CoChat
Sign Up
Cited by 17

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Mast Cell Targeted Chimeric Toxin Can Be Developed as an Adjunctive Therapy in Colon Cancer Treatment

Wang, Shan, Li, Linmei, Shi, Renren, Liu, Xueting, Zhang, Junyan, Zou, Zehong, Hao, Zhuofang, Tao, Ailin·2016·Toxins
DOI 10.3390/toxins8030071PMC PMC4810216
Open this paper in CoChat — free account

Abstract

The association of colitis with colorectal cancer has become increasingly clear with mast cells being identified as important inflammatory cells in the process. In view of the relationship between mast cells and cancer, we studied the effect and mechanisms of mast cells in the development of colon cancer. Functional and mechanistic insights were gained from ex vivo and in vivo studies of cell interactions between mast cells and CT26 cells. Further evidence was reversely obtained in studies of mast cell targeted Fcε-PE40 chimeric toxin. Experiments revealed mast cells could induce colon tumor cell proliferation and invasion. Cancer progression was found to be related to the density of mast cells in colonic submucosa. The activation of MAPK, Rho-GTPase, and STAT pathways in colon cancer cells was triggered by mast cells during cell-to-cell interaction. Lastly, using an Fcε-PE40 chimeric toxin we constructed, we confirmed the promoting effect of mast cells in development of colon cancer. Mast cells are a promoting factor of colon cancer and thus also a potential therapeutic target. The Fcε-PE40 chimeric toxin targeting mast cells could effectively prevent colon cancer in vitro and in vivo. Consequently, these data may demonstrate a novel immunotherapeutic approach for the treatment of tumors.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3390/toxins8030071

