Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Immunotherapy After Surgery in Treating Patients With Breast Cancer, Colon Cancer, or Melanoma

ABSTRACT: RATIONALE: Immunotherapy uses different ways to stimulate the immune system and stop cancer cells from growing. Immunotherapy biological extracts may be useful as adjuvant therapy in treating patients who have had surgery for breast cancer, colon cancer, or melanoma. PURPOSE: Phase III trial to study the effectiveness of Corynebacterium granulosum extract as maintenance immunotherapy following surgery in treating patients with breast cancer, colon cancer, or melanoma.

DISEASE(S): Melanoma,Colorectal Cancer,Melanoma (skin),Breast Neoplasms,Breast Cancer,Colonic Neoplasms

PROVIDER: 2002148 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

ACCESS DATA

Json Xml

Similar Datasets

Comparative genomic hybridization of cell lines from 9 different cancer tissue of origin types (Breast, Central Nervous System, Colon, Leukemia, Melanoma, Non-Small Cell Lung, Ovarian, Prostate, Renal) from NCI-60 panel

Project description:Array comparative genomic hybridization characterization and comparison of cell lines from 9 different cancer tissue of origin types (Breast, Central Nervous System, Colon, Leukemia, Melanoma, Non-Small Cell Lung, Ovarian, Prostate, Renal) from NCI-60 panel.

2005-11-23 | E-TABM-65 | biostudies-arrayexpress

Modulation of gene expression induced by supercritical fluid rosemary extract in colon cancer cells

Project description:Supercritical rosemary extract (containing 16.90% carnosic acid, 1.90% carnosol and 13.59% volatile compounds) showed antitumor activity on colon cancer cells in vitro. We treated colon cancer cells with the extract and we employed whole genome microarray expression profiling to identify genes potentially involved in its antitumor mechanism of action. We analyzed gene expression of colon cancer SW620 cells after treating during 48h with supercritical rosemary extract at concentrations that cause 50% inhibition of cell viability (30 M-NM-<g/mL), citostatic effect (60 M-NM-<g/mL) and 50% cell death (100 M-NM-<g/mL), in comparison to control cells (0 M-NM-<g/mL). Two independent experiments were performed in triplicate. Each sample is the pool of the triplicates of one of the experiments (a or b) at the indicated concentration.

2014-04-04 | E-GEOD-56496 | biostudies-arrayexpress

Mitochondrial calcium uniporter controls melanoma aggressive behavior through a redox-controlled phenotype switch

Project description:Melanoma is the deadliest of skin cancers and has a high tendency to metastasize to distant organs. Calcium and metabolic signals contribute to melanoma invasiveness; however, the underlying molecular details are elusive. The mitochondrial calcium uniporter (MCU) complex is a major route for calcium into the mitochondrial matrix but if and how MCU affects melanoma pathobiology is not understood. Here, we show that MCUA expression correlates with melanoma patient survival, similarly as in kidney, cervical and other cancers, while in pancreatic, breast and liver cancer, this correlation is inverse. Knockdown (KD) of MCUA suppressed melanoma cell growth but promoted migration and invasion in 2D and 3D cultures. In melanoma xenografts, MCUA_KD reduced tumor volumes but promoted lung metastases. Proteomic analyses and protein microarrays identified pathways that link MCUA abundance and melanoma cell phenotype and suggested a major role for metabolic and redox regulation. Accordingly, antioxidants enhanced melanoma cell migration, while pro-oxidants diminished the MCUA_KD-induced invasive phenotype. Furthermore, MCUA_KD amplified the resistance of melanoma cells to immunotherapies and ferroptosis. Col¬lectively, we demonstrate that MCUA controls melanoma aggressive behavior and therapeutic sen¬sitivity. Manipulations of mitochondrial calcium and redox homeostasis, in combination with cur¬rent therapies, should be considered in treating advanced melanoma.

2022-10-30 | PXD029132 | Pride

Proteomic profiling of exosomes isolated from invasive and proliferative melanoma cell lines and correlation with exosomes from plasma of human melanoma patients pre- and post-checkpoint inhibitor treatment

Project description:Over the last decades, exosomes have received increasing attention due to their involvement in numerous pathologies including cancer. Tumor-derived exosomes and exosomes derived from the tumor microenvironment are implicated in multiple mechanisms that support disease progression such as the escape of malignant cells from immunosurveillance, tumor cell growth, tumor angiogenesis, preparation of a pre-metastatic niche and remodeling of the extracellular matrix, thereby promoting dissemination and metastasis. Here, we performed protein expression phenotyping of exosomes derived from different invasive and proliferative melanoma cell lines (n=8) to provide a solid framework of gene expression programs, which - in a clinical setting - would be useful for prognosis and may also predict treatment response. Cell line characteristics have been published previously (Wenzina et al.,2020). Having identified a set of differentially expressed proteins in proliferative and invasive melanoma cell lines, we correlated them to the protein composition of plasma exosomes from melanoma patients pre and post immunotherapy treatment (n=7) as well as healthy controls (n=5).

