Comparison of the performance of anti-CD7 and anti-CD38 bispecific antibodies and immunotoxins for the delivery of saporin to a human T-cell acute lymphoblastic leukemia cell line

1995 ◽  
Vol 13 (4) ◽  
pp. 185-200 ◽  
Author(s):  
David J. Flavell ◽  
Sue Cooper ◽  
Keiko Okayama ◽  
Loretta Emery ◽  
Sopsamorn U. Flavell
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Cell Line ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cell ◽  
Bispecific Antibodies ◽  
Leukemia Cell Line ◽  
Human T Cell ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia Cell Line

scholarly journals The oxidation of (−)-epigallocatechin-3-gallate inhibits T-cell acute lymphoblastic leukemia cell line HPB-ALL via the regulation of Notch1 expression

RSC Advances ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 1679-1684 ◽  
Author(s):  
Yu-Na Wang ◽  
Jing Wang ◽  
Hao-Nan Yang ◽  
Bang-Lei Zhang ◽  
Pan Zhang ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Cell Line ◽  
Hematological Malignancy ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Activating Mutations ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia Cell Line

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy, and commonly associated with activating mutations in the Notch1 pathway.

Mechanism of CAG Regimen Eliminating Human T Cell Acute Lymphoblastic Leukemia Cell Line, A3

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5051-5051
Author(s):  
Aining Sun ◽  
Yanling Wu ◽  
Shengli Xue ◽  
Wu Depei ◽  
Weirong Chang
Keyword(s):  
Cell Cycle ◽  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cell ◽  
S Phase ◽  
Leukemia Cell Line ◽  
Human T Cell ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia Cell Line

Abstract Objective To explore the mechanism of CAG regimen eliminating human T cell acute lymphoblastic leukemia cell line, A3 and evaluate the role played by G-CSF/G-CSFR system in this process. Methods The expression of G-CSFR on A3 cells was detected by flow cytometric analysis. Cell cycle parameters of A3 cells treated with different concentration of G-CSF(5ng/ml A10ng/ml A15ng/ml A20ng/ml G0ng/ml as control) were examined by propidium iodide staining. The inhibition and apoptosis rates of A3 cells caused by treatment with various combination of G-CSF, cytarabine (Ara-C), and aclarubicin (ACR) after incubation for 48h were analyzed by Cell Counting Kit (CCK-8) and AnnexinV staining, respectively. After incubation for 48 hours with G-CSF and PD98059(the specific inhibitor of MEK in Ras-MAPK signaling pathway), cell cycle and cell dynamic change were examined. Results The expression frenquency of G-CSFR on A3 cells was 94.2% which was comparable to that of KG-1 cells. The proportion of A3 cells in S-phase was elevated concomitantly with the increasing G-CSF concentrations within 0–20ng/ml, highest at 15ng/ml of G-CSF. After incubation with Ara-C and G-CSF for 48 hours, the proliferation of A3 cells was inhibited more significantly than incubation with incubation with Ara-C alone (P<0.05, Ara-C 10−5M and 10−6M) by CCK-8 assay. Incubated with Ara-C, ACR, and G-CSF for 48 hours, the apoptosis of A3 cells was increased than that treated with Ara-C and ACR. With the concentration of PD98059 increased gradually, the proportion of A3 cells in S-phase and OD values of A3 cells decreased, which was less than that of control group (p<0.05). Conclusion G-CSFR was expressed on A3 cells. G-CSF/G-CSFR system had a synergetic effect on eliminating A3 cells when administrated simultaneously with chemical agents by driving G0-phase cells into S-phase. Apoptosis was one of the mechanisms of CAG regimen eliminating A3 cells. The interaction between G-CSF and G-CSFR activates a series of signaling pathways which includes Ras-MAPK. The inhibition of MAPK phosphorylation by PD98059 contributed partially to the effect of G-CSF on A3 cells.

scholarly journals The t(11;14)(p15;q11) in a T-cell acute lymphoblastic leukemia cell line activates multiple transcripts, including Ttg-1, a gene encoding a potential zinc finger protein

