The Cystatin S gene maps to rat Chromosome 3, to which Dlmgh18 is re-assigned from Chromosome 1

1997 ◽  
Vol 8 (12) ◽  
pp. 946-947 ◽  
Author(s):  
M. Beatriz Duran Alonso ◽  
Paul Shiels ◽  
Andrew S. McCallion ◽  
Neil K. Bennett ◽  
Anthony P. Payne ◽  
...  
Keyword(s):  
Chromosome 1 ◽  
Chromosome 3 ◽  
S Gene ◽  
Gene Maps

Mouse Thioredoxin Gene Maps on Chromosome 4, whereas Its Pseudogene Maps on Chromosome 1

Genomics ◽  
1994 ◽  
Vol 21 (1) ◽  
pp. 251-253 ◽  
Author(s):  
Makoto Taketo ◽  
Minoru Matsui ◽  
Julie M. Rochelle ◽  
Junji Yodoi ◽  
Michael F. Seldin
Keyword(s):  
Chromosome 1 ◽  
Chromosome 4 ◽  
Gene Maps

Integration of gene maps: updating chromosome 1

1995 ◽  
Vol 59 (3) ◽  
pp. 291-305 ◽  
Author(s):  
P. FORABOSCO ◽  
A. COLLINS ◽  
N. E. MORTON
Keyword(s):  
Chromosome 1 ◽  
Gene Maps

A human SHC-related sequence maps to chromosome 17, the SHC gene maps to chromosome 1

1995 ◽  
Vol 96 (2) ◽  
pp. 245-248 ◽  
Author(s):  
IsikG. Yulug ◽  
SeanE. Egan ◽  
CheeGee See ◽  
ElizabethM.C. Fisher
Keyword(s):  
Chromosome 17 ◽  
Chromosome 1 ◽  
Related Sequence ◽  
Gene Maps

Specific end-to-end attachment of chromosomes in Ornithogalum virens

1979 ◽  
Vol 38 (1) ◽  
pp. 357-367
Author(s):  
T. Ashley
Keyword(s):  
Chromosome 1 ◽  
Chromosome 3 ◽  
Chromosome 2 ◽  
Root Tips ◽  
End To End ◽  
Specific Association ◽  
High Degree ◽  
Ornithogalum Virens ◽  
Homologous Alignment ◽  
Generative Nuclei

C-banding of nonhomologous chromosomes in haploid generative nuclei of Ornithogalum virens (n = 3) reveals a high degree of specificity with respect to end-to-end connexions. The centromeric end of chromosome 2 preferentially associates with the centromeric end of chromosome 3 and the telomeric end of chromosome 3 associates preferentially with the telomeric end of chromosome 1. This same association of nonhomologous chromosomes persists in prophase nuclei of diploid root tips. In addition, the telomeric ends of the 2 chromosome 2s are connected to one another as are the centromeric ends of the chromosome 1s. This results in a ring of chromosomes in which homologues lie opposite one another. Centromeric ends lie on one side of the nucleus and telomeric ends on the other. It is proposed that this specific association of chromosome ends reflects an order which was probably established at the preceding anaphase or telophase and which persists throughout interphase. The suggestion is made that the proximity of homologous ends and consequently homologous alignment may facilitate initiation of pairing at meiosis.

Discordant Rates of Chromosome Evolution in the Drosophila virilis Species Group

Genetics ◽  
1997 ◽  
Vol 147 (1) ◽  
pp. 223-230 ◽  
Author(s):  
Jorge Vieira ◽  
Cristina P Vieira ◽  
Daniel L Hartl ◽  
Elena R Lozovskaya
Keyword(s):  
Polytene Chromosome ◽  
Genomic Dna ◽  
Chromosome Evolution ◽  
Species Group ◽  
Drosophila Virilis ◽  
Chromosome 1 ◽  
Chromosome 3 ◽  
Bacteriophage P1 ◽  
Minimum Number ◽  
Chromosome Maps

Abstract In Drosophila, the availability of polytene chromosome maps and of sets of probes covering most regions of the chromosomes allows a direct comparison of the organization of the genome in different species. In this work, we report the localization, in Drosophila virilis, D. montana, and D. novamexicana, of >100 bacteriophage P1 clones containing ~65 kilobase inserts of genomic DNA from D. virilis. Each clone hybridizes with a single euchromatic site in either chromosome 1 or chromosome 3 in D. virilis. From these data, it is possible to estimate the minimum number of inversions required to transform the map positions of the probes in one species into the map positions of the same probes in a related species. The data indicate that, in the D. virilis species group, the X chromosome has up to four times the number of inversions as are observed in chromosome 3. The first photographic polytene chromosome maps for D. montana and D. novamexicana are also presented.

