Comparative abilities of athymic nude mice and severe combined immune deficient (SCID) mice to accept transplants of induced rat mammary carcinomas: Enhanced transplantation efficiency of those rat mammary carcinomas that have elevated expression of <i>neu</i> oncogene

Oakley, Cori S.; Welsch, Margaret A.; Zhai, Yifan; Chang, Chia‐Cheng; Gould, Michael N.; Welsch, Clifford W.

doi:10.1002/ijc.2910530624

Cited by 13 publications

(2 citation statements)

References 29 publications

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“…And immune analysis showed that IL‐33 could enhance anti‐MM immunity. So we could not completely rule out that the enhancement of IL‐33 on BTZ‐mediated anti‐MM efficacy was related to the effect of IL‐33 on the microenvironment, 43,44 severe combined immunodeficient mice may be more suitable for our study.…”

Section: Discussionmentioning

confidence: 98%

Interleukin‐33 increases the sensitivity of multiple myeloma cells to the proteasome inhibitor bortezomib through reactive oxygen species‐mediated inhibition of nuclear factor kappa‐B signal and stemness properties

Shao,

Liu,

Liu

et al. 2024

MedComm

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The proteasome inhibitor bortezomib (BTZ) is the first‐line therapy for multiple myeloma (MM). BTZ resistance largely limits its clinical application in MM. Interleukin‐33 (IL‐33) exerts antitumor effects through various mechanisms, including enhancing antitumor immunity and promoting the apoptosis of cancer cells. Here, the synergistic anti‐MM effect of IL‐33 and BTZ was verified, and the underlying mechanisms were elucidated. Bioinformatic analysis indicated that IL‐33 expression levels were downregulated in MM, and that BTZ‐treated MM patients with high IL‐33 levels had better prognosis than those with low IL‐33 levels. Moreover, the patients with high IL‐33 levels had a better treatment response to BTZ. Further immune analysis suggested that IL‐33 can enhance the anti‐MM immunity. IL‐33 and BTZ synergistically inhibited proliferation and induced apoptosis of MM cells, which was mediated by the excessive accumulation of cellular reactive oxygen species (ROS). Furthermore, increased ROS hindered the nuclear translocation of NF‐κB‐p65, thereby decreasing the transcription of target stemness‐related genes (SOX2, MYC, and OCT3/4). These effects induced by the combination therapy could be reversed by eliminating ROS by N‐acetylcysteine. In conclusion, our results indicated that IL‐33 enhanced the sensitivity of MM to BTZ through ROS‐mediated inhibition of nuclear factor kappa‐B (NF‐κB) signal and stemness properties.

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Section: Discussionmentioning

confidence: 98%

Interleukin‐33 increases the sensitivity of multiple myeloma cells to the proteasome inhibitor bortezomib through reactive oxygen species‐mediated inhibition of nuclear factor kappa‐B signal and stemness properties

Shao,

Liu,

Liu

et al. 2024

MedComm

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“…Lack of T, B, NK cells. It is a ideal strain for cancer modeling and studies in immune-oncology and efficacy testing [15,16].…”

Section: Introductionmentioning

confidence: 99%

A novel retinoic acid analog, 4-Amino-2-Trifluoromethyl-Phenyl Retinate (ATPR) triggers differentiation and is effective in the treatment of Acute Promyelocytic Leukemia

Bao

et al. 2020

Preprint

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Acute promyelocytic leukemia (APL), form RARα fusion genes and proteins is one of the most prevalent forms of leukemia. 4-Amino-2-Trifluoromethyl-Phenyl Retinate (ATPR), a derivative of all-trans-retinoic acid (ATRA), is of potent functions in the induce of cell differentiation, growth arrest, and apoptosis. Nowadays, we aimed to investigate the therapeutic effect of ATPR on this APL pathological model, and whether the mechanism involves PI3K/AKT, ERK and Notch signaling. We established a human xenograft mouse model using NB4 cells and found that ATPR significantly increased the protein concentration in the CD11b and suppressed the PI3K/AKT signaling and activated the ERK and Notch signaling in tumor tissue. Collectively, these data suggest that ATPR shows antileukemic effects by regulating PI3K/AKT, ERK and Notch signaling.

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BXD recombinant inbred mice represent a novel T cell–mediated immune response tumor model

Grizzle

Mountz

Yang

et al. 2002

Intl Journal of Cancer

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To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2 d RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to Characterization of the effect of the host environment on the development and progression of tumors has proven difficult due, in part, to the lack of informative models. The immune surveillance system, which is thought to play a key role in determining susceptibility or resistance to tumor growth, shows considerable variation among individuals. Although immunodeficient nude and SCID mice are useful tools for the characterization of the role of the host environment in the development and progression of human-derived tumors, 1,2 the lack of an intact immune system in these mice results in an incomplete picture of the potential mechanisms involved and their relative contribution to tumor growth. Comparative analysis of implanted syngeneic TS/A tumor cells in C57BL/6 mice, which are resistant to implanted tumors, and DBA/2 mice, which are susceptible, is a good model for the dissection of the host immune response to tumors but is limited by the lack of response diversity. [3][4][5] The genetically well-characterized BXD RI strain of mice was derived by intercrossing F 2 mice derived from DBA/2 and C57BL/6 mice for more than 20 generations to fix homozygous loci. These strains exhibit a broad spectrum of traits, including diversity in the types and intensity of the immune responses. 6 -12 The availability of these mice therefore presented an opportunity to develop an alternative model to analyze the mechanisms that determine the immune response to tumor cells. BXD mice have been used for genetic mapping of disease susceptibility 13,14 and for studying the development of the nervous system 15-17 and alcohol abuse. 6,18 Several investigators have recognized the advantage of using these mice to identify both MHCrelated and non-MHC-related genetic loci that affect the shaping of the repertoire and the function of the immune system. 7,13,19 -21 Waters et al. 22 utilized these mice to show that the genetic restriction involved in KLH antigen-specific proliferation maps to the mls gene on chromosome 1. Scalzo et al. 20 showed that the resistance of mice to lethal infection by MCMV is associated ...

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Comparative abilities of athymic nude mice and severe combined immune deficient (SCID) mice to accept transplants of induced rat mammary carcinomas: Enhanced transplantation efficiency of those rat mammary carcinomas that have elevated expression of neu oncogene

Cited by 13 publications

References 29 publications

Interleukin‐33 increases the sensitivity of multiple myeloma cells to the proteasome inhibitor bortezomib through reactive oxygen species‐mediated inhibition of nuclear factor kappa‐B signal and stemness properties

Interleukin‐33 increases the sensitivity of multiple myeloma cells to the proteasome inhibitor bortezomib through reactive oxygen species‐mediated inhibition of nuclear factor kappa‐B signal and stemness properties

A novel retinoic acid analog, 4-Amino-2-Trifluoromethyl-Phenyl Retinate (ATPR) triggers differentiation and is effective in the treatment of Acute Promyelocytic Leukemia

BXD recombinant inbred mice represent a novel T cell–mediated immune response tumor model

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