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[PMID]: 29523612
[Au] Autor:Miliaras S; Ziogas IA; Mylonas KS; Papadopoulos VN
[Ad] Address:1st Department of Surgery, Papageorgiou University General Hospital, Aristotle University of Thessaloniki School of Medicine, Thessaloniki, Greece.
[Ti] Title:Primary malignant melanoma of the ascending colon.
[So] Source:BMJ Case Rep;2018, 2018 Mar 09.
[Is] ISSN:1757-790X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Malignant gastrointestinal melanoma is usually a metastatic lesion. We report the case of a 67-year-old female patient who presented with intermittent abdominal pain, fever, rigor and diarrhoea. CT scan of the abdomen revealed a large mass at the right iliac fossa with features concerning for intra-abdominal abscess. Exploratory laparotomy confirmed the preoperative diagnosis of abscess, and a right hemicolectomy was performed. Histopathological examination of the surgical specimen was indicative of malignant melanoma, and immunohistochemical examination showed positivity to S100 protein, Melan-A, HMB-45 and vimentin. A series of postoperative clinical, laboratory and imaging examinations revealed no suspicious lesions in the skin, eye, leptomeninges or other sites. Therefore, the diagnosis of primary colonic melanoma was confirmed. Only 36 additional cases of primary colonic melanoma have been reported to date. These rare neoplasms are challenging to diagnose and usually require a multidisciplinary treatment approach, including surgery, chemotherapy and possibly immunotherapy or radiotherapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process

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[PMID]: 29267503
[Au] Autor:Wang ZK; Yang L; Wu LL; Mao H; Zhou YH; Zhang PF; Dai GH
[Ad] Address:The Second Department of Medical Oncology, Chinese People's Liberation Army General Hospital, Beijing, China.
[Ti] Title:Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy.
[So] Source:Braz J Med Biol Res;51(2):e6793, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] Country of publication:Brazil
[La] Language:eng
[Ab] Abstract:Colon cancer is one of the most common digestive tumors. The present study aimed to explore the functional role, as well as the underlying mechanism of long non-coding RNA LINC00261 in colon cancer. Expression of LINC00261 was analyzed in colon cancer cell lines and human normal cell lines. Acquired resistance cell lines were then built and the acquired resistance efficiency was detected by evaluating cell viability. Thereafter, the effects of LINC00261 overexpression on cisplatin-resistant colon cancer cells were measured, as well as cell apoptosis, viability, migration, and invasion. Subsequently, we investigated the interaction of LINC00261 and ß-catenin. The results showed that the LINC00261 gene was down-regulated in colon cancer cell lines and tissues, and in cisplatin-resistant cells. LINC00261 overexpression might relieve cisplatin resistance of colon cancer cells via promoting cell apoptosis, and inhibiting cell viability, migration, and invasion. Moreover, LINC00261 might down-regulate nuclear ß-catenin through restraining ß-catenin from cytoplasm into nuclei or it could also promote ß-catenin degradation and inhibit activation of Wnt pathway. Finally, LINC00261 reduced cisplatin resistance of colon cancer in vivo and enhanced the anti-colon cancer effect of cisplatin through reducing tumor volume and weight.
[Mh] MeSH terms primary: Antineoplastic Agents/pharmacology
Cisplatin/pharmacology
Colonic Neoplasms/drug therapy
Colonic Neoplasms/genetics
Colonic Neoplasms/pathology
RNA, Long Noncoding/physiology
[Mh] MeSH terms secundary: Analysis of Variance
Apoptosis/drug effects
Apoptosis/physiology
Apoptosis Regulatory Proteins/drug effects
Apoptosis Regulatory Proteins/physiology
Blotting, Western
Cell Migration Assays
Cell Proliferation/drug effects
Cell Proliferation/physiology
Down-Regulation
Gene Expression Regulation, Neoplastic/drug effects
Gene Expression Regulation, Neoplastic/physiology
HCT116 Cells
HT29 Cells
Humans
RNA, Long Noncoding/analysis
RNA, Long Noncoding/drug effects
RNA, Long Noncoding/genetics
Reproducibility of Results
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction/drug effects
Signal Transduction/physiology
Tetrazolium Salts
Thiazoles
beta Catenin/drug effects
beta Catenin/physiology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antineoplastic Agents); 0 (Apoptosis Regulatory Proteins); 0 (RNA, Long Noncoding); 0 (Tetrazolium Salts); 0 (Thiazoles); 0 (beta Catenin); 0 (long non-coding RNA 00261, human); EUY85H477I (thiazolyl blue); Q20Q21Q62J (Cisplatin)
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:171222
[St] Status:MEDLINE

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[PMID]: 29203759
[Au] Autor:Cwiertnia G; Dyaczynski M
[Ad] Address:Oddzial Chirurgii Ogolnej, Szpital Miejski W Siemianowicach Slaskich, Siemianowice Slaskie, Polska.
