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A technique for spectroscopic imaging based on a new concept of dual encoding (i.e., both phase and frequency encoding) of position along the direction of the read-out gradient is proposed. The phase encoding is produced by changing the amplitude of the dephasing gradient as in conventional phase encoding. High-resolution spectroscopic images of a normal human thigh obtained by a 2.0 Tesla whole body MR imaging system are presented.

In summary, of 64 patients with total or partial monosomy 7, 21 cases showed a deletion of 7q, and a translocation resulting in loss of the whole or major portion of 7q was detected in six other cases; a consistent translocation involving chromosomes #7 and #17 was observed in four of the latter cases, resulting in an effective loss of 7q. In 23 of these 27 patients reviewed with loss of 7q, the common segment deleted involved 7q32 to 7q34 (Table). The most common abnormalities associated with -7 or 7q- were -5 or 5q- (26 cases) and monosomy 17 (16 cases); except for two patients, all of the latter also had -5 or 5q-. Fifteen of the 64 patients with -7 or 7q- had a secondary leukemia (23.4%). Other abnormalities, such as complete and partial trisomy 7 and various balanced translocations involving #7, were far less common. Only one of 16 cases had an associated 5q- chromosome, one was -17, and only one case had secondary leukemia.

Cytogenetic analysis was successfully performed on 31 of 40 patients with chronic B cell leukemia. Clonal abnormalities were seen in 16 patients using various culture methods. Fourteen of these had unstimulated cultures established of which 13 had the clonal abnormality. Trisomy 12 was observed in seven patients while a 14q32 translocation was present in four. Race, age, hemoglobin, WBC, percentage of lymphocytes and prolymphocytes in BM and PB, platelets, Smig, lymph node, spleen, liver, pattern of bone marrow infiltration, therapy free interval, and overall survival were all compared. Significant correlations between the presence of clonal abnormalities and prior therapy (p less than 0.005) and an increase in prolymphocytes in bone marrow (p = 0.05) and/or peripheral blood (p = 0.0014) were observed.

Chromosomes of six patients with plasma cell leukemia and one patient with leukemic macroglobulinemia were examined from peripheral blood, bone marrow, and/or pleural fluid. All the patients had a clonal chromosomal abnormality. The modal chromosome number was near tetraploid in two, pseudodiploid in two, and hypodiploid in three patients. Rearrangements of chromosome 1 were found in all the patients. The most consistent abnormality was a large marker involving the long arm of No. 1, found in six patients, including the patient with macroglobulinemia. Each patient had one to four large markers which resulted in partial trisomy to hexasomy for the long arm of No. 1. The translocations occurred with No. 9 in two, with No. 16 in two, and Nos. 8, 17, and 18 each in one patient. The survival time from the diagnosis was less than 1 year in five of them and over 2 years in one. The only patient whose cells lacked an extra 1q lived for over 3 years. Five 14q+ marker chromosomes were detected in three patients. The donor chromosome was No. 11 in one of these and was undetermined in the others; the size of each 14q+ marker seemed quite different which suggested different donor chromosomes. Loss of a sex chromosome was found in five patients. Loss of No. 13 and gain of No. 7 or 7q were each found in two patients. Rearrangement or deletion of the short arm of No. 8 was found in five patients. A rearrangement of 9p was found in three patients. The myeloma cells had a different morphology in the peripheral blood, bone marrow, and/or pleural fluid before and after the leukemic phase of one patient; however, chromosome analysis revealed the same clone despite the altered morphology.