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Figures

Figure 1 Mast cell infiltration relates with colon cancer development. (A) Immunohistochemistry-stained pictures of CD117 and tryptase show mast cells infiltration in different colonic tumor tissues. Magnification, ×400. Scale bar, 100 μm. (B) Mast cell counts carried out on tryptase Immunohistochemistry-stained colonic tumor sections in per 400× field. Tumor tissues are characterized by colonic adenoma, well differentiated adenocarcinoma, and poor differentiated adenocarcinoma. (C) Mast cell counts carried out on tryptase immunohistochemistry-stained colonic tumor sections. Tumor tissues are characterized by non-metastatic colon cancer and metastatic colon cancer. Arrows indicate mast cells.
Figure 1 Mast cell infiltration relates with colon cancer development. (A) Immunohistochemistry-stained pictures of CD117 and tryptase show mast cells infiltration in different colonic tumor tissues. Magnification, ×400. Scale bar, 100 μm. (B) Mast cell counts carried out on tryptase Immunohistochemistry-stained colonic tumor sections in per 400× field. Tumor tissues are characterized by colonic adenoma, well differentiated adenocarcinoma, and poor differentiated adenocarcinoma. (C) Mast cell counts carried out on tryptase immunohistochemistry-stained colonic tumor sections. Tumor tissues are characterized by non-metastatic colon cancer and metastatic colon cancer. Arrows indicate mast cells.CC BY · PubMed Central
Figure 2 Piecemeal degranulation of mast cells can promote colon cancer cell proliferation and migration. (A) Toluidine blue staining of bone marrow-derived mast cells induced for 4 weeks and 6 weeks. Arrows indicate mature mast cells enriching with granules. Magnification, ×1000, Scale bar, 20 μm. (B) Histogram of bone marrow-derived mast cells (BMMCs) induced for 4 weeks and 6 weeks. Mast cells were identified by flow cytometry as CD117+ cells which were 13.9% at 4 weeks and 76.7% at 6 weeks. (C) Histamine release analysis shows bone marrow-derived mast cell “piecemeal degranulation” without stimulation and Calcium Ionophore (CaIO) makes bone marrow-derived mast cells degranulation with a dose-dependent way. (D) Quantification of CT26 cells proliferation cultured with or without BMMCs after 48 h by MTS. (E,F) The wound healing assay showed different cell migration in CT26 cells and CT26 cells co-cultured with BMMCs. (E) Representative images were taken at different time points. (F) Quantification of CT26 cells migration by measuring the wound width. The amount of motility was expressed as a percent of migration at the time point 0. ** p < 0.01; and *** p < 0.001.
Figure 2 Piecemeal degranulation of mast cells can promote colon cancer cell proliferation and migration. (A) Toluidine blue staining of bone marrow-derived mast cells induced for 4 weeks and 6 weeks. Arrows indicate mature mast cells enriching with granules. Magnification, ×1000, Scale bar, 20 μm. (B) Histogram of bone marrow-derived mast cells (BMMCs) induced for 4 weeks and 6 weeks. Mast cells were identified by flow cytometry as CD117+ cells which were 13.9% at 4 weeks and 76.7% at 6 weeks. (C) Histamine release analysis shows bone marrow-derived mast cell “piecemeal degranulation” without stimulation and Calcium Ionophore (CaIO) makes bone marrow-derived mast cells degranulation with a dose-dependent way. (D) Quantification of CT26 cells proliferation cultured with or without BMMCs after 48 h by MTS. (E,F) The wound healing assay showed different cell migration in CT26 cells and CT26 cells co-cultured with BMMCs. (E) Representative images were taken at different time points. (F) Quantification of CT26 cells migration by measuring the wound width. The amount of motility was expressed as a percent of migration at the time point 0. ** p < 0.01; and *** p < 0.001.CC BY · PubMed Central
Figure 3 Mast cells up-regulate the expression of RhoA and VEGFc in colon cancer cells. (A) Western blotting analysis of the expression levels of RhoA in CT26 cells with different stimulation conditions. (B,C) RT-PCR analysis detected the VEGF-A/B/C and TGF-β expression in CT26 cells with or without BMMCs co-cultured.
Figure 3 Mast cells up-regulate the expression of RhoA and VEGFc in colon cancer cells. (A) Western blotting analysis of the expression levels of RhoA in CT26 cells with different stimulation conditions. (B,C) RT-PCR analysis detected the VEGF-A/B/C and TGF-β expression in CT26 cells with or without BMMCs co-cultured.CC BY · PubMed Central