[Ti] Title:[Right hemicolectomy under spinal anesthesia due to cancer of ascending large bowel - case report].
[So] Source:Wiad Lek;70(5):1013-1015, 2017.
[Is] ISSN:0043-5147
[Cp] Country of publication:Poland
[La] Language:pol
[Ab] Abstract:Surgery procedures of the abdomen cavity are commonly performed in general anaesthesia. Patients from high risk group with circulatory insufficiency, respiratory failure pose a problem. They undergo surgical procedures for life indications and emergency cases. Regional anaesthesia can be an alternative for general anaesthesia, and makes planned surgical treatment possible for this group of patients. The study presents the case of 79-year-old male with chronic obstructive pulmonary disease, after left lung upper lobectomy, arterial hypertension, who underwent operation due to ascending large bowel cancer under spinal anaesthesia as planned.
[Mh] MeSH terms primary: Anesthesia, Spinal/methods
Colectomy/methods
Colonic Neoplasms/surgery
[Mh] MeSH terms secundary: Aged
Humans
Male
Treatment Outcome
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:171206
[St] Status:MEDLINE

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[PMID]: 29203747
[Au] Autor:Mielczarek-Puta M; Chrzanowska A; Otto-Slusarczyk D; Grabon W; Baranczyk-Kuzma A
[Ad] Address:Katedra I Zaklad Biochemii, Warszawski Uniwersytet Medyczny, Warszawa, Polska.
[Ti] Title:[Effect of antioxidants on human primary and metastatic colon cancer cells at hypoxia and normoxia].
[So] Source:Wiad Lek;70(5):946-952, 2017.
[Is] ISSN:0043-5147
[Cp] Country of publication:Poland
[La] Language:pol
[Ab] Abstract:THE AIM: Evaluation of some antioxidants on human colon cancer cells viability and proliferation at various oxygen levels. MATERIAL AND METHODS: Human primary (SW480) and metastatic (SW620) colon cancer cells were cultured at hypoxia (1% oxygen), tissues (10% oxygen) and atmospheric (21% oxygen) normoxia with quercetin, epigallocatechin gallate, lipoic acid, hydroxycitric acid, their mixture, and without studied compounds (control). Antioxidants were used at physiological concentrations. The cell viability was determined by trypan blue dye exclusion and proliferation by MTT assay. RESULTS: The viability of each line ranged from 80% to 97%, and it was independent on the compound and oxygen availability. At hypoxia the cell count of both lines was lower than for the controls in the presence of each studied compound. At tissue normoxia the cell count of primary cancer cells was decreased only with epigallocatechin gallate, whereas metastatic cells were sensitive for each antioxidant. CONCLUSIONS: Our results indicated, that the studied antioxidants were not cytotoxic at physiological levels for both pirmary and metastatic colon cancer. Their cytostatic effect depend on the type of cell, oxygen availability and antioxidant concentration.
[Mh] MeSH terms primary: Antioxidants/pharmacology
Cell Hypoxia/drug effects
Colonic Neoplasms/drug therapy
[Mh] MeSH terms secundary: Catechin/analogs & derivatives
Catechin/pharmacology
Cell Line, Tumor/drug effects
Citrates/pharmacology
Colonic Neoplasms/pathology
Humans
Neoplasm Metastasis
Oxygen/pharmacology
Thioctic Acid/pharmacology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antioxidants); 0 (Citrates); 73Y7P0K73Y (Thioctic Acid); 8R1V1STN48 (Catechin); 8W94T9026R (hydroxycitric acid); BQM438CTEL (epigallocatechin gallate); S88TT14065 (Oxygen)
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:171206
[St] Status:MEDLINE

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[PMID]: 29516325
[Au] Autor:Cooper GS; Markowitz SD; Chen Z; Tuck M; Willis JE; Berger BM; Brenner DE; Li L
[Ad] Address:Division of Gastroenterology, Case Comprehensive Cancer Center, University Hospitals Cleveland Medical Center, 11100 Euclid Avenue, Wearn 244, Cleveland, OH, 44106-5066, USA. Gregory.Cooper@Uhhospitals.org.
