scholarly journals Piperlongumine and immune cytokine TRAIL synergize to promote tumor death

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Jiahe Li ◽  
Charles C. Sharkey ◽  
Michael R. King
Keyword(s):  
2020 ◽  
Vol 21 (21) ◽  
pp. 8151
Author(s):  
Sharda Kumari ◽  
Shibani Mukherjee ◽  
Debapriya Sinha ◽  
Salim Abdisalaam ◽  
Sunil Krishnan ◽  
...  

Radiation therapy (RT), an integral component of curative treatment for many malignancies, can be administered via an increasing array of techniques. In this review, we summarize the properties and application of different types of RT, specifically, conventional therapy with x-rays, stereotactic body RT, and proton and carbon particle therapies. We highlight how low-linear energy transfer (LET) radiation induces simple DNA lesions that are efficiently repaired by cells, whereas high-LET radiation causes complex DNA lesions that are difficult to repair and that ultimately enhance cancer cell killing. Additionally, we discuss the immunogenicity of radiation-induced tumor death, elucidate the molecular mechanisms by which radiation mounts innate and adaptive immune responses and explore strategies by which we can increase the efficacy of these mechanisms. Understanding the mechanisms by which RT modulates immune signaling and the key players involved in modulating the RT-mediated immune response will help to improve therapeutic efficacy and to identify novel immunomodulatory drugs that will benefit cancer patients undergoing targeted RT.


2021 ◽  
Vol 20 ◽  
pp. 153303382110330
Author(s):  
Wenwen Tang ◽  
Shaomi Zhu ◽  
Xin Liang ◽  
Chi Liu ◽  
Linjiang Song

With the increasing aging population, cancer has become one of the leading causes of death worldwide, and the number of cancer cases and deaths is only anticipated to grow further. Long non-coding RNAs (lncRNAs), which are closely associated with the expression level of downstream genes and various types of bioactivity, are regarded as one of the key regulators of cancer cell proliferation and death. Cell death, including apoptosis, necrosis, autophagy, pyroptosis, and ferroptosis, plays a vital role in the progression of cancer. A better understanding of the regulatory relationships between lncRNAs and these various types of cancer cell death is therefore urgently required. The occurrence and development of tumors can be controlled by increasing or decreasing the expression of lncRNAs, a method which confers broad prospects for cancer treatment. Therefore, it is urgent for us to understand the influence of lncRNAs on the development of different modes of tumor death, and to evaluate whether lncRNAs have the potential to be used as biological targets for inducing cell death and predicting prognosis and recurrence of chemotherapy. The purpose of this review is to provide an overview of the various forms of cancer cell death, including apoptosis, necrosis, autophagy, pyroptosis, and ferroptosis, and to describe the mechanisms of different types of cancer cell death that are regulated by lncRNAs in order to explore potential targets for cancer therapy.


10.1038/5505 ◽  
1999 ◽  
Vol 5 (2) ◽  
pp. 146-147 ◽  
Author(s):  
Lars E. French ◽  
Jürg Tschopp
Keyword(s):  

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 925-925 ◽  
Author(s):  
Andreas Lundqvist ◽  
Kristy Greeneltch ◽  
Maria Berg ◽  
Shivani Srivastava ◽  
Nanae Harashima ◽  
...  