Figure 4 MAPK/Rho-GTPase/STATs pathways participate in the regulation mechanism of mast cells function to colon cancer cells. (A) CT26 cells were co-cultured with BMMCs for different time. Suspended BMMCs were then washed out and CT26 cells were further processed to cell lysates for western blotting analysis. Western blotting analysis detected the phosphorylation of signaling proteins in CT26 cells after BMMCs stimulation, including ERK 1/2, P38 MAPK, JNK/SAPK, and Rac1. (B) Western blotting analysis detected the phosphorylation of STATs pathway signaling protein in CT26 cells after BMMCs stimulation, including STAT3, STAT5 and STAT6. (C) Relative quantization of the pathways activation included Figure 4A,B during BMMCs stimulation. The band intensity was quantized by the Quantity One.
Figure 4 MAPK/Rho-GTPase/STATs pathways participate in the regulation mechanism of mast cells function to colon cancer cells. (A) CT26 cells were co-cultured with BMMCs for different time. Suspended BMMCs were then washed out and CT26 cells were further processed to cell lysates for western blotting analysis. Western blotting analysis detected the phosphorylation of signaling proteins in CT26 cells after BMMCs stimulation, including ERK 1/2, P38 MAPK, JNK/SAPK, and Rac1. (B) Western blotting analysis detected the phosphorylation of STATs pathway signaling protein in CT26 cells after BMMCs stimulation, including STAT3, STAT5 and STAT6. (C) Relative quantization of the pathways activation included Figure 4A,B during BMMCs stimulation. The band intensity was quantized by the Quantity One.CC BY · PubMed Central
Figure 5 Mast cell targeted Fcε-PE40 chimeric toxin induce mast cells apoptosis without degranulation. (A) The purity and concentration of recombinant protein Fcε-PE40 chimeric toxin were measured by 12% SDS-PAGE (arrow indicating). (B) The protein Fcε (17 KD) and Fcε-PE40 chimeric toxin (55 KD) were verified by western blotting with Pseudomonas Exotoxin A antibody (a) and mouse IgE antibody (b). (C) Images show the growth of CT26 cells and BMMCs with or without Fcε-PE40 chimeric toxin (1 μg/mL) after 24 h. Magnification, ×100. Scale bar, 100 μm. (D) Cell death dose dependent curves after CT26 cells and BMMCs co-cultured with Fcε-PE40 for 24 h were assessed by MTS assay. (E) Mast cells’ degranulation after treated by Fcε-PE40 for 24 h was assessed by histamine release analysis. (F) Expression level of cleaved caspase3 in CT26 cells and BMMCs co-cultured with Fcε-PE40 for 24 h was detected by western blotting.
Figure 5 Mast cell targeted Fcε-PE40 chimeric toxin induce mast cells apoptosis without degranulation. (A) The purity and concentration of recombinant protein Fcε-PE40 chimeric toxin were measured by 12% SDS-PAGE (arrow indicating). (B) The protein Fcε (17 KD) and Fcε-PE40 chimeric toxin (55 KD) were verified by western blotting with Pseudomonas Exotoxin A antibody (a) and mouse IgE antibody (b). (C) Images show the growth of CT26 cells and BMMCs with or without Fcε-PE40 chimeric toxin (1 μg/mL) after 24 h. Magnification, ×100. Scale bar, 100 μm. (D) Cell death dose dependent curves after CT26 cells and BMMCs co-cultured with Fcε-PE40 for 24 h were assessed by MTS assay. (E) Mast cells’ degranulation after treated by Fcε-PE40 for 24 h was assessed by histamine release analysis. (F) Expression level of cleaved caspase3 in CT26 cells and BMMCs co-cultured with Fcε-PE40 for 24 h was detected by western blotting.CC BY · PubMed Central
Figure 6 Mast cells targeted Fcε-PE40 chimeric toxin can assist colon cancer control in vivo. (A) Tumor growth in mice implanted with CT26 cells and CT26 cells together with BMMCs. Tumor growth is measured by the weight of solid tumor mass. (B) Solid tumor masses obtained from mice implanted with CT26 cells and CT26 cells together with BMMCs. (C) H & E staining and Immunohistochemistry of tryptase sections of tumor mass implanted with CT26 cells and CT26 cells together with BMMCs. Arrows indicate mast cells rich in tryptase in tumor tissues. Scale bar, 50 μm. (D) Determination of the tumor growth. Tumor weight was calculated 4 weeks after injection. (E) Representative image for tumor growth is shown. BAL B/C mice were subcutaneously injected with 2.0 × 106 CT26 cells. Fcε-PE40 chimeric toxin was injected after 2 weeks. * p < 0.05; ** p < 0.01.
Figure 6 Mast cells targeted Fcε-PE40 chimeric toxin can assist colon cancer control in vivo. (A) Tumor growth in mice implanted with CT26 cells and CT26 cells together with BMMCs. Tumor growth is measured by the weight of solid tumor mass. (B) Solid tumor masses obtained from mice implanted with CT26 cells and CT26 cells together with BMMCs. (C) H & E staining and Immunohistochemistry of tryptase sections of tumor mass implanted with CT26 cells and CT26 cells together with BMMCs. Arrows indicate mast cells rich in tryptase in tumor tissues. Scale bar, 50 μm. (D) Determination of the tumor growth. Tumor weight was calculated 4 weeks after injection. (E) Representative image for tumor growth is shown. BAL B/C mice were subcutaneously injected with 2.0 × 106 CT26 cells. Fcε-PE40 chimeric toxin was injected after 2 weeks. * p < 0.05; ** p < 0.01.CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Research works printed but not linked: 65