[Ti] Title:Evaluation of Patients with an Apparent False Positive Stool DNA Test: The Role of Repeat Stool DNA Testing.
[So] Source:Dig Dis Sci;, 2018 Mar 07.
[Is] ISSN:1573-2568
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: There is uncertainty as to the appropriate follow-up of patients who test positive on multimarker stool DNA (sDNA) testing and have a colonoscopy without neoplasia. AIMS: To determine the prevalence of missed colonic or occult upper gastrointestinal neoplasia in patients with an apparent false positive sDNA. METHODS: We prospectively identified 30 patients who tested positive with a commercially available sDNA followed by colonoscopy without neoplastic lesions. Patients were invited to undergo repeat sDNA at 11-29 months after the initial test followed by repeat colonoscopy and upper endoscopy. We determined the presence of neoplastic lesions on repeat evaluation stratified by results of repeat sDNA. RESULTS: Twelve patients were restudied. Seven patients had a negative second sDNA test and a normal second colonoscopy and upper endoscopy. In contrast, 5 of 12 subjects had a persistently positive second sDNA test, and 3 had positive findings, including a 3-cm sessile transverse colon adenoma with high-grade dysplasia, a 2-cm right colon sessile serrated adenoma with dysplasia, and a nonadvanced colon adenoma (p = 0.045). These corresponded to a positive predictive value of 0.60 (95% CI 0.17-1.00) and a negative predictive value of 1.00 (95% CI 1.00-1.00) for the second sDNA test. In addition, the medical records of all 30 subjects with apparent false positive testing were reviewed and no documented cases of malignant tumors were recorded. CONCLUSIONS: Repeat positive sDNA testing may identify a subset of patients with missed or occult colorectal neoplasia after negative colonoscopy for an initially positive sDNA. High-quality colonoscopy with careful attention to the right colon in patients with positive sDNA is critically important and may avoid false negative colonoscopy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1007/s10620-018-5001-z

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[PMID]: 28453697
[Au] Autor:Dienstmann R; Mason MJ; Sinicrope FA; Phipps AI; Tejpar S; Nesbakken A; Danielsen SA; Sveen A; Buchanan DD; Clendenning M; Rosty C; Bot B; Alberts SR; Milburn Jessup J; Lothe RA; Delorenzi M; Newcomb PA; Sargent D; Guinney J
[Ad] Address:Computational Oncology, Sage Bionetworks, Seattle, USA.
[Ti] Title:Prediction of overall survival in stage II and III colon cancer beyond TNM system: a retrospective, pooled biomarker study.
[So] Source:Ann Oncol;28(5):1023-1031, 2017 05 01.
[Is] ISSN:1569-8041
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background: TNM staging alone does not accurately predict outcome in colon cancer (CC) patients who may be eligible for adjuvant chemotherapy. It is unknown to what extent the molecular markers microsatellite instability (MSI) and mutations in BRAF or KRAS improve prognostic estimation in multivariable models that include detailed clinicopathological annotation. Patients and methods: After imputation of missing at random data, a subset of patients accrued in phase 3 trials with adjuvant chemotherapy (n = 3016)-N0147 (NCT00079274) and PETACC3 (NCT00026273)-was aggregated to construct multivariable Cox models for 5-year overall survival that were subsequently validated internally in the remaining clinical trial samples (n = 1499), and also externally in different population cohorts of chemotherapy-treated (n = 949) or -untreated (n = 1080) CC patients, and an additional series without treatment annotation (n = 782). Results: TNM staging, MSI and BRAFV600E mutation status remained independent prognostic factors in multivariable models across clinical trials cohorts and observational studies. Concordance indices increased from 0.61-0.68 in the TNM alone model to 0.63-0.71 in models with added molecular markers, 0.65-0.73 with clinicopathological features and 0.66-0.74 with all covariates. In validation cohorts with complete annotation, the integrated time-dependent AUC rose from 0.64 for the TNM alone model to 0.67 for models that included clinicopathological features, with or without molecular markers. In patient cohorts that received adjuvant chemotherapy, the relative proportion of variance explained (R2) by TNM, clinicopathological features and molecular markers was on an average 65%, 25% and 10%, respectively. Conclusions: Incorporation of MSI, BRAFV600E and KRAS mutation status to overall survival models with TNM staging improves the ability to precisely prognosticate in stage II and III CC patients, but only modestly increases prediction accuracy in multivariable models that include clinicopathological features, particularly in chemotherapy-treated patients.