Abstract Killer IgG like receptor (KIR) inactivation of NK cells by self HLA molecules has been proposed as a mechanism through which malignant cells evade host NK cell-mediated immunity. To overcome this limitation, we sought to develop a method to sensitize the patient’s tumor to autologous NK cell cytotoxicity. The proteasome inhibitor bortezomib has recently been shown to enhance the activity of tumor death receptors. We found that exposure of a variety of different leukemia, lymphoma and solid tumor cancer cell lines to sub-apoptotic doses of bortezomib sensitized tumor cells in vitro to lysis by allogeneic NK cells. Importantly, this sensitizing effect also occurs with autologous NK cells normally rendered inactive via tumor KIR ligands; NK cells expanded from patients with metastatic renal cell carcinoma were significantly more cytotoxic against the patient’s own autologous tumor cells when pretreated with bortezomib compared to untreated tumors. This sensitization to autologous NK cell killing was also observed in vivo in two different murine tumor models. A significant delay in tumor growth in C57BL/6 mice bearing LLC1 tumors (figure) and a delay in tumor growth and a significant prolongation (p<0.01) in survival were observed in RENCA tumor bearing Balb/c mice treated with bortezomib and syngeneic NK cell infusions compared to untreated mice or animals treated with bortezomib alone or NK cells alone. An investigation into the mechanism through which NK cell cytotoxicity was potentiated revealed bortezomib enhanced the activity of tumor death receptor-dependent and -independent apoptotic pathways. More specifically, bortezomib sensitized human and murine tumor cells to TRAIL and perforin/granzyme mediated NK cell cytotoxicity respectively. These observations suggest that pretreatment of malignant cells with bortezomib could be used as a strategy to override NK cell inhibition via tumor KIR ligands, thus potentiating the activity of adoptively infused autologous NK cells. A clinical trial evaluating the safety and anti-tumor efficacy of adoptively infused autologous NK cells in patients with advanced malignancies with and without tumor sensitization using bortezomib is currently being explored. Figure: Tumor growth in LLC1 bearing C57BL/6 mice. Fourteen days following s.c. injection of 3x105 LLC1 tumor cells, mice received 15μg (i.p) bortezomib and/or an adoptive infusion of 1x106 NK cells from C57BL/6 mice (i.v) given on day 15. Each dot represents the tumor volume of individual mice measured on day 28 post tumor injection. Tumors were significantly smaller in mice treated with bortezomib followed by NK cells compared to controls or mice that received either NK cells alone or bortezomib alone (p<0.04 for all groups). Figure:. Tumor growth in LLC1 bearing C57BL/6 mice. . / Fourteen days following s.c. injection of 3x105 LLC1 tumor cells, mice received 15μg (i.p) bortezomib and/or an adoptive infusion of 1x106 NK cells from C57BL/6 mice (i.v) given on day 15. Each dot represents the tumor volume of individual mice measured on day 28 post tumor injection. Tumors were significantly smaller in mice treated with bortezomib followed by NK cells compared to controls or mice that received either NK cells alone or bortezomib alone (p<0.04 for all groups).


2020 ◽  
Vol 231 (4) ◽  
pp. e159-e160
Author(s):  
Sara Daniel ◽  
Kevin Michael Sullivan ◽  
Xiuyun Jiang ◽  
Heidi L. Kenerson ◽  
Alan Fremder Utria ◽  
...  

2003 ◽  
Vol 127 (3) ◽  
pp. e147-e150 ◽  
Author(s):  
Li Huang ◽  
Carmen Espinoza ◽  
Ronald Welsh

Abstract Right posterior thigh malignant peripheral nerve sheath tumor with malignant glandular and rhabdomyoblastic components was diagnosed in a 24-year-old African American man. Malignant glands and rhabdomyoblastic cells were admixed with the spindle cells. Immunohistochemistry demonstrated spindle cells positive for S100 and vimentin; the glandular component was positive for chromogranin, and rare cells were positive for CK20 but negative for CK7. Rhabdomyoblastic cells were positive for muscle-specific actin and desmin. A single pulmonary metastasis occurred 5 months after surgical resection of the tumor. Death occurred 1 month later and was probably due to a pulmonary embolus.


2003 ◽  
Vol 84 (2) ◽  
pp. 263-266 ◽  
Author(s):  
Takeo Ohsugi ◽  
Kazunari Yamaguchi ◽  
Toshio Kumasaka ◽  
Takaomi Ishida ◽  
Ryouichi Horie ◽  
...  

2014 ◽  
Vol 32 (2) ◽  
pp. 182-190 ◽  
Author(s):  
Shawn T Beug ◽  
Vera A Tang ◽  
Eric C LaCasse ◽  
Herman H Cheung ◽  
Caroline E Beauregard ◽  
...  

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