ATM-dependent spontaneous regression of early Eμ-myc–induced murine B-cell leukemia depends on natural killer and T cells

Croxford, J. Ludovic; Tang, Melissa Li Fang; Pan, Meng; Huang, Caleb; Kamran, Neha; Phua, Cindy; Chng, Wee Joo; Ng, Siok Bian; Raulet, David H.; Gasser, Stephan

doi:10.1182/blood-2012-08-449025

Cited by 57 publications

(42 citation statements)

References 52 publications

(55 reference statements)

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“…41,49,[53][54][55][56][57] Further evidence of the role of DNAM-1 in tumor immune surveillance is provided by studies using experimental and spontaneous models of cancer in vivo showing enhanced tumor spread in the absence of DNAM-1. [47][48][49][50]58 As NKG2D and DNAM-1 ligands are frequently expressed on stressed cells, many studies have sought to determine the mechanisms that underpin these observations. The guiding hypothesis for these studies is that cell-intrinsic responses to stress are directly linked to cell-extrinsic responses that can trigger rapid NK cell surveillance and elimination of stressed cells.…”

Section: Cellular Stress and Natural Killer (Nk) Cells-an Overviewmentioning

confidence: 99%

“…58,65,70 For example, in the Em-myc spontaneous B-cell lymphoma model, activation of the DNA-damage response leads to the upregulation of CD155 in the early-stage transformed B cells, subsequently activating spontaneous tumor regression in an NK cell-and T-cell-dependent manner. 58 The DNA-damage response can also regulate the expression of the death receptor DR5. 71 The engagement of DR5 by the effector molecule TRAIL, which is expressed by NK cells and T cells, can induce apoptosis of target cells and has been shown to have a key role in immune surveillance against tumors.…”

Section: The Dna-damage Responsementioning

confidence: 99%

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Molecular mechanisms of natural killer cell activation in response to cellular stress

2013

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Protection against cellular stress from various sources, such as nutritional, physical, pathogenic, or oncogenic, results in the induction of both intrinsic and extrinsic cellular protection mechanisms that collectively limit the damage these insults inflict on the host. The major extrinsic protection mechanism against cellular stress is the immune system. Indeed, it has been well described that cells that are stressed due to association with viral infection or early malignant transformation can be directly sensed by the immune system, particularly natural killer (NK) cells. Although the ability of NK cells to directly recognize and respond to stressed cells is well appreciated, the mechanisms and the breadth of cell-intrinsic responses that are intimately linked with their activation are only beginning to be uncovered. This review will provide a brief introduction to NK cells and the relevant receptors and ligands involved in direct responses to cellular stress. This will be followed by an in-depth discussion surrounding the various intrinsic responses to stress that can naturally engage NK cells, and how therapeutic agents may induce specific activation of NK cells and other innate immune cells by activating cellular responses to stress.

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Section: Cellular Stress and Natural Killer (Nk) Cells-an Overviewmentioning

confidence: 99%

Section: The Dna-damage Responsementioning

confidence: 99%

Molecular mechanisms of natural killer cell activation in response to cellular stress

2013

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“…[29][30][31] We used the well-established Bcr/Abl leukemia model to test the effect of deleting STAT3. We subcutaneously injected v-abl Finally we injected newborn mice with a replication-incompetent ecotropic retrovirus encoding for v-abl.…”

Section: Loss Of Stat3 In Nk Cells Improves Tumor Surveillance Againsmentioning

confidence: 99%

Loss of STAT3 in murine NK cells enhances NK cell–dependent tumor surveillance

Gotthardt

Putz

Straka

et al. 2014

Blood

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“…6A). Of note, the elevated WBC counts represent an early burst of pre‐B cells, caused by MYC overexpression 39, and the WBC counts subsided by 4 weeks of age (data not shown). Cell counts from the bone marrow and spleen of 2‐week‐old mice were comparable between all the genotypes (data not shown).…”

Section: Resultsmentioning

confidence: 94%

Differential effects of Vav‐promoter‐driven overexpression of BCLX and BFL1 on lymphocyte survival and B cell lymphomagenesis

et al. 2018

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Overexpression of BCLX and BFL1/A1 has been reported in various human malignancies and is associated with poor prognosis and drug resistance, identifying these prosurvival BCL2 family members as putative drug targets. We have generated transgenic mice that express human BFL1 or human BCLX protein throughout the haematopoietic system under the control of the Vav gene promoter. Haematopoiesis is normal in both the Vav‐BFL1 and Vav‐BCLX transgenic (TG) mice and susceptibility to spontaneous haematopoietic malignancies is not increased. Lymphoid cells from Vav‐BCLX TG mice exhibit increased resistance to apoptosis in vitro while most blood cell types form Vav‐BFL1 TG mice were poorly protected. Both transgenes significantly accelerated lymphomagenesis in Eμ‐MYC TG mice and, surprisingly, the Vav‐BFL1 transgene was the more potent. Unexpectedly, expression of transgenic BFL1 RNA and protein is significantly elevated in B lymphoid cells of Vav‐BFL1/Eμ‐MYC double‐transgenic compared to Vav‐BFL1 mice, even during the preleukaemic phase, providing a rationale for the potent synergy. In contrast, Vav‐BCLX expression was not notably different. These mouse models of BFL1 and BCLX overexpression in lymphomas should be useful tools for the testing the efficacy of novel human BFL1‐ and BCLX‐specific inhibitors.

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ATM-dependent spontaneous regression of early Eμ-myc–induced murine B-cell leukemia depends on natural killer and T cells

Abstract: • Spontaneous regression of B-cell tumors in Em-myc mice.• Regression depends on DNAM-1, natural killer cells, and T cells.

Cited by 57 publications

References 52 publications

Molecular mechanisms of natural killer cell activation in response to cellular stress

Molecular mechanisms of natural killer cell activation in response to cellular stress

Loss of STAT3 in murine NK cells enhances NK cell–dependent tumor surveillance

Differential effects of Vav‐promoter‐driven overexpression of BCLX and BFL1 on lymphocyte survival and B cell lymphomagenesis

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