[Mh] MeSH terms primary: Biomarkers, Tumor/metabolism
Colonic Neoplasms/mortality
[Mh] MeSH terms secundary: Adult
Aged
Aged, 80 and over
Colonic Neoplasms/metabolism
Colonic Neoplasms/pathology
Female
Humans
Kaplan-Meier Estimate
Male
Middle Aged
Neoplasm Staging
Proportional Hazards Models
Retrospective Studies
Treatment Outcome
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Biomarkers, Tumor)
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:170429
[St] Status:MEDLINE
[do] DOI:10.1093/annonc/mdx052

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[PMID]: 27770401
[Au] Autor:Schulte ML; Hight MR; Ayers GD; Liu Q; Shyr Y; Washington MK; Manning HC
[Ad] Address:Vanderbilt Center for Molecular Probes, Vanderbilt University Medical Center, Nashville, TN, 37232, USA.
[Ti] Title:Non-Invasive Glutamine PET Reflects Pharmacological Inhibition of BRAF In Vivo.
[So] Source:Mol Imaging Biol;19(3):421-428, 2017 06.
[Is] ISSN:1860-2002
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: This study aimed to study whether cancer cells possess distinguishing metabolic features compared with surrounding normal cells, such as increased glutamine uptake. Given this, quantitative measures of glutamine uptake may reflect critical processes in oncology. Approximately, 10 % of patients with colorectal cancer (CRC) express BRAF , which may be actionable with selective BRAF inhibitors or in combination with inhibitors of complementary signaling axes. Non-invasive and quantitative predictive measures of response to these targeted therapies remain poorly developed in this setting. The primary objective of this study was to explore 4-[ F]fluoroglutamine (4-[ F]F-GLN) positron emission tomography (PET) to predict response to BRAF -targeted therapy in preclinical models of colon cancer. PROCEDURES: Tumor microarrays from patients with primary human colon cancers (n = 115) and CRC liver metastases (n = 111) were used to evaluate the prevalence of ASCT2, the primary glutamine transporter in oncology, by immunohistochemistry. Subsequently, 4-[ F]F-GLN PET was evaluated in mouse models of human BRAF -expressing and BRAF wild-type CRC. RESULTS: Approximately 70 % of primary colon cancers and 53 % of metastases exhibited positive ASCT2 immunoreactivity, suggesting that [ F]4-F-GLN PET could be applicable to a majority of patients with colon cancer. ASCT2 expression was not associated selectively with the expression of mutant BRAF. Decreased 4-[ F]F-GLN predicted pharmacological response to single-agent BRAF and combination BRAF and PI3K/mTOR inhibition in BRAF -mutant Colo-205 tumors. In contrast, a similar decrease was not observed in BRAF wild-type HCT-116 tumors, a setting where BRAF -targeted therapies are ineffective. CONCLUSIONS: 4-[ F]F-GLN PET selectively reflected pharmacodynamic response to BRAF inhibition when compared with 2-deoxy-2[ F]fluoro-D-glucose PET, which was decreased non-specifically for all treated cohorts, regardless of downstream pathway inhibition. These findings illustrate the utility of non-invasive PET imaging measures of glutamine uptake to selectively predict response to BRAF-targeted therapy in colon cancer and may suggest further opportunities to inform colon cancer clinical trials using targeted therapies against MAPK activation.