1989 ◽  
Vol 9 (5) ◽  
pp. 2124-2132
Author(s):  
E A McGuire ◽  
R D Hockett ◽  
K M Pollock ◽  
M F Bartholdi ◽  
S J O'Brien ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Cell Line ◽  
Zinc Finger Protein ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
New Genes ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia Cell Line

Interchromosomal translocations within lymphoid neoplasms frequently involve the antigen receptor genes. We cloned the breakpoints of the t(11;14)(p15;q11) in a CD3-negative T-cell acute lymphoblastic leukemia cell line (RPMI 8402) in order to identify new genes potentially involved in T-cell neoplasia. An extensive comparison of both breakpoints and their germ line counterparts indicated that an inadvertant recombinase-mediated break at chromosome segment 11p15 recombined with the delta T-cell receptor at 14q11. The derivative 11 breakpoint resembles a coding joint in which 11p15 rather than a variable region was introduced 5' to a D delta 1 D delta 2 J delta 1 intermediate rearrangement. Conversely, the derivative 14 breakpoint corresponds to a signal joint between the 5' heptamer-spacer-nonamer recombinational signal of D delta 1 and an isolated heptamer at 11p15. Multiple, apparently distinct transcripts were found flanking both breakpoints of 8402. RNAs of 3.5, 4.4, 1.4, and 8.0 kilobases originating from either side of the derivative 14 breakpoint were highly expressed in 8402 compared with other cells. This suggests that this translocation deregulated multiple genes and provides the opportunity to assess any multifactorial contribution they may have to malignancy. We cloned and sequenced several cDNAs representing the 1.4-kilobase transcript (termed Ttg-1 [T-cell translocation gene 1]) from an 8402 library. The predicted protein of 156 amino acids contained two internal repeats which could potentially form zinc fingers.

scholarly journals The t(11;14)(p15;q11) in a T-cell acute lymphoblastic leukemia cell line activates multiple transcripts, including Ttg-1, a gene encoding a potential zinc finger protein.

1989 ◽  
Vol 9 (5) ◽  
pp. 2124-2132 ◽  
Author(s):  
E A McGuire ◽  
R D Hockett ◽  
K M Pollock ◽  
M F Bartholdi ◽  
S J O'Brien ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Cell Line ◽  
Zinc Finger Protein ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
New Genes ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia Cell Line

Interchromosomal translocations within lymphoid neoplasms frequently involve the antigen receptor genes. We cloned the breakpoints of the t(11;14)(p15;q11) in a CD3-negative T-cell acute lymphoblastic leukemia cell line (RPMI 8402) in order to identify new genes potentially involved in T-cell neoplasia. An extensive comparison of both breakpoints and their germ line counterparts indicated that an inadvertant recombinase-mediated break at chromosome segment 11p15 recombined with the delta T-cell receptor at 14q11. The derivative 11 breakpoint resembles a coding joint in which 11p15 rather than a variable region was introduced 5' to a D delta 1 D delta 2 J delta 1 intermediate rearrangement. Conversely, the derivative 14 breakpoint corresponds to a signal joint between the 5' heptamer-spacer-nonamer recombinational signal of D delta 1 and an isolated heptamer at 11p15. Multiple, apparently distinct transcripts were found flanking both breakpoints of 8402. RNAs of 3.5, 4.4, 1.4, and 8.0 kilobases originating from either side of the derivative 14 breakpoint were highly expressed in 8402 compared with other cells. This suggests that this translocation deregulated multiple genes and provides the opportunity to assess any multifactorial contribution they may have to malignancy. We cloned and sequenced several cDNAs representing the 1.4-kilobase transcript (termed Ttg-1 [T-cell translocation gene 1]) from an 8402 library. The predicted protein of 156 amino acids contained two internal repeats which could potentially form zinc fingers.

scholarly journals Targeting FoxM1 transcription factor in T-cell acute lymphoblastic leukemia cell line

2015 ◽  
Vol 39 (3) ◽  
pp. 342-347 ◽  
Author(s):  
Özlem Tüfekçi ◽  
Melis Kartal Yandım ◽  
Hale Ören ◽  
Gülersu İrken ◽  
Yusuf Baran
Keyword(s):  
Transcription Factor ◽  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Cell Line ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia Cell Line
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