  1. Eichten, 2006, Paradoxical roles of the immune system during cancer development, Nat. Rev. Cancer, 6, 24, 10.1038/nrc1782 · DOI
  2. Grivennikov, 2010, Immunity, inflammation, and cancer, Cell, 140, 883, 10.1016/j.cell.2010.01.025 · DOI · Paper page
  3. Quante, 2013, The gastrointestinal tumor microenvironment, Gastroenterology, 145, 63, 10.1053/j.gastro.2013.03.052 · DOI
  4. Wood, 2014, The role of the tumor-microenvironment in lung cancer-metastasis and its relationship to potential therapeutic targets, Cancer Treat. Rev., 40, 558, 10.1016/j.ctrv.2013.10.001 · DOI
  5. Riese, 2014, Epiregulin: Roles in normal physiology and cancer, Semin. Cell Dev. Biol., 28, 49, 10.1016/j.semcdb.2014.03.005 · DOI
  6. Loesch, 2008, The p38 mapk stress pathway as a tumor suppressor or more?, Front. Biosci., 13, 3581, 10.2741/2951 · DOI
  7. Kim, 2010, Pathological roles of mapk signaling pathways in human diseases, Biochim. Biophys. Acta, 1802, 396, 10.1016/j.bbadis.2009.12.009 · DOI · Paper page
  8. Zhang, 2013, Interleukin-6 is required for pancreatic cancer progression by promoting mapk signaling activation and oxidative stress resistance, Cancer Res., 73, 6359, 10.1158/0008-5472.CAN-13-1558-T · DOI
  9. Taylor, C.A., Zheng, Q., Liu, Z., and Thompson, J.E. (2013). Role of p38 and jnk mapk signaling pathways and tumor suppressor p53 on induction of apoptosis in response to ad-eif5a1 in a549 lung cancer cells. Mol. Cancer. · DOI
  10. Sanders, 2010, The type ii transmembrane serine protease, matriptase-2: Possible links to cancer?, Anti-Cancer Agents Med. Chem., 10, 64, 10.2174/1871520611009010064 · DOI
  11. Chia, 2014, Breast cancer cell invasion mediated by galpha12 signaling involves expression of interleukins-6 and -8, and matrix metalloproteinase-2, J. Mol. Signal., 9, 1, 10.1186/1750-2187-9-6 · DOI
  12. Lin, 2007, Il-6 induces ags gastric cancer cell invasion via activation of the c-src/rhoa/rock signaling pathway, Int. J. Cancer., 120, 2600, 10.1002/ijc.22599 · DOI
  13. Geng, Y., Chandrasekaran, S., Hsu, J.W., Gidwani, M., Hughes, A.D., and King, M.R. (2013). Phenotypic switch in blood: Effects of pro-inflammatory cytokines on breast cancer cell aggregation and adhesion. PLoS ONE, 8. · DOI
  14. Gacche, 2013, Targeting tumor micro-environment for design and development of novel anti-angiogenic agents arresting tumor growth, Prog. Biophys. Mol. Biol., 113, 333, 10.1016/j.pbiomolbio.2013.10.001 · DOI
  15. Allavena, 2012, Immunology in the clinic review series; focus on cancer: Tumour-associated macrophages: Undisputed stars of the inflammatory tumour microenvironment, Clin. Exp. Immunol., 167, 195, 10.1111/j.1365-2249.2011.04515.x · DOI
  16. Sakurai, 2012, Targeting of tak1 in inflammatory disorders and cancer, Trends Pharmacol. Sci., 33, 522, 10.1016/j.tips.2012.06.007 · DOI
  17. Vaiopoulos, 2010, Colon carcinogenesis: Learning from nf-kappab and ap-1, Int. J. Biochem. Cell Biol., 42, 1061, 10.1016/j.biocel.2010.03.018 · DOI
  18. Verstovsek, 2013, Molecular pathways: Jak/stat pathway: Mutations, inhibitors, and resistance, Clin. Cancer Res., 19, 1933, 10.1158/1078-0432.CCR-12-0284 · DOI
  19. Laveti, 2013, Anti-inflammatory treatments for chronic diseases: A review, Inflamm. Allergy Drug Targets, 12, 349, 10.2174/18715281113129990053 · DOI
  20. Yu, 2009, Stats in cancer inflammation and immunity: A leading role for stat3, Nat. Rev. Cancer, 9, 798, 10.1038/nrc2734 · DOI · Paper page
  21. Crivellato, 2003, Paul ehrlich’s doctoral thesis: A milestone in the study of mast cells, Br. J. Haematol., 123, 19, 10.1046/j.1365-2141.2003.04573.x · DOI
  22. Wedemeyer, 2000, Roles of mast cells and basophils in innate and acquired immunity, Curr. Opin. Immunol., 12, 624, 10.1016/S0952-7915(00)00154-0 · DOI
  23. Ali, 2010, Regulation of human mast cell and basophil function by anaphylatoxins c3a and c5a, Immunol. Lett., 128, 36, 10.1016/j.imlet.2009.10.007 · DOI