[Mh] MeSH terms primary: Glutamine/chemistry
Mutation/genetics
Positron-Emission Tomography
Proto-Oncogene Proteins B-raf/antagonists & inhibitors
Proto-Oncogene Proteins B-raf/genetics
[Mh] MeSH terms secundary: Amino Acid Transport System ASC/metabolism
Animals
Cell Line, Tumor
Colonic Neoplasms/drug therapy
Colonic Neoplasms/metabolism
Colonic Neoplasms/pathology
Female
Humans
Liver Neoplasms/secondary
Mice, Nude
Minor Histocompatibility Antigens/metabolism
Protein Kinase Inhibitors/pharmacology
Protein Kinase Inhibitors/therapeutic use
Xenograft Model Antitumor Assays
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Amino Acid Transport System ASC); 0 (Minor Histocompatibility Antigens); 0 (Protein Kinase Inhibitors); 0 (SLC1A5 protein, human); 0RH81L854J (Glutamine); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:161023
[St] Status:MEDLINE
[do] DOI:10.1007/s11307-016-1008-z

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[PMID]: 29173578
[Au] Autor:Jones LA; Ferrans CE; Polite BN; Brewer KC; Maker AV; Pauls HA; Rauscher GH
[Ad] Address:Division of Epidemiology and Biostatistics, School of Public Health, University of Illinois, Chicago.
[Ti] Title:Examining racial disparities in colon cancer clinical delay in the Colon Cancer Patterns of Care in Chicago study.
[So] Source:Ann Epidemiol;27(11):731-738.e1, 2017 Nov.
[Is] ISSN:1873-2585
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: We explored a potential racial disparity in clinical delay among non-Hispanic (nH) Black and White colon cancer patients and examined factors that might account for the observed disparity. METHODS: Patients aged 30-79 years with a newly diagnosed colon cancer from 2010 to 2014 (n = 386) were recruited from a diverse sample of nine public, private, and academic hospitals in and around Chicago. Prolonged clinical delay was defined as 60 days or more or 90 days or more between medical presentation (symptoms or a screen-detected lesion) and treatment initiation (surgery or chemotherapy). Multivariable logistic regression with model-based standardization was used to estimate the disparity as a difference in prevalence of prolonged delay by race. RESULTS: Prevalence of delay in excess of 60 days was 12 percentage points (95% confidence interval: 2%, 22%) higher among nH Blacks versus Whites after adjusting for age, facility, and county of residence. Travel burden (time and distance traveled from residence to facility) explained roughly one-third of the disparity (33%, P = .05), individual and area-level socioeconomic status measures explained roughly one-half (51%, P = .21), and socioeconomic measures together with travel burden explained roughly four-fifths (79%, P = .08). CONCLUSIONS: Low socioeconomic status and increased travel burden are barriers to care disproportionately experienced by nH Black colon cancer patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Process

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[PMID]: 29489644
[Au] Autor:Attademo L; De Falco S; Rosanova M; Esposito M; Mazio F; Foschini F; Santaniello A; Fiore G; Matano E; Manganelli F; Carlomagno C
[Ad] Address:Department of Clinical Medicine and Surgery.
[Ti] Title:A case report of limbic encephalitis in a metastatic colon cancer patient during first-line bevacizumab-combined chemotherapy.
[So] Source:Medicine (Baltimore);97(9):e0011, 2018 Mar.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: Paraneoplastic limbic encephalitis (PLE) is one of the most common causes of neurologic paraneoplastic syndromes, with unclear pathogenesis. While several reports published in the last decades showed the occurrence of PLE in a variety of cancers, only a few cases have been associated with colon cancer. PATIENT CONCERNS: In February 2017, a 54-year-old man with clinical history of radically resected colon cancer started first line chemotherapy with FOLFOXIRI plus bevacizumab, after radiological diagnosis of multiple liver and bone metastases. During the third cycle of treatment, the patient developed psychomotor agitation and hallucinations followed by severe consciousness level reduction and cognitive impairment. DIAGNOSES: Magnetic resonance imaging showed hyperintense signals in both hippocampal areas, insula and right cingulate gyrus on fluid attenuated inversion recovery, diffusion weighted imaging, and T2-weighted images, highly suggestive of limbic encephalitis. Other causes (brain metastases, toxicity of chemotherapeutic agents, and infections) were excluded. INTERVENTIONS: Empirical immunosuppressive treatment (high-dose immunoglobulins and corticosteroids) was administered and chemotherapy was resumed. OUTCOMES: A slowly progressive improvement in neurological condition has been observed, even though radiological signs of limbic encephalitis are still evident. LESSONS: The present case highlights the complex diagnostic process of PLE, and the lack of a standard treatment. Moreover, the absence of correlation between PLE and tumor progression or tumor burden, and the opportunity of treating underlying neoplasm is discussed.