The clinicopathologic features of 53 patients with various types of non-T-cell malignancies were compared with the karyotypic findings. Although all chromosomes underwent numerical and structural rearrangements, a 14q+ marker chromosome (14q32 translocation), which was found in 31 patients, was the single most common abnormality. In terms of survival, no significant difference was noted between the 14q+ positive and negative patients. Donor chromosomes of a 14q32 translocation, which were identified in 27 patients, were quite variable. However, certain chromosomes were predisposed to act as donor chromosomes in the 14q32 translocation. An 8;14 translocation [t(8;14) (q24;q32)] was found in six patients with diffuse non-Burkitt's lymphoma and in four patients with Burkitt's lymphoma-leukemia; in all these patients a stem line or the subline with a t(8;14) had partial trisomy for 1q. An 11;14 translocation [t(11;14) (q13;q32)] was observed in one patient each with diffuse or follicular lymphoma and in two with myeloma; three of the four patients had also structural rearrangements of chromosome 1 in the same cells. A 14;18 translocation [t(14;18) (q32;q21)] was found in six patients with follicular lymphoma and in one with diffuse lymphoma; however, no common involvement of other chromosomes was detected among clones of these abnormal cells with a t(14;18). The median survival was 8 months for patients with a t(8;14) and 39 months for patients with a t(11;14). The difference between the two survival curves was of borderline significance [p = 0.06]. In contrast, patients with a t(14;18) survived significantly longer than those with a t(8;14) [p less than 0.001] or those with a t(11;14) [p = 0.03]. These findings revealed that in non-T-cell malignancies, the clinicopathologic features of the patients with a 14q+ marker depend upon the precise 14q32 translocation and the subsequent karyotypic evolution, although the translocation was not always correlated with a particular type of lymphoid malignancy.

Four of 30 patients with a diagnosis of B-CLL or prolymphocytic transformation of CLL, who had an adequate cytogenetic analysis, had abnormalities involving 14q32. Three of the 4 had a translocation involving chr. 19; in 2 of them it appeared to be t(14;19) (q32;q13.1). The third patient probably had the same translocation. All 3 patients had received therapy prior to cytogenetic analysis.

In three patients with non-Hodgkin lymphomas and in one cell line (HPL-Hod) derived from pleural effusion cells of a patient with Hodgkin's disease, rearrangements of the long arm of chromosome No. 14(14q) were observed. These rearrangements appeared to be consistently associated with a 14q translocation, suggestive of occurrence of a break at 14q13. The translocation in an individual case could occur with 1p, 2q, 4q, and another 14q. A 14q13 translocation may be comparable with a 14q32 translocation, which has often been observed in various types of lymphoid malignancy.

An insertion (10;11)(p11;q23q24) was found in bone marrow metaphase cells from two children with acute monocytic leukemia (AMoL-M5b). This rearrangement involves a small chromosomal segment of 11q and may be misinterpreted as a deletion of 11q. Insertion (10;11) may represent a new recurring abnormality involving 11q associated with acute leukemia of the M5b type.

Clonal chromosome abnormalities were observed in 30 patients with non-Hodgkin's lymphoma; the type of lymphoma was characterized on the basis of the International Working Formulation. The 30 patients were classified into five groups according to the chromosome abnormality. There were 8 patients with t(14;18), 3 with t(8;14), 7 with a translocation to the long arm of chromosome 3 (a 3q+ chromosome), 5 with near-tetraploidy, and 7 with other abnormalities. Among the 8 patients with t(14;18), 5 had follicular small cleaved-cell lymphoma (FSC), I had follicular mixed cell lymphoma (FM), and 2 had diffuse large-cell lymphoma (DL); the diagnosis in these 2 patients was based on extranodal tissue. All 3 patients with t(8;14) had DL and B-cell markers. Except for 1 patient, all those with a 3q+ chromosome had DL; 4 of those who were tested had B-cell or pre-B-cell markers. Four of the 5 patients with near-tetraploidy had follicular mixed-cell lymphoma, and 2 of the 7 patients with other abnormalities had T-cell lymphoma. Thus, patients with a t(8;14), a 14q+ chromosome, or a 3q+ chromosome all tend to have diffuse large-cell lymphoma, usually of the non-cleaved type. On the other hand, our data suggest that patients with FSC generally have a t(14;18) whereas those with follicular and diffuse mixed small cleaved cells and large noncleaved cells have a different pattern with modal chromosome numbers in the tetraploid range. We added 17 previously reported patients to the 30 presented here and correlated the karyotype with survival. The 6 patients with near-tetraploidy had the longest median survival, 69 months, the 15 patients with t(14;18) had the next longest, 48 months. The 4 patients with t(8;14) had the shortest survival, 12 months, and the 9 with other abnormalities had the next shortest, 17 months. Intermediate survivals of 27 and 30 months were observed in patients with a 14q+ or a 3q+ chromosome, respectively. The median survival of these various categories differs and our data, thus, indicate that the karyotypic pattern of the malignant cell may be a significant independent prognostic feature influencing the survival of patients with non-Hodgkin's lymphoma.