 and 1983. Three children with acute myelomonocytic leukemia (AMMoL; M4, FAB classification) had the following unique bone marrow morphology and cytogenetic abnormality: eosinophilic precursors with dysplastic violaceous granules and a pericentric inversion of chromosome 16. Surface marker analysis of leukemic cells from these patients, using a panel of monoclonal antibodies, revealed the expression of a series of monocyte markers. The association of an inversion of chromosome 16 with abnormal eosinophil morphology in the M4 subtype of ANLL appears to represent a unique subgroup of patients.

scholarly journals A pericentric inversion of chromosome 16 is associated with dysplastic marrow eosinophils in acute myelomonocytic leukemia

Blood ◽  
1984 ◽  
Vol 63 (4) ◽  
pp. 800-802
Author(s):  
R Tantravahi ◽  
M Schwenn ◽  
C Henkle ◽  
M Nell ◽  
PR Leavitt ◽  
...  
Keyword(s):  
Pericentric Inversion ◽  
Surface Marker ◽  
Leukemic Cells ◽  
Acute Nonlymphocytic Leukemia ◽  
Chromosome 16 ◽  
Cytogenetic Studies ◽  
Fab Classification ◽  
Acute Myelomonocytic Leukemia ◽  
Surface Marker Analysis ◽  
Myelomonocytic Leukemia

Cytogenetic studies were performed in 18 consecutive children with acute nonlymphocytic leukemia (ANLL) between 1981 and 1983. Three children with acute myelomonocytic leukemia (AMMoL; M4, FAB classification) had the following unique bone marrow morphology and cytogenetic abnormality: eosinophilic precursors with dysplastic violaceous granules and a pericentric inversion of chromosome 16. Surface marker analysis of leukemic cells from these patients, using a panel of monoclonal antibodies, revealed the expression of a series of monocyte markers. The association of an inversion of chromosome 16 with abnormal eosinophil morphology in the M4 subtype of ANLL appears to represent a unique subgroup of patients.

Extensive cross-homology between the long and the short arm of chromosome 16 may explain leukemic inversions and translocations

Blood ◽  
1992 ◽  
Vol 79 (5) ◽  
pp. 1299-1304 ◽  
Author(s):  
JG Dauwerse ◽  
EA Jumelet ◽  
JW Wessels ◽  
JJ Saris ◽  
A Hagemeijer ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Acute Leukemia ◽  
Fluorescence In Situ Hybridization ◽  
Pericentric Inversion ◽  
Repetitive Elements ◽  
Leukemic Cells ◽  
Acute Nonlymphocytic Leukemia ◽  
Chromosome 16

Abstract Specific rearrangements of chromosome 16 are well known in acute nonlymphocytic leukemia with abnormal eosinophils. While mapping cosmids relative to breakpoints in chromosome 16 in leukemic cells with fluorescence in situ hybridization (FISH), we have identified three areas of extensive cross-homology between 16p and 16q. Three cosmids among 99 tested showed two large signals on the short arm and one signal on the long arm of chromosome 16. A fourth cosmid showed mainly two signals on the short arm. With the 16p-specific cosmid we can demonstrate that the breakpoints of a pericentric inversion and a reciprocal (16;16) translocation, both of which are characteristic for acute leukemia, map to the most distal of two blocks on the short arm. We suggest that there may be at least two distinct repetitive elements specific for chromosome 16 interdigitated on 16p. The presence of a similar repeat in the short, as well as the long arm of the chromosome, may play a role in the origin of chromosome 16 rearrangements in acute leukemia.

Karyotypic evolution in acute myelomonocytic leukemia with pericentric inversion of chromosome 16

1987 ◽  
Vol 24 (2) ◽  
pp. 257-262 ◽  
Author(s):  
Masafumi Taniwaki ◽  
Johji Inazawa ◽  
Shigeo Horiike ◽  
Shinichi Misawa ◽  
Tatsuo Abe ◽  
...  
Keyword(s):  
Pericentric Inversion ◽  
Karyotypic Evolution ◽  
Chromosome 16 ◽  
Acute Myelomonocytic Leukemia ◽  
Myelomonocytic Leukemia

Abnormalities of chromosome 16 in association with acute myelomonocytic leukemia and dysplastic bone marrow eosinophils.

1984 ◽  
Vol 2 (6) ◽  
pp. 550-557 ◽  
Author(s):  
D E Hogge ◽  
S Misawa ◽  
N Z Parsa ◽  
A Pollak ◽  
J R Testa
Keyword(s):  
Bone Marrow ◽  
Pericentric Inversion ◽  
Bone Marrow Cells ◽  
Absolute Number ◽  
Chromosome 16 ◽  
Abnormal Bone Marrow ◽  
Acute Myelomonocytic Leukemia ◽  
Prognostic Importance ◽  
Myelomonocytic Leukemia ◽  
Marrow Cells

