ライフサイエンスコーパス: T-PLL

1 T-PLL is also seen in non-A-T individuals where expressi

2 T-PLL, defined as a T-cell leukemia showing rapidly risi

3 Among 17 T-PLL tumour samples, three rearrangements were detected

4 ing IL2RG, JAK1, JAK3, or STAT5B in 38 of 50 T-PLL genomes (76.0%).

5 In a series of 86 T-PLL tumors, we show that expression of TCR, and levels

6 c lymphocytic/prolymphocytic leukemia (T-CLL/T-PLL) is a lymphoproliferative disease derived from imm

7 Some additional role for ATM during T-PLL tumorigenesis is possible since nucleotide changes

8 that ATM acts as a tumour suppressor during T-PLL tumorigenesis.

9 High-level TCL1 in TCR-expressing T-PLL is associated with higher presenting white blood c

10 T and non-A-T patients and the age range for T-PLL may also be different in A-T and non-A-T patients.

11 Currently, the best treatment for T-PLL is intravenous alemtuzumab, which has resulted in

12 t to identify novel effective treatments for T-PLL patients.

13 nduced activation of Akt, which causes human T-PLL.

14 ivo and in humans, offering a novel agent in T-PLL.

15 Campath-1H is an active drug in T-PLL patients for whom first-line therapy has failed.

16 y altered genes not previously implicated in T-PLL including EZH2, FBXW10, and CHEK2.

17 data suggest ATM is frequently rearranged in T-PLL, it was decided to investigate such rearrangements

18 STAT5B have not been previously reported in T-PLL.

19 We propose that in T-PLL, TCL1 represents a highly regulated, targetable mo

20 s that CAMPATH-1H is an effective therapy in T-PLL, producing remissions in more than two thirds of p

21 owed to the point to which they develop into T-PLL.

22 T-prolymphocytic leukaemia (T-PLL) is a rare, sporadic leukaemia similar to a mature

23 evelop into T cell prolymphocytic leukaemia (T-PLL).

24 hogenesis of T-cell prolymphocytic leukemia (T-PLL) are unknown.

25 T-cell prolymphocytic leukemia (T-PLL) is a chemotherapy-resistant malignancy with a med

26 T-cell prolymphocytic leukemia (T-PLL) is a rare and aggressive T-lymphoid malignancy us

27 malignancy, T-cell prolymphocytic leukemia (T-PLL) is remarkable for frequently harbouring somatic m

28 reviously treated T-prolymphocytic leukemia (T-PLL) patients in a compassionate-use program.

29 ark of human T-cell prolymphocytic leukemia (T-PLL), a form of adult leukemia.

30 ee developed T-cell prolymphocytic leukemia (T-PLL), and eight developed carcinoma at a median age of

31 c leukemia (CLL), T-prolymphocytic leukemia (T-PLL), and mantle cell lymphoma (MCL) and is associated

32 ia including T-cell prolymphocytic leukemia (T-PLL), Sezary syndrome (SS), and T-cell large granular

33 reatment for T-cell prolymphocytic leukemia (T-PLL).

34 of cases of T-cell prolymphocytic leukemia (T-PLL).

35 the exception of T-prolymphocytic leukemia (T-PLL).

36 uence mutations have been reported in 46% of T-PLL cases, but some cases also have karyotypic abnorma

37 and Sanger resequencing of a large cohort of T-PLL.

38 By the time of diagnosis of T-PLL, the clone contains many more genetic changes in t

39 de a portrait of the mutational landscape of T-PLL and implicate deregulation of DNA repair and epige

40 JAK1-JAK3-STAT5B axis in the pathogenesis of T-PLL.

41 teristically associated with either T-ALL or T-PLL in non-A-T patients.

42 ny age and may be T-ALL, T-cell lymphoma, or T-PLL; most strikingly, there may be a fourfold to fivef

43 Importantly, primary T-PLL cells exhibited constitutive activation of STAT5,

44 5 with pimozide induced apoptosis in primary T-PLL cells.

45 ent was commenced in 2 late-stage refractory T-PLL patients resulting in clinical responses.

46 etoclax (ABT-199) demonstrated the strongest T-PLL-specific response when comparing individual ex viv

47 urred at a relatively high level only in two T-PLL tumours from A-T patients with t(X;14) translocati

48 treatment of choice for previously untreated T-PLL.

49 is study reports results in 39 patients with T-PLL treated with CAMPATH-1H between March 1993 and May

50 tion in 9 previously untreated patients with T-PLL.

51 s in these patients were uncontaminated with T-PLL cells as demonstrated by dual-color flow cytometry