  24. Huang, 2008, Scf-mediated mast cell infiltration and activation exacerbate the inflammation and immunosuppression in tumor microenvironment, Blood, 112, 1269, 10.1182/blood-2008-03-147033 · DOI
  25. Kanbe, 1999, Human mast cells produce matrix metalloproteinase 9, Eur. J. Immunol., 29, 2645, 10.1002/(SICI)1521-4141(199908)29:08<2645::AID-IMMU2645>3.0.CO;2-1 · DOI
  26. Crivellato, 2005, Piecemeal degranulation in human tumour pheochromocytes, J. Anat., 206, 47, 10.1111/j.0021-8782.2005.00365.x · DOI
  27. Caruso, 2005, Degranulation patterns of eosinophils in advanced gastric carcinoma: An electron microscopic study, Ultrastruct. Pathol., 29, 29, 10.1080/019131290882303 · DOI
  28. Theoharides, 2004, Mast cells: The jekyll and hyde of tumor growth, Trends Immunol., 25, 235, 10.1016/j.it.2004.02.013 · DOI
  29. McNeil, 2007, Mast cell-restricted tryptases: Structure and function in inflammation and pathogen defense, J. Biol. Chem., 282, 20785, 10.1074/jbc.R700017200 · DOI
  30. Coussens, 2000, Mmp-9 supplied by bone marrow-derived cells contributes to skin carcinogenesis, Cell, 103, 481, 10.1016/S0092-8674(00)00139-2 · DOI · Paper page
  31. Maltby, 2009, Mast cells in tumor growth: Angiogenesis, tissue remodelling and immune-modulation, Biochim. Biophys. Acta, 1796, 19
  32. Crivellato, 2008, Mast cells and tumour angiogenesis: New insight from experimental carcinogenesis, Cancer Lett., 269, 1, 10.1016/j.canlet.2008.03.031 · DOI
  33. Ribatti, 2013, Mast cells and macrophages exert beneficial and detrimental effects on tumor progression and angiogenesis, Immunol. Lett., 152, 83, 10.1016/j.imlet.2013.05.003 · DOI
  34. Adams, 1994, Short-course cimetidine and survival with colorectal cancer, Lancet, 344, 1768, 10.1016/S0140-6736(94)92907-6 · DOI
  35. Matsumoto, 1995, Cimetidine and survival with colorectal cancer, Lancet, 346, 115, 10.1016/S0140-6736(95)92136-2 · DOI
  36. Matsumoto, 2002, Cimetidine increases survival of colorectal cancer patients with high levels of sialyl lewis-x and sialyl lewis-a epitope expression on tumour cells, Br. J. Cancer, 86, 161, 10.1038/sj.bjc.6600048 · DOI
  37. Khazaie, 2011, The significant role of mast cells in cancer, Cancer Metastasis Rev., 30, 45, 10.1007/s10555-011-9286-z · DOI
  38. Galinsky, 2008, Mast cells and cancer—No longer just basic science, Crit. Rev. Oncol. Hematol., 68, 115, 10.1016/j.critrevonc.2008.06.001 · DOI
  39. Nonomura, 2007, Decreased number of mast cells infiltrating into needle biopsy specimens leads to a better prognosis of prostate cancer, Br. J. Cancer, 97, 952, 10.1038/sj.bjc.6603962 · DOI
  40. Strouch, 2010, Crosstalk between mast cells and pancreatic cancer cells contributes to pancreatic tumor progression, Clin. Cancer Res., 16, 2257, 10.1158/1078-0432.CCR-09-1230 · DOI
  41. Goffredo, 2013, Tryptase serum levels in patients suffering from hepatocellular carcinoma undergoing intra-arterial chemoembolization: Possible predictive role of response to treatment, Mol. Clin. Oncol., 1, 385, 10.3892/mco.2013.59 · DOI
  42. Tan, 2005, P53 and c-kit (cd117) protein expression as prognostic indicators in breast phyllodes tumors: A tissue microarray study, Mod. Pathol., 18, 1527, 10.1038/modpathol.3800488 · DOI
  43. Gulubova, 2009, Prognostic significance of mast cell number and microvascular density for the survival of patients with primary colorectal cancer, J. Gastroenterol. Hepatol., 24, 1265, 10.1111/j.1440-1746.2007.05009.x · DOI
  44. Yodavudh, 2008, Prognostic significance of microvessel density and mast cell density for the survival of thai patients with primary colorectal cancer, J. Med. Assoc. Thail., 91, 723
  45. Acikalin, 2005, Tumour angiogenesis and mast cell density in the prognostic assessment of colorectal carcinomas, Dig. Liver Dis., 37, 162, 10.1016/j.dld.2004.09.028 · DOI
  46. Fishman, 1997, Targeted elimination of cells expressing the high-affinity receptor for ige (fc epsilon ri) by a pseudomonas exotoxin-based chimeric protein, Eur. J. Immunol., 27, 486, 10.1002/eji.1830270220 · DOI