Additional Chromosomal Abnormalities in Patients with Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia Treated with Tyrosine Kinase Inhibitors: Differential Outcomes According to Type of Chromosomal Abnormality

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 1737-1737
Author(s):  
Nicholas J. Short ◽  
Elias J. Jabbour ◽  
Koji Sasaki ◽  
Heidi Ko ◽  
Farhad Ravandi ◽  
...  
Keyword(s):  
Research Funding ◽  
Kinase Inhibitors ◽  
Chromosomal Abnormalities ◽  
Lymphoblastic Leukemia ◽  
Philadelphia Chromosome ◽  
Chromosome 1 ◽  
Chromosome 3 ◽  
Poor Risk ◽  
Evaluable Population ◽  
Additional Chromosomal Abnormalities

Abstract Background: Prior to the introduction of tyrosine kinase inhibitors (TKIs), additional chromosomal abnormalities (ACAs) in patients (pts) with Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) were associated with worse outcomes. However, in pts treated with chemotherapy plus a TKI regimen, the prognostic impact of ACAs is not well-established. Methods: Between 6/2001 and 1/2016, we identified 152 adult pts with newly diagnosed Ph+ ALL treated at our institution on 3 protocols with hyper-CVAD plus a TKI. 27 pts were positive for BCR-ABL1 by FISH and/or PCR but did not have a Ph chromosome identified on baseline karyotype and therefore were excluded from the analysis. In the remaining evaluable population of 125 pts with a Ph+ karyotype, complete molecular response (CMR) after 3 months of therapy, relapse-free survival (RFS) and overall survival (OS) were compared among pts with and without ACAs. Results: The median age of the evaluable population was 55 years (range, 23-85 years). All pts received hyper-CVAD plus imatinib (n=34, 27%), dasatinib (n=51, 41%) or ponatinib (n=40, 32%). Of the 125 evaluable pts in whom the Ph chromosome was detected, 28 (22%) had Ph alone and 97 (78%) had Ph plus one or more ACAs. Among the 97 pts with ACAs, 22 (23%) were high hyperdiploid (HeH; defined as 51-65 chromosomes); no pts with low hypodiploidy (defined as 30-39 chromosomes) were identified. Excluding ACAs associated with chromosomal gain in the 22 pts with HeH, the recurrent ACAs identified in >5% of the ACA population were: -7/7q in 21 pts (22%), der(22) in 18 pts (19%), -9/9p in 11 pts (11%), translocations of chromosome 1 in 9 pts (9%), +21 in 7 pts (7%), and abnormalities of chromosome 3 in 5 pts (5%). The median duration of follow-up for the evaluable population was 51 months (range, 4-173 months). The 5-year RFS and OS rates were similar between the Ph alone and ACA groups (RFS: 56% and 57%, respectively, P=0.57; OS: 54% and 58%, respectively, P=0.78). However, when individual ACA groups were compared, distinct prognostic groups were identified (Table 1). Pts with der(22), -9/9p, translocations of chromosome 1, or abnormalities of chromosome 3 (n=35, 36% of the ACA cohort and 28% of the evaluable population) had a particularly poor prognosis with a median RFS of 15 months, 14 months, 21 months and 12 months, respectively. These 4 ACAs constituted a poor-risk ACA group with a median RFS of 21 months and 5-year RFS rate of 38%. In contrast, pts with ACAs other than der(22), -9/9p, translocations of chromosome 1, or abnormalities of chromosome 3 (n=62, 64% of the ACA cohort) had a median RFS of 124 months and a 5-year RFS rate of 65%. These pts with non-poor-risk ACAs had similar RFS to those with Ph alone (P=0.82). The 3-month CMR rate for the pooled group of pts with Ph alone or non-poor-risk ACAs compared to the group of poor-risk ACA pts was 63% vs. 50% (P=0.29). Pts with poor-risk ACAs had significantly shorter RFS (median 21 months vs. 124 months and 5-year RFS rate 38% vs. 62%, P=0.02; Figure 1A) and OS (median 28 months vs. 125 months and 5-year OS rate 38% vs. 65%, P=0.03; Figure 1B). The rate of allogeneic stem cell transplant was similar between the Ph alone / non-poor-risk ACA group and the poor-risk ACA group (23% vs. 17%, respectively; P=0.45). Compared to pts with only 1 poor-risk ACA (n=27), pts with 2 poor-risk ACAs (n=8) had significantly shorter RFS and OS (P=0.004 and P=0.02, respectively). By univariate analysis including age, WBC count, platelets, BM blasts, performance status, CD20 expression, presence of CNS leukemia, BCR-ABL1 transcript type, TKI received, and ACA risk group, the factors associated with RFS were poor-risk ACAs (P=0.02) and TKI (P=0.04); the factors associated with OS were poor-risk ACAs (P=0.03), age (P=0.03) and TKI (P=0.02). By multivariate analysis, only poor-risk ACAs were associated with worse RFS (HR 1.88 [95% CI 1.07-3.30], P=0.03). In contrast, the factors independently associated with OS were age (HR 1.02 [95% CI 1.00-1.04], P=0.04) and TKI (HR 0.59 [0.39-0.89], P=0.02) but not poor-risk ACAs (HR 1.48 [95% CI 1.06-3.24], P=0.19). Conclusions: In pts with Ph+ ALL receiving chemotherapy plus a TKI, der(22), -9/9p, translocations of chromosome 1, or abnormalities of chromosome 3 constitute a group of poor-risk ACAs that confers inferior RFS and OS. These poor-risk ACAs should be taken into account when planning post-remission strategies in pts with Ph+ ALL. Disclosures Jabbour: ARIAD: Consultancy, Research Funding; Pfizer: Consultancy, Research Funding; Novartis: Research Funding; BMS: Consultancy. Cortes:ARIAD: Consultancy, Research Funding; BMS: Consultancy, Research Funding; Novartis: Consultancy, Research Funding; Pfizer: Consultancy, Research Funding; Teva: Research Funding. O'Brien:Pharmacyclics, LLC, an AbbVie Company: Consultancy, Honoraria, Research Funding; Janssen: Consultancy, Honoraria. Daver:Ariad: Research Funding; Pfizer: Consultancy, Research Funding; Karyopharm: Honoraria, Research Funding; Sunesis: Consultancy, Research Funding; Kiromic: Research Funding; BMS: Research Funding; Otsuka: Consultancy, Honoraria. Jain:Pharmacyclics: Consultancy, Honoraria, Research Funding; Seattle Genetics: Research Funding; Abbvie: Research Funding; Celgene: Research Funding; Incyte: Research Funding; Infinity: Research Funding; Genentech: Research Funding; Pfizer: Consultancy, Honoraria, Research Funding; Servier: Consultancy, Honoraria; Novartis: Consultancy, Honoraria; BMS: Research Funding; Novimmune: Consultancy, Honoraria; ADC Therapeutics: Consultancy, Honoraria, Research Funding. Konopleva:Cellectis: Research Funding; Calithera: Research Funding.