Six patients with M4 acute myelomonocytic leukemia ( AMMoL ) were identified who had abnormalities of chromosome 16 in bone marrow cells. Five had a pericentric inversion, inv(16)( p13q22 ), and a sixth patient had a translocation, t(16;16)(p13.1;q22). Each of these six patients had bone marrow eosinophils that were abnormal in morphology on light and/or electron microscopy and by cytochemical stains. The eosinophils constituted 1%-24% of nucleated marrow cells. Of 61 acute nonlymphocytic leukemia (ANLL) patients, all those with AMMoL and abnormal bone marrow eosinophils had an inv(16) or a t(16;16). One other patient in this group had a rearrangement of chromosome 16 (with a break in the short arm at band p13); however, the ANLL type was M1 and no abnormal eosinophils were present. Four patients with ANLL types other than M4 had an increase in marrow eosinophils; three in whom the eosinophils appeared normal and one with ANLL-M2 and bizarre eosinophils morphologically distinct from those seen in AMMoL . Chromosome pair 16 was normal in the latter four patients. AMMoL with dysplastic bone marrow eosinophils appears to represent a unique clinicopathologic entity associated with several related abnormalities affecting 16q . The morphologic features of both blasts and eosinophils may be more important than the absolute number of eosinophils in the marrow in identifying this group of patients. This may have prognostic importance as five of six patients achieved complete remission with standard antileukemic therapy and are still alive.

scholarly journals Extensive cross-homology between the long and the short arm of chromosome 16 may explain leukemic inversions and translocations

Blood ◽  
1992 ◽  
Vol 79 (5) ◽  
pp. 1299-1304 ◽  
Author(s):  
JG Dauwerse ◽  
EA Jumelet ◽  
JW Wessels ◽  
JJ Saris ◽  
A Hagemeijer ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Acute Leukemia ◽  
Fluorescence In Situ Hybridization ◽  
Pericentric Inversion ◽  
Repetitive Elements ◽  
Leukemic Cells ◽  
Acute Nonlymphocytic Leukemia ◽  
Chromosome 16

Specific rearrangements of chromosome 16 are well known in acute nonlymphocytic leukemia with abnormal eosinophils. While mapping cosmids relative to breakpoints in chromosome 16 in leukemic cells with fluorescence in situ hybridization (FISH), we have identified three areas of extensive cross-homology between 16p and 16q. Three cosmids among 99 tested showed two large signals on the short arm and one signal on the long arm of chromosome 16. A fourth cosmid showed mainly two signals on the short arm. With the 16p-specific cosmid we can demonstrate that the breakpoints of a pericentric inversion and a reciprocal (16;16) translocation, both of which are characteristic for acute leukemia, map to the most distal of two blocks on the short arm. We suggest that there may be at least two distinct repetitive elements specific for chromosome 16 interdigitated on 16p. The presence of a similar repeat in the short, as well as the long arm of the chromosome, may play a role in the origin of chromosome 16 rearrangements in acute leukemia.

scholarly journals Leukemia with Down's syndrome: translocation between chromosomes 1 and 19 in acute myelomonocytic leukemia following transient congenital myeloproliferative syndrome

Blood ◽  
1985 ◽  
Vol 66 (6) ◽  
pp. 1466-1468 ◽  
Author(s):  
R Morgan ◽  
F Hecht ◽  
ML Cleary ◽  
J Sklar ◽  
MP Link
Keyword(s):  
Spontaneous Regression ◽  
Down's Syndrome ◽  
Down’S Syndrome ◽  
Myeloproliferative Disorder ◽  
Leukemic Cells ◽  
Immunoglobulin Gene ◽  
Acute Nonlymphocytic Leukemia ◽  
Myeloproliferative Syndrome ◽  
Acute Myelomonocytic Leukemia ◽  
Myelomonocytic Leukemia

Abstract A girl with Down's syndrome was born with a myeloproliferative disorder. The child had spontaneous regression of the myeloproliferation, with acute leukemia developing at a later date. Morphologic, cytochemical, immunologic, and immunoglobulin gene configuration studies all supported the diagnosis of acute nonlymphocytic leukemia. High-resolution chromosome studies revealed that the leukemic cells consistently contained a translocation between chromosomes 1 and 19: der(19)t(1;19)(q25;p13). Spontaneous regression of the transient myeloproliferative syndrome of the newborn with Down's syndrome may not always be permanent, and the transient myeloproliferative syndrome may sometimes represent an early sign of acute nonlymphocytic leukemia.

scholarly journals Leukemia with Down's syndrome: translocation between chromosomes 1 and 19 in acute myelomonocytic leukemia following transient congenital myeloproliferative syndrome

Blood ◽  
1985 ◽  
Vol 66 (6) ◽  
pp. 1466-1468 ◽  
Author(s):  
R Morgan ◽  
F Hecht ◽  
ML Cleary ◽  
J Sklar ◽  
MP Link
Keyword(s):  
Spontaneous Regression ◽  
Down's Syndrome ◽  
Down’S Syndrome ◽  
Myeloproliferative Disorder ◽  
Leukemic Cells ◽  
Immunoglobulin Gene ◽  
Acute Nonlymphocytic Leukemia ◽  
Myeloproliferative Syndrome ◽  
Acute Myelomonocytic Leukemia ◽  
Myelomonocytic Leukemia

A girl with Down's syndrome was born with a myeloproliferative disorder. The child had spontaneous regression of the myeloproliferation, with acute leukemia developing at a later date. Morphologic, cytochemical, immunologic, and immunoglobulin gene configuration studies all supported the diagnosis of acute nonlymphocytic leukemia. High-resolution chromosome studies revealed that the leukemic cells consistently contained a translocation between chromosomes 1 and 19: der(19)t(1;19)(q25;p13). Spontaneous regression of the transient myeloproliferative syndrome of the newborn with Down's syndrome may not always be permanent, and the transient myeloproliferative syndrome may sometimes represent an early sign of acute nonlymphocytic leukemia.