2022-07-14 | PXD025475 | Pride

Proteomics of melanoma response to immunotherapy reveals dependence on mitochondrial function

Project description:Immunotherapy has revolutionized cancer treatment, yet most patients do not respond. Here, we investigated mechanisms of response by deeply profiling the proteome of clinical samples from advanced stage melanoma patients undergoing either tumor infiltrating lymphocytes (TIL)-based or anti-PD1 immunotherapy. Using high-resolution mass spectrometry, we quantified over 10,300 proteins with high accuracy. Statistical analyses revealed higher oxidative phosphorylation and lipid metabolism in responders in both treatments, and identified proteomic signatures for response. Aiming to elucidate the effects of the metabolic state on the immune response, we examined melanoma cells upon metabolic perturbations or Crisp-Cas9 knockouts. These experiments indicated lipid metabolism as a regulatory mechanism that increases melanoma immunogenicity by elevating antigen presentation, thereby affecting the sensitivity to T-cell mediated killing both in-vitro and in-vivo. Altogether, our proteomic analyses revealed novel association between the melanoma metabolic state and the response to immunotherapy, which can be the basis for future improvement of therapeutic response.

2019-07-29 | PXD006003 | Pride

Oxidized methionine melanoma epitopes

Project description:One of the most promising alternatives to chemotherapy in cancer treatment is immunotherapy, particularly, peptide-based immunotherapy in which synthetic peptides derived from tumor-specific antigens are used to trigger an immune response to specifically target cancer cells. Here using custom nanoLC-MS/MS based workflows we examine the possible presentation of peptide-based oxidative variants in complex with Major Histocompatibility Complex (MHC) class I proteins at the surface of melanoma cells. The deposited data contains the raw files associated with mild acidic elutions (MAE) of MHC class I associated peptides from various melanoma cell lines. These were analysed using Data Independent Acquisition (DIA), employing a custom method for MS/MS fragmentation of the native and Met-oxidative modifications of a tyrosinase derived peptide (YMDGTMSQV denoted as YMD peptide). The data contains also the raw files referring to the nanoLC-MS/MS analysis of HPLC purified fractions of various oxidative derivatives of the YMD peptide but also of MAGE-10 native and oxidized forms.

2023-07-25 | PXD039318 | Pride

Gene Expression patterns in mouse B16-OVA melanoma tumors

Project description:This laboratory focuses on selectin mediated recruitment during adoptive immunotherapy for metastatic cancer. This study seeks to determine changes in the expression levels of Fucosyltransferases, Selectins, and cytokines in normal and inflamed mouse skin, melanoma tumor tissue of different sizes, and tumor cells grown in culture. Since the ability to treat the tumor effectively is directly related to the size of the tumor, differences in glyco-expression patterns may be of interest. In this study, five groups were hybridized and analyzed using the GLYCOv2 array. Each group was analyzed in triplicate. The groups were: Normal mouse skin, normal mouse skin inflamed by treatment with Oxazolone, B16-OVA melanoma tissue from 6 day tumors, B16-OVA melanoma tissue from 11 day tumors, and B16-OVA grown in cell culture.

2011-02-17 | E-GEOD-27355 | biostudies-arrayexpress

Engineered Antibody Cytokine Chimera Synergizes with DNA-Launched Nanoparticle Vaccines to Potentiate Suppression of Melanoma Proliferation in vivo

Project description:Cancer immunotherapy has demonstrated great promise with the checkpoint inhibitors being approved as the first-line therapy for some types of cancer, and engineered cytokines like Neo2/15 being evaluated in many studies. In this work, we designed Antibody Cytokine Chimera (ACC) scaffolding cytokine mimetics with full-length tumor-specific antibody. We characterized the pharmacokinetic (PK) and pharmacodynamic (PD) properties of first-generation ACC TA99-Neo2/15, which synergized with DLnano-vaccines in suppressing in vivo melanoma proliferation but caused significant systemic cytokine activation. A novel second-generation ACC TA99-HL2-KOA1, with retained IL-2Rβ/γ binding and attenuated but preserved IL-2Rα, caused significantly lower systemic cytokine activation and non-inferior protection in murine tumor studies. Transcriptomic experiment demonstrated up-regulation of Type I interferon responsive genes, particularly ISG15, in dendritic cells, macrophages and monocytes following TA99-HL2-KOA1 treatment. Characterization of additional ACCs in combination with cancer vaccines will likely be an important area of research for treating melanoma and other types of cancer.

2023-03-15 | GSE159553 | GEO

Progressing vs regressing melanoma metastases

Project description:We documented the transcriptional pattern of 3 progressing and 2 regressing synchronous melanoma metastases from the same patient following M-VAX treatment. Two-condition experiment, Progressing vs regressing metastases. 3 progressing and 2 regressing metastases extracted from the same patient after M-VAX immunotherapy. One replicate per array.

2010-09-11 | E-GEOD-24067 | biostudies-arrayexpress

RNF31 inhibition sensitizes tumors to bystander killing by innate and adaptive immune cells

Project description:Tumor escape mechanisms for immunotherapy include deficiencies in antigen presentation, diminishing adaptive CD8+ T cell antitumor activity. Although innate NK cells are triggered by loss of MHC class I, their response is often inadequate. To increase tumor susceptibility to both innate and adaptive immune elimination, we performed parallel genome-wide CRISPR-Cas9 screens. This identified all components, RNF31, RBCK1, and SHARPIN, of the linear ubiquitination chain assembly complex (LUBAC). Genetic and pharmacologic ablation of RNF31, an E3 ubiquitin ligase, strongly sensitized melanoma, breast and colorectal cancer cells to both NK and CD8+ T cell killing. This occurred in a TNF-dependent manner, causing loss of A20 and non-canonical IKK complexes from TNF Receptor Complex I. Corroborating this preclinically, a small molecule RNF31 inhibitor sensitized human colon carcinoma organoids to TNF and greatly enhanced immune bystander killing of antigen-loss and antigen presentation machinery-deficient tumor cells. These results merit exploration of RNF31 inhibition as a clinical pharmacological opportunity for immunotherapy-refractory cancers.

2022-05-30 | PXD029489 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data