Immunodeficiency and cancer: prospects for correction

Hadden, John W.

doi:10.1016/s1567-5769(03)00060-2

Cited by 123 publications

(82 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Modern cancer immunotherapies are therefore designed to induce or enhance T cell reactivity against tumor antigens (23). Evidence indicates that many tumors induce T cell apoptosis as a mechanism of inhibiting anti-tumor activity (24). Recent studies suggest that human carcinoma cells of various origins can activate intrinsic programmed cell death in lymphocytes interacting with the tumor in vivo and in vitro (25)(26)(27).…”

Section: Discussionmentioning

confidence: 99%

Curcumin Prevents Tumor-induced T Cell Apoptosis through Stat-5a-mediated Bcl-2 Induction

Bhattacharyya

Mandal

Saha

et al. 2007

Journal of Biological Chemistry

View full text Add to dashboard Cite

Patients with advanced cancer exhibit multifaceted defects in their immune capacity, which are likely to contribute to an increased susceptibility to infections and disease progression. We demonstrated earlier that curcumin inhibits tumor growth and prevents immune cell death in tumor-bearing hosts. Here we report that tumor-induced immunodepletion involves apoptosis of thymic CD4 ؉ /CD8 ؉ single/double positive cells as well as loss of circulating CD4؉ /CD8 ؉ T cells. Administration of curcumin to tumor-bearing animals resulted in restoration of progenitor, effecter, and circulating T cells. In fact, tumor burden decreased the expression level of the pro-proliferative protein Bcl-2 while increasing the pro-apoptotic protein Bax in T cells. Curcumin down-regulated the Bax level while augmenting Bcl-2 expression in these cells, thereby protecting the immunocytes from tumor-induced apoptosis. A search for the upstream mechanism revealed down-regulation of the common cytokine receptor ␥ chain (␥c) expression in T cells by tumor-secreted prostaglandin E 2 . As a result, Jak-3 and Stat-5a phosphorylation and to a lesser extent Stat-5b phosphorylation were also decreased in T cells. These entire phenomena could be reverted back by curcumin, indicating that this phytochemical restored the cytokine-dependent Jak-3/Stat-5a signaling pathway in T cells of tumor bearers. Overexpressed Stat-5a/constitutively active Stat-5a1*6 but not Stat-5b could efficiently elevate Bcl-2 levels and protect T cells from tumor-induced death, whereas C-terminal truncated Stat-5a 713 overexpression failed to do so, indicating the importance of Stat-5a signaling in T cell survival. Thus, these results raise the possibility of inclusion of curcumin in successful therapeutic regimens against cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

Curcumin Prevents Tumor-induced T Cell Apoptosis through Stat-5a-mediated Bcl-2 Induction

Bhattacharyya

Mandal

Saha

et al. 2007

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Several cancers have been correlated with immunodeficiency and it is known that the spleen plays a crucial role in the immune response hence, one might argue that splenectomy might be a risk factor for cancer, but the exact mechanism is still unknown (30,31).…”