Pericentric inversion of chromosome 16 and eosinophilia in chronic myelomonocytic leukemia

1997 ◽  
Vol 94 (2) ◽  
pp. 99-102 ◽  
Author(s):  
Toshihiro Miyamoto ◽  
Koichi Akashi ◽  
Shin Hayashi ◽  
Akiko Oogami ◽  
Takashi Okamura ◽  
...  
Keyword(s):  
Pericentric Inversion ◽  
Chronic Myelomonocytic Leukemia ◽  
Chromosome 16 ◽  
Myelomonocytic Leukemia

scholarly journals A unique pattern of central nervous system leukemia in acute myelomonocytic leukemia associated with inv(16)(p13q22)

Blood ◽  
1985 ◽  
Vol 65 (5) ◽  
pp. 1071-1078
Author(s):  
R Holmes ◽  
MJ Keating ◽  
A Cork ◽  
Y Broach ◽  
J Trujillo ◽  
...  
Keyword(s):  
Median Duration ◽  
Myeloid Leukemia ◽  
Chromosome Analysis ◽  
Leptomeningeal Disease ◽  
Brain Scan ◽  
Fab Classification ◽  
Additional Chromosome ◽  
Acute Myelomonocytic Leukemia ◽  
Immature Cells ◽  
Myelomonocytic Leukemia

Twenty-six patients with inv(16)(p13q22) or del(16)(q22) in association with acute myelomonocytic leukemia (AMML-M4, FAB classification), and abnormal marrow eosinophils have been treated at this institute. Initial bone marrow eosinophilia (greater than or equal to 4%) was observed in 22 of 26 patients (85%), and abnormal eosinophil morphology, characterized by immature cells with some interspersed basophilic granules, was evident in 26 of 26 (100%). Giemsa-banded chromosome analysis performed in all patients revealed 16 cases with inv(16)(p13q22) alone, and ten cases with additional chromosome changes. Twenty-five patients received combination induction chemotherapy, and 23 (92%) achieved complete remission (CR). The median duration of remission was 18 months (range, six to 72 + months), and the median duration of survival was 34 months (range, 0.5 to 133 months). Nine patients (35%) relapsed in the CNS at a median time of 19 months (range, six to 133 months) from first marrow CR. All patients had leptomeningeal disease, and in addition, six of nine (66%) demonstrated two or more enhancing lesions on computed tomography brain scan, consistent with intracerebral myeloblastomas. Review of 384 Giemsa-banded patients with acute myeloid leukemia revealed no other morphologic or cytogenetic subgroup with either an equivalent incidence of CNS leukemia or documented intracerebral myeloblastomas. This series of inv(16)(p13q22)/del(16)(q22) AMML reports a favorable prognosis for such patients and associates a specific clonal cytogenetic subgroup of acute leukemia with a distinct propensity for CNS relapse, manifesting as leptomeningeal disease and intracerebral myeloblastomas.

scholarly journals A unique surface marker profile in T-cell acute lymphocytic leukemia

Blood ◽  
1980 ◽  
Vol 55 (4) ◽  
pp. 702-705
Author(s):  
ER Richie ◽  
MP Sullivan ◽  
J van Eys
Keyword(s):  
T Cell ◽  
Peripheral Blood ◽  
Acute Lymphocytic Leukemia ◽  
Early Stage ◽  
Mixed Lymphocyte Culture ◽  
Lymphocyte Culture ◽  
Surface Marker ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
Surface Marker Analysis

A 5-yr-old girl with acute lymphocytic leukemia presented with moderate hepatomegaly, marked splenomegaly, but no evidence of a mediastinal mass. The peripheral blood white count was 270 x 10(9)/liter with 99% leukemic cells. Surface marker analysis showed the lymphoblasts to be E- rosette negative and complement receptor positive. The patient's leukemic cells were unreactive with anti-p23,30, which detects Ia-like antigens, and strongly reactive with A99 anti-T-cell serum, which reacts with normal human thymocytes and peripheral blood T cells. The percentage of leukemic cells bearing complement receptors diminished during relapse. The leukemic cells obtained at diagnosis and during relapse were nonreactive to mitogens and alloantigens and failed to stimulate proliferation of normal lymphocytes in mixed lymphocyte culture. There was no evidence for active suppression of normal lymphocyte reactivity mediated by the leukemic cells. The surface marker and functional profile of these leukemic cells is consistent with that of an early stage in T-cell maturation.

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