Therapy-related acute leukemia associated with t(11q23) after primary acute myeloid leukemia with t(8;21): a report of two cases [letter]

Roulston, Diane; Anastasi, John; Rudinsky, R; Nucifora, Giuseppina; Zeleznik‐Le, Nancy J.; Rowley, J.D.; McGavran, Loris; Tsuchida, Mineko; Hayashi, Yasuhide

doi:10.1182/blood.v86.9.3613.bloodjournal8693613

Cited by 20 publications

(4 citation statements)

References 1 publication

(1 reference statement)

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“…An MLL rearrangement was reported in three patients with t(11;16)(q23;p13)-associated, therapyrelated acute leukemia (Hunger et al, 1993;Roulston et al, 1995;Rowley et al, 1996). We found the same translocation in a child with therapy-related chronic myelomonocytic leukemia (t-CMML) (Bennett et al, 1976), and we detected a novel MLL-CBP fusion transcript in his neoplastic cells.…”

Section: Introductionsupporting

confidence: 69%

NovelMLL-CBP fusion transcript in therapy-related chronic myelomonocytic leukemia with a t(11;16) (q23;p13) chromosome translocation

Satake

Ishida

Otoh

et al. 1997

Genes Chromosom. Cancer

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CBP, which is located on 16p13 and encodes a transcriptional adaptor/coactivator protein, has been shown to fuse by the t(8;16)(p11;p13) translocation to MOZ on 8p11 in acute myeloid leukemia. We found a t(11;16)(q23;p13) in a child with therapy‐related chronic myelomonocytic leukemia. Subsequent reverse transcriptase‐polymerase chain reaction and direct sequencing analyses revealed the MLL‐CBP fusion transcript in CMML cells. Because 11q23 translocations involving MLL and t(8;16) involving MOZ and CBP have been reported in therapy‐related leukemias, both the MLL and CBP genes may be targets for topoisomerase II inhibitors. Accordingly, we believe that most t(11;16)‐associated leukemias may develop in patients who have been treated with cytotoxic chemotherapy for primary malignant diseases. Genes Chromosom. Cancer 20:60–63, 1997. © 1997 Wiley‐Liss, Inc.

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Section: Introductionsupporting

confidence: 69%

NovelMLL-CBP fusion transcript in therapy-related chronic myelomonocytic leukemia with a t(11;16) (q23;p13) chromosome translocation

Satake

Ishida

Otoh

et al. 1997

Genes Chromosom. Cancer

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“…Other etiologies for late relapse need to be considered. True secondary ALL, as has been well described in AML, 22‐24 is very uncommon and its existence is, in fact, uncertain 25 . However, a second de novo ALL has been suggested in some cases of relapsed ALL 26 .…”

Section: Discussionmentioning

confidence: 95%

At three years, patients with acute lymphoblastic leukaemia are still at risk for relapse. Results of the international MRC UKALLXII/ECOG E2993 trial

et al. 2020

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Late relapse [>3 years from complete remission (CR)] in acute lymphoblastic leukaemia (ALL), is unusual. Data from the MRC UKALLXII/ECOG E2993 trial are presented to evaluate the incidence and characteristics of late relapse in adult ALL. Of 1,909 patients, 1,752 (92%) achieved CR and among these 757 (43Á2%) relapsed; 691 (91Á3%) within three years and 66 (8Á7%) beyond. Among these 66 patients, median time to relapse was 47 (37-144) months. Relapse beyond three years occurred in 3Á8% of all who achieved CR. The cumulative risk of relapse was 40%, 43% and 45% at three, five and ten years respectively. Out of the 1 752 patients who achieved CR, 11Á7% underwent autologous and 40Á6% allogeneic transplant, while in CR1. Of the autologous patients, 43Á2% relapsed early and 3Á4% relapsed late. However, among the allogeneic patients, 13Á2% relapsed early and only 1Á3% late. The five-year overall survival from relapse was 5Á8% and 20% in the early and late relapse patients respectively. In conclusion, late relapse in adults with ALL is not uncommon, and is associated with better outcome after relapse compared to early relapse.

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“…Because these agents generate a “lesion” that includes DNA strand breaks and proteins covalently bound to DNA, they have been known as topo II poisons. Unfortunately, in certain cases, the use of these agents has resulted in serious drawbacks, including the induction of secondary malignancies [ 33 , 34 , 35 , 36 ]. On the other hand, the second class of DNA topo II inhibitors only diminished the enzymatic activity of topo II proteins [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Cracking the Cytotoxicity Code: Apoptotic Induction of 10-Acetylirciformonin B is Mediated through ROS Generation and Mitochondrial Dysfunction

et al. 2014

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A marine furanoterpenoid derivative, 10-acetylirciformonin B (10AB), was found to inhibit the proliferation of leukemia, hepatoma, and colon cancer cell lines, with selective and significant potency against leukemia cells. It induced DNA damage and apoptosis in leukemia HL 60 cells. To fully understand the mechanism behind the 10AB apoptotic induction against HL 60 cells, we extended our previous findings and further explored the precise molecular targets of 10AB. We found that the use of 10AB increased apoptosis by 8.9%–87.6% and caused disruption of mitochondrial membrane potential (MMP) by 15.2%–95.2% in a dose-dependent manner, as demonstrated by annexin-V/PI and JC-1 staining assays, respectively. Moreover, our findings indicated that the pretreatment of HL 60 cells with N-acetyl-l-cysteine (NAC), a reactive oxygen species (ROS) scavenger, diminished MMP disruption and apoptosis induced by 10AB, suggesting that ROS overproduction plays a crucial rule in the cytotoxic activity of 10AB. The results of a cell-free system assay indicated that 10AB could act as a topoisomerase catalytic inhibitor through the inhibition of topoisomerase IIα. On the protein level, the expression of the anti-apoptotic proteins Bcl-xL and Bcl-2, caspase inhibitors XIAP and survivin, as well as hexokinase II were inhibited by the use of 10AB. On the other hand, the expression of the pro-apoptotic protein Bax was increased after 10AB treatment. Taken together, our results suggest that 10AB-induced apoptosis is mediated through the overproduction of ROS and the disruption of mitochondrial metabolism.

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Therapy-related acute leukemia associated with t(11q23) after primary acute myeloid leukemia with t(8;21): a report of two cases [letter]

Cited by 20 publications

References 1 publication

NovelMLL-CBP fusion transcript in therapy-related chronic myelomonocytic leukemia with a t(11;16) (q23;p13) chromosome translocation

NovelMLL-CBP fusion transcript in therapy-related chronic myelomonocytic leukemia with a t(11;16) (q23;p13) chromosome translocation

At three years, patients with acute lymphoblastic leukaemia are still at risk for relapse. Results of the international MRC UKALLXII/ECOG E2993 trial

Cracking the Cytotoxicity Code: Apoptotic Induction of 10-Acetylirciformonin B is Mediated through ROS Generation and Mitochondrial Dysfunction

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