Section: Splenectomy and Cancer Riskmentioning

confidence: 99%

Patients After Splenectomy: Old Risks and New Perspectives

Dragomir¹,

Petrescu²,

Manga³

et al. 2016

chr

View full text Add to dashboard Cite

Rezumat Pacienåii post-splenectomie: complicaåii cunoscute aei perspective noiComplicaåiile care survin în urma splenectomiei pot fi împãråite în infecåioase aei non-infecåioase. Legãtura dintre splenectomie aei aceste riscuri este doar paråial înåeleasã. Rãspunsul imun al gazdei împotriva infecåiei este profund modificat post-splenectomie, iar aceaeti indivizi sunt mai susceptibili sã dezvolte sepsis aei infecåia are o evoluåie fulminantã. Splenectomia este de asemenea un potenåial factor de risc pentru numeroase complicaåii vasculare care rezultã în urma obstrucåiei paråiale sau totale ale unei artere sau vene. În plus, hipertensiunea pulmonarã poate fi o complicaåie severã aei uneori fatalã a splenectomiei. Unii autori includ aei neoplaziile, diabetul zaharat aei pancreatita acutã în categoria complicaåiilor non-infecåioase post-splenectomie. Cea mai de temut complicaåie pentru pacienåii splenectomizaåi rãmâne sepsisul. Fiziopatologia sepsisului încã este controversatã. Decesul în sepsis poate surveni fie în urma hiperinflamaåiei, fie în urma imunosupresiei. Multiple dovezi experimentale au dovedit implicarea microRNA-urilor celulare aei virale în sepsis. Considerãm faptul cã microRNA-urile sunt de asemenea asociate cu imunosupresia pacientului asplenic, ceea ce determinã o creaetere a riscului de sepsis fatal. Studierea nivelului expresiei plasmatice a microRNA-urilor circulante la pacienåii asplenici, ar putea conduce la o mai bunã înåelegere a imunosupresiei post-splenectomie aei la dezvoltarea unor noi metode diagnostice aei terapeutice.Cuvinte cheie: splenectomie, microRNA, sepsis, microRNA-uri virale, OPSI AbstractThe risks that arise after splenectomy can be divided in infectious and non-infectious. The link between splenectomy and these hazards remains partially unknown. Host defense against infection is altered after splenectomy and such individuals develop sepsis more easily and the infection has a fulminant course. Splenectomy is also a potential risk factor for several vascular complications that result from partial or total obstruction of an arterial or venous blood vessel. Furthermore, pulmonary hypertensioncan be a severe and sometimes fatal complication following splenectomy. Some authors also consider that malignancies, diabetes mellitus and acute pancreatitis are non-infectious complications after splenectomy. The most feared complication for splenectomized patients remains sepsis. The pathophysiology of sepsis is still controversial. Death in sepsis can occur due to either hyper-inflammation or "immune paralysis". Multiple experimental evidences link cellular and viral microRNAs with sepsis. We presume that General ReportChirurgia (2016)

show abstract

“…Tumors can evade destruction by inhibiting immune response directly. Therefore, enhancement of the immune response in tumor-bearing host can restore the dynamic balance between the tumor cells and the immune system, and thus exert potential antitumor effects (Hadden, 2003;Li et al, 2011). Some botanical polysaccharides have been shown to promote immune functions in various ways, and their antitumor activities might be mediated via augmentation of the immune response Liu et al, 2013).…”

Section: Immunological Activity Of Ccpsmentioning

confidence: 99%

Polysaccharides fromCymbopogon citratuswith antitumor and immunomodulatory activity

Bao

Yuan

Wang

et al. 2014

Pharmaceutical Biology

View full text Add to dashboard Cite

Context: Most of the present studies on the antitumor efficiency of Cymbopogon citratus (DC.) Stapf (Gramineae) are limited to its low-mass compounds, and little information about the antitumor activity of polysaccharides from this plant is available. Objectives: This study focused on the potential antitumor and immunomodulatory activities of polysaccharides (CCPS) from C. citratus. Materials and methods: CCPS was isolated using the water extraction-ethanol precipitation method. The sarcoma 180 (S180) cells-inoculated mice were intraperitoneally administrated with CCPS (30-200 mg/kg/d) for seven consecutive days. The effects of CCPS on tumor growth, thymus and spleen weights, splenocyte proliferation, and cytokine secretion in the tumorbearing mice were measured. The cytotoxicity of CCPS (50-800 lg/mL) towards S180 cells was also studied. Results: CCPS significantly inhibited the growth of the transplanted S180 tumors, with the inhibition rates ranging from 14.8 to 37.8%. Simultaneously, CCPS dose-dependently improved the immunity of the tumor-bearing mice. With the highest dose of 200 mg/kg/d, the thymus and spleen indices were increased by 21.9 and 91.9%, respectively; ConA-and LSP-induced splenocyte proliferations were increased by 32.7 and 35.3%, respectively. The secretions of interleukin 2 (IL-2), interleukin 6 (IL-6), interleukin 2 (IL-12), and tumor necrosis factor-a (TNF-a) were increased by 103.2, 40.2, 23.6, and 26.3%, respectively. Nevertheless, almost no toxicity of CCPS towards S180 cells was observed, with the maximal inhibition rate less than 15% at the CCPS concentration of 800 lg/mL. Conclusion: CCPS exhibited antitumor activity in vivo, and this activity might be achieved by immunoenhancement rather than direct cytotoxicity.

show abstract

Immunodeficiency and cancer: prospects for correction

Cited by 123 publications

References 70 publications

Curcumin Prevents Tumor-induced T Cell Apoptosis through Stat-5a-mediated Bcl-2 Induction

Curcumin Prevents Tumor-induced T Cell Apoptosis through Stat-5a-mediated Bcl-2 Induction

Patients After Splenectomy: Old Risks and New Perspectives

Polysaccharides fromCymbopogon citratuswith antitumor and immunomodulatory activity

Contact Info

Product

Resources

About