Effect of splenectomy on the growth of murine colon tumors

Sato, Noriyuki; Michaelides, Maria C.; Wallack, Marc K.

doi:10.1002/jso.2930220202

Cited by 19 publications

(10 citation statements)

References 9 publications

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“…While some studies suggest that splenectomy increases tumor growth, others advocate that splenectomy might inhibit tumor progression (37)(38)(39).…”

Section: Splenectomy and Cancer Riskmentioning

confidence: 99%

Patients After Splenectomy: Old Risks and New Perspectives

Dragomir¹,

Petrescu²,

Manga³

et al. 2016

chr

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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)

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“…While some studies suggest that splenectomy increases tumor growth, others advocate that splenectomy might inhibit tumor progression (37)(38)(39).…”

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

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“…Because the multifactors participate in such mechanisms, data on the effect of splenectomy on tumor growth yield conflicting results in experimental animals, which may be related to 1) whether the tumor is allogeneic or syngeneic, 2) its relative immunogenicity and dose of injected tumor cells, 3) the timing of the operation relative to tumor inoculation, 4) the manner and site of the tumor inoculum, and 5 ) the species used for the experimental model [13,16,24]. On the other hand, in clinical investigation, the role of splenectomy in cancer patients, such as gastric cancer patients, also has been explored, providing the same conflicts [6,25].…”

Section: Discussionmentioning

confidence: 99%

Changes of peripheral t‐cell subsets in asplenic w256 tumor‐bearing rats

Han

Xiantao

1989

Journal of Surgical Oncology

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In exploring the mechanism of the effect of splenectomy on tumor growth, splenectomized rats and other control rats were implanted subcutaneously with Walker 256 carcinosarcoma cells (5 x 10(5] on day 10 after splenic operation; meanwhile, peripheral T-lymphocyte subsets were analysed successively. It was found that splenectomy enhanced the rate of tumor appearance and mean tumor diameter and disturbed the equation of T-lymphocyte subsets in peripheral blood, i.e., a subnormal level of Th/Ts ratio. Interestingly, a significant correlation was noted between decreasing values of Th/Ts ratio and increasing average diameters of implanted tumor in splenectomized rats, but not in sham-splenectomized or nonoperated rats with tumor growth. In spleen cells from tumor-bearing rats, a distinct increase of B-lymphocytes and a decrease of T cells were demonstrated. Data from this investigation provide striking evidence that a relationship exists between enhancement of tumor growth and disproportion of T-lymphocyte subsets in peripheral blood and offer some reasonable explanation for the causes of the promotive role of tumor growth following splenectomy.

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“…The CT26 murine colon tumor line was originated by intrarectal injections of N-nitroso-N-methylurethane into BALB/c mice (26), with CT26-P provided by D. M. Pardoll (The Johns Hopkins University, Baltimore, MD) (39) and CT26-C by M. Colombo (University of Milan, Milan, Italy) without any genetic modification. C26 is a BALB/c-derived colon carcinoma cell line (40). A20 B lymphoma cells were obtained from the American Type Culture Collection (ATCC) (Manassas, VA).…”

Section: Methodsmentioning

confidence: 99%

Folding of an MHC class II-restricted tumor antigen controls its antigenicity via MHC-guided processing

Mimura

Mimura‐Kimura

Doores

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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antigen presentation ͉ immunodominance ͉ protein folding T wo antigen-processing pathways have been described for the loading of MHC class II molecules (MHC-IIs) with peptides for presentation to CD4 ϩ T cells. In the classical pathway, exogenous antigens taken up by antigen-presenting cells (APCs) are unfolded and cleaved into fragments during transport through the increasingly acidic endosomal network, from early endosomes to lysosomes. Newly synthesized MHC-IIs associated with the invariant chains (Iis) are transported to a late endocytic compartment where the Ii is removed by proteolytic cleavage, leaving the class II Ii-derived peptide (CLIP) bound to the peptide-binding groove (1, 2). This is followed by peptide editing, which is catalyzed by the MHC-encoded DM molecule (3-6). The initial forms of antigen that bind to MHC-IIs may be short peptides, 12-26 aa in length, generated by lysosomal proteases (7,8). A second pathway has been described in which mature MHC-IIs recycle from the cell surface to early endosomes and load antigenic peptides that are made available in less acidic and less aggressively proteolytic environments, independently of newly synthesized MHC-IIs, Iis, and DM molecules (9-12).A long-standing question concerning antigen processing in the MHC class II pathway is whether peptides are always generated first and then loaded (trim/bind model) or whether epitopes can be generated after the binding of intact antigen to MHC-IIs (bind/trim model) (13-16). The former model has been presumed to prevail, but Sercarz et al. (13,14) have suggested that immunodominant epitopes within an intact, partially unfolding antigen might first bind to MHC-IIs and subsequently be trimmed to short peptide epitopes that roughly corresponded to the ''footprint'' of the MHC binding site. This latter model, or MHC-guided processing, has its roots in reports of MHC-IIs binding to long polypeptides (17-19). It remains unclear, however, whether these large polypeptides were the precursors of immunogenic peptides or whether they were presented as large polypeptides. The structure of several MHC-II/peptide complexes has now been solved, and it seems likely that peptides preferentially interact with the peptide-binding groove in an extended conformation, although some ''bulging'' is permitted for certain MHC-II/peptide combinations (20, 21). These data preclude the binding of MHC-IIs to elements of a protein antigen containing significant secondary structure. One mechanism by which large proteins or polypeptides bind to MHC-IIs might therefore be solvent-exposed regions of eight or more amino acids that adopt an extended or random conformation. Several proteins are known to display a more ''relaxed'' conformation during either thermal or chemical denaturation or during biogenesis. The latter may therefore give rise to a pool of substrates capable of binding to MHC-IIs and engaging in MHC-guided processing.Here we describe how the notion of MHC-guided processing is related to the immunodominance of a recently identified M...

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Effect of splenectomy on the growth of murine colon tumors

Cited by 19 publications

References 9 publications

Patients After Splenectomy: Old Risks and New Perspectives

Patients After Splenectomy: Old Risks and New Perspectives

Changes of peripheral t‐cell subsets in asplenic w256 tumor‐bearing rats

Folding of an MHC class II-restricted tumor antigen controls its antigenicity via MHC-guided processing

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