[Mh] MeSH terms primary: Antineoplastic Agents, Immunological/therapeutic use
Antineoplastic Combined Chemotherapy Protocols/therapeutic use
Bevacizumab/therapeutic use
Colonic Neoplasms/drug therapy
Colonic Neoplasms/pathology
Limbic Encephalitis/diagnosis
[Mh] MeSH terms secundary: Bone Neoplasms/drug therapy
Bone Neoplasms/secondary
Colonic Neoplasms/complications
Electroencephalography
Humans
Limbic Encephalitis/complications
Liver Neoplasms/drug therapy
Liver Neoplasms/secondary
Magnetic Resonance Imaging
Male
Middle Aged
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (Antineoplastic Agents, Immunological); 2S9ZZM9Q9V (Bevacizumab)
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180301
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000010011

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[PMID]: 28460478
[Au] Autor:Vo MC; Nguyen-Pham TN; Lee HJ; Jaya Lakshmi T; Yang S; Jung SH; Kim HJ; Lee JJ
[Ad] Address:Research Center for Cancer Immunotherapy, Chonnam National University Hwasun Hospital, Hwasun, Jeollanamdo, Republic of Korea.
[Ti] Title:Combination therapy with dendritic cells and lenalidomide is an effective approach to enhance antitumor immunity in a mouse colon cancer model.
[So] Source:Oncotarget;8(16):27252-27262, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In this study, we investigated efficacy of lenalidomide in combination with tumor antigen-loaded dendritic cells (DCs) in murine colon cancer model. MC-38 cell lines were injected subcutaneously to establish colon cancer-bearing mice. After tumor growth, lenalidomide (50 mg/kg/day) was injected intraperitoneally on 3 consecutive days in combination with tumor antigen-loaded DC vaccination on days 8, 12, 16, and 20. The tumor antigen-loaded DCs plus lenalidomide combination treatment exhibited a significant inhibition of tumor growth compared with the other groups. These effects were associated with a reduction in immune suppressor cells, such as myeloid-derived suppressor cells and regulatory T cells, with the induction of immune effector cells, such as natural killer cells, CD4+ T cells and CD8+ T cells in spleen, and with the activation of cytotoxic T lymphocytes and NK cells. This study suggests that a combination of tumor antigen-loaded DC vaccination and lenalidomide synergistically enhanced antitumor immune response in the murine colon cancer model, by inhibiting the generation of immune suppressive cells and recovery of effector cells, and demonstrated superior polarization of Th1/Th2 balance in favor of Th1 immune response. This combination approach with DCs and lenalidomide may provide a new therapeutic option to improve the treatment of colon cancer.
[Mh] MeSH terms primary: Colonic Neoplasms/immunology
Colonic Neoplasms/pathology
Dendritic Cells/immunology
Immunity
Thalidomide/analogs & derivatives
[Mh] MeSH terms secundary: Animals
Antigens, Neoplasm/immunology
Cancer Vaccines/administration & dosage
Cancer Vaccines/immunology
Cell Line, Tumor
Cell Survival/drug effects
Colonic Neoplasms/genetics
Colonic Neoplasms/therapy
Combined Modality Therapy
Cytokines/biosynthesis
Dendritic Cells/metabolism
Disease Models, Animal
Female
Gene Expression
Immunity/drug effects
Immunotherapy
Killer Cells, Natural/immunology
Killer Cells, Natural/metabolism
Mice
T-Lymphocytes, Cytotoxic/drug effects
T-Lymphocytes, Cytotoxic/immunology
T-Lymphocytes, Cytotoxic/metabolism
T-Lymphocytes, Regulatory/drug effects
T-Lymphocytes, Regulatory/immunology
T-Lymphocytes, Regulatory/metabolism
Thalidomide/pharmacology
Vaccination
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antigens, Neoplasm); 0 (Cancer Vaccines); 0 (Cytokines); 4Z8R6ORS6L (Thalidomide); F0P408N6V4 (lenalidomide)
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:IM
[Da] Date of entry for processing:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15917


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