One method to establish Epstein‐Barr virus‐associated <scp>NK</scp>/T cell lymphoma mouse models

Xue, Weili; Li, Weiming; Shang, Yufeng; Zhang, Yanjie; Liu, Xuan; Wang, Guannan; Li, Zhaoming; Zhang, Xudong; Song, Yue; Wu, Baopeng; Meng, Di; Wang, Xinhua; Zhang, Mingzhi

doi:10.1111/jcmm.14057

Cited by 5 publications

(5 citation statements)

References 24 publications

(33 reference statements)

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“…No primary patient cell culture systems have been documented. Only a handful of xenograft mouse models from cell lines 66,67 and one single case of a patient-derived xenograft model from a patient with NKTCL 68 have been described, and they all tend to be unstable models, questioning their relevance.…”

Section: Discussionmentioning

confidence: 99%

Selective drug combination vulnerabilities in STAT3- and TP53-mutant malignant NK cells

et al. 2021

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Mature natural killer (NK) cell neoplasms are rare but very aggressive types of cancers. With currently available treatments, they have a very poor prognosis and, as such, are an example of group of cancers in which the development of effective precision therapies is needed. Using both short- and long-term drug sensitivity testing, we explored novel ways to target NK-cell neoplasms by combining the clinically approved JAK inhibitor ruxolitinib with other targeted agents. We profiled 7 malignant NK-cell lines in drug sensitivity screens and identified that these exhibit differential drug sensitivities based on their genetic background. In short-term assays, various classes of drugs combined with ruxolitinib seemed highly potent. Strikingly, resistance to most of these combinations emerged rapidly when explored in long-term assays. However, 4 combinations were identified that selectively eradicated the cancer cells and did not allow for development of resistance: ruxolitinib combined with the mouse double-minute 2 homolog (MDM2) inhibitor idasanutlin in STAT3-mutant, TP53 wild-type cell lines; ruxolitinib combined with the farnesyltransferase inhibitor tipifarnib in TP53-mutant cell lines; and ruxolitinib combined with either the glucocorticoid dexamethasone or the myeloid cell leukemia-1 (MCL-1) inhibitor S63845 but both without a clear link to underlying genetic features. In conclusion, using a new drug sensitivity screening approach, we identified drug combinations that selectively target mature NK-cell neoplasms and do not allow for development of resistance, some of which can be applied in a genetically stratified manner.

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Section: Discussionmentioning

confidence: 99%

Selective drug combination vulnerabilities in STAT3- and TP53-mutant malignant NK cells

et al. 2021

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“…NOD/SCID mice were inoculated into right axillary region with 1.0 × 10 7 NKYS cells ( n = 5). The mice were given intraperitoneal injection of 20,000 IU/kg rhIL‐2 twice a week 27 . Tumors were allowed to develop until the average tumor volume reached approximately 200 mm 3 .…”

Section: Methodsmentioning

confidence: 99%

“…The mice were given intraperitoneal injection of 20,000 IU/kg rhIL-2 twice a week. 27 Tumors were allowed to develop until the average tumor volume reached approximately 200 mm 3 . Tumorbearing mice were then randomly divided into treatment groups and were left untreated or were treated with BV、bendamustine or combinations.…”

Section: Xenograft Mouse Models Of Nk/t Cell Lymphoma Diseasementioning

confidence: 99%

Brentuxinmab vedotin, alone or combine with bendamustine in the treatment of natural killer T cell lymphoma

Zhang

Shi

Song

et al. 2022

Hematological Oncology

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Natural killer (NK)/T cell lymphoma is a highly aggressive subtype of non‐Hodgkin lymphoma. The prognosis of patients with natural killer T cell lymphoma (NKTCL) remains poor. More potent treatment strategies are urgently needed to improve the survival of these patients with R/R NKTCL. CD30 expression has been reported to occur in about 40% of NK/T cell lymphoma. Brentuximab vedotin (BV), a monomethyl auristatin E conjugated CD30 antibody, targets CD30 to kill cancer cells. Therapeutic combination of BV and bendamustine has been shown to be highly effective in Hodgkin lymphoma. We investigated efficacy of BV in treating NKTCL as a single therapy, and in combination with bendamustine in vitro and in vivo. We determined CD30 expression levels in 6 NKTCL cell lines. The efficiency of lymphoma cell inhibition by BV correlates with CD30 expression. We also determined the efficacy of BV in combination with bendamustine and found synergistic effects with bendamustine in NKTCL. Combined BV and bendamustine treatment exerted synergistic antiproliferation effect and enhanced cell apoptotic in vitro and in vivo. Brentuximab vedotin and bendamustine synergistically arrested cell cycle at the G2/M phase in NKTCL cell lines. The combination of BV and bendamustine was demonstrated to synergistically damage DNA in NKTCL. This study provides a reference for possible application on using BV for the treatment of NKTCL, either as a single agent or in combination with bendamustine.

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“…In Xue W et al, 1 Figures 2, 4 and 7 were incorrect due to an error in the preparation of these figures for publication. It was noticed that the image for CD56 and Perforin of YT F9 in Figure 2, were coming from photographs of YT F0.…”

Section: Figurementioning

confidence: 99%

Corrigendum

2023

J Cellular Molecular Medi

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In Xue W et al., 1 Figures 2, 4 and 7 were incorrect due to an error in the preparation of these figures for publication. It was noticed that the image for CD56 and Perforin of YT F9 in Figure 2, were coming from photographs of YT F0. In addition, the images for TIA1 of NKYS F4 and F7 in Figure 4, the image for EBER of YT F5 in Figure 7, are the same with the left panel (images for CD56 of NKYS F4 and F7 in Figure 4, the image for EBER of YT F0 in Figure 7). The corrected figures appear below. The authors confirmed all results and conclusions of this article remain unchanged. We apologize for any confusion this may have caused.

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One method to establish Epstein‐Barr virus‐associated NK/T cell lymphoma mouse models

Cited by 5 publications

References 24 publications

Selective drug combination vulnerabilities in STAT3- and TP53-mutant malignant NK cells

Selective drug combination vulnerabilities in STAT3- and TP53-mutant malignant NK cells

Brentuxinmab vedotin, alone or combine with bendamustine in the treatment of natural killer T cell lymphoma

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