scholarly journals Disruption of the SCL gene by a t(1;3) translocation in a patient with T cell acute lymphoblastic leukemia.

1992 ◽  
Vol 176 (5) ◽  
pp. 1303-1310 ◽  
Author(s):  
P D Aplan ◽  
S C Raimondi ◽  
I R Kirsch
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Interstitial Deletion ◽  
Chromosome 1 ◽  
Chromosome 3 ◽  
Evolutionarily Conserved ◽  
Nucleotide Addition ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Causal Event

SCL gene disruptions are the most common chromosomal abnormality associated with the development of T cell acute lymphoblastic leukemia (ALL). Such disruptions can be the result of t(1;14) and t(1;7) translocations, as well as a cytogenetically undetectable interstitial deletion of chromosome 1. We present here a case of T cell ALL with a t(1;3)(p34;p21) translocation that also disrupts the SCL locus and leads to dysregulated SCL gene expression. This translocation, similar to previously reported SCL gene disruptions, appears to have been mediated, at least in part, by the V(D)J recombinase complex, since cryptic heptamer recognition sequences, as well as nontemplated N region nucleotide addition, are present at the breakpoints. The t(1;3) also disrupts a region on chromosome 3 characterized by alternating purine and pyrimidine residues, which can form a Z-DNA structure, reported to be prone to recombination events. A previously undescribed, evolutionarily conserved transcript unit is detected within 8 kb of the breakpoint on chromosome 3. This report extends the spectrum of recognized SCL translocations associated with T cell ALL, and underscores the contention that dysregulated SCL expression may be a causal event in T cell ALL.

scholarly journals Integration of gene maps: chromosome 1.

1992 ◽  
Vol 89 (10) ◽  
pp. 4598-4602 ◽  
Author(s):  
A. Collins ◽  
B. J. Keats ◽  
N. Dracopoli ◽  
D. C. Shields ◽  
N. E. Morton
Keyword(s):  
Chromosome 1 ◽  
Gene Maps
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