  47. Fishman, 2000, Targeted fc2′-3-pe40 chimeric protein abolishes passive cutaneous anaphylaxis in mice, Clin. Exp. Immunol., 119, 398, 10.1046/j.1365-2249.2000.01151.x · DOI
  48. Kruger, 1974, Structural features of histamine release in rat peritoneal mast cells. A study with toluidine blue, Int. Arch. Allergy Appl. Immunol., 46, 740, 10.1159/000231174 · DOI
  49. Nitta, 2009, Image analysis of mast cell degranulation in a concentration gradient of stimuli formed in the channel between a glass plate and a silicon substrate, Eur. J. Cell Biol., 88, 541, 10.1016/j.ejcb.2009.03.004 · DOI
  50. Kovarikova, 2014, Methods for studying tumor cell migration and invasiveness, Klin. Onkol., 27, S22, 10.14735/amko20141S22 · DOI
  51. Hill, 1996, Stem cell factor enhances immunoglobulin e-dependent mediator release from cultured rat bone marrow-derived mast cells: Activation of previously unresponsive cells demonstrated by a novel elispot assay, Immunology, 87, 326, 10.1046/j.1365-2567.1996.455545.x · DOI
  52. Oliveira, 2002, Stem cell factor induces eosinophil activation and degranulation: Mediator release and gene array analysis, Blood, 100, 4291, 10.1182/blood.V100.13.4291 · DOI
  53. Mantovani, 2008, Cancer-related inflammation, Nature, 454, 436, 10.1038/nature07205 · DOI · Paper page
  54. Grimbaldeston, 2004, Association between melanoma and dermal mast cell prevalence in sun-unexposed skin, Br. J. Dermatol., 150, 895, 10.1111/j.1365-2133.2004.05966.x · DOI
  55. Anuradha, A., Kiran Kumar Naik, B., Vijay Srinivas, G., Devi, R.S., and Puneet, H.K. (2014). Incidence of mast cells in oral squamous cell carcinoma: A short study. J. Oncol. · DOI
  56. Rabenhorst, 2012, Mast cells play a protumorigenic role in primary cutaneous lymphoma, Blood, 120, 2042, 10.1182/blood-2012-03-415638 · DOI
  57. Ribatti, 2009, The controversial role of mast cells in tumor growth, Int. Rev. Cell Mol. Biol., 275, 89, 10.1016/S1937-6448(09)75004-X · DOI
  58. Marichal, 2013, Mast cells: Potential positive and negative roles in tumor biology, Cancer Immunol. Res., 1, 269, 10.1158/2326-6066.CIR-13-0119 · DOI
  59. Shantikumar, 2013, Immune system: A double-edged sword in cancer, Inflamm. Res., 62, 823, 10.1007/s00011-013-0645-9 · DOI · Paper page
  60. Noguchi, 2013, Antibody-based therapy in colorectal cancer, Immunotherapy, 5, 533, 10.2217/imt.13.35 · DOI
  61. Brinkmann, 1998, Role of caspases in immunotoxin-induced apoptosis of cancer cells, Biochemistry, 37, 16934, 10.1021/bi980995m · DOI
  62. Perentesis, 1997, Induction of apoptosis in multidrug-resistant and radiation-resistant acute myeloid leukemia cells by a recombinant fusion toxin directed against the human granulocyte macrophage colony-stimulating factor receptor, Clin. Cancer Res., 3, 347
  63. Turcotte, 2011, Immunotherapy for metastatic solid cancers, Adv. Surg., 45, 341, 10.1016/j.yasu.2011.04.003 · DOI · Paper page
  64. Tartour, 2011, Cancer immunotherapy: Recent breakthroughs and perspectives, Med. Sci., 27, 833
  65. Dalton, 2012, The roles of mast cells in anticancer immunity. Cancer immunology, immunotherapy, Cancer Immunol. Immunother., 61, 1511, 10.1007/s00262-012-1246-0 · DOI

Cited by

Sorted by citations

See all 17

Metadata

Authors
Wang, S., Li, L., Shi, R., Liu, X., Zhang, J., Zou, Z., Hao, Z., & Tao, A.
Affiliations
  • The Second Affiliated Hospital of Guangzhou Medical University, Guangdong Provincial Key Laboratory of Allergy &amp; Clinical Immunology, The State Key Clinical Specialty in Allergy, The State Key Laboratory of Respiratory Disease; Guangzhou 510260, China
  • The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, China
Venue
Toxins
Publisher
MDPI AG
Published
2016-03-11
Volume
8
Issue
3
Pages
71
ISSN
2072-6651
DOI
10.3390/toxins8030071
PMC
PMC4810216
Cited by
17
References
2
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • the National Natural Science Foundation of China (81373128, 81402025)
  • Guangdong provincal public welfare research and capacity building special fundation (2014A020212363)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review