> Disorders > Neoplastic Process > Splenic Neoplasms

Splenic Neoplasms

Splenic Neoplasms are a diverse group of tumors that originate within the spleen.
These include benign and malignant growths, such as hemangiomas, lymphomas, and sarcomas.
Accurate identification and characterization of Splenic Neoplasms is crucial for effective treatment planning and patient outcomes.
PubCompare.ai's AI-driven protocol optimization can help improve research accuracy by effortlessly locating the best protocols from literature, preprints, and patents using intelligent comparisons.
This streamlines the research process and supports informed decision-making with PubCompare.ai's powerfull AI-fueled capabilities.

Most cited protocols related to «Splenic Neoplasms»

Evaluating MDSC Suppression of T Cell Responses

Cited 15 times

MDSC and their subsets were isolated from spleens of tumor-bearing or control mice using cell sorting on FACSAria cell sorter (Becton Dickinson). The purity of cell populations was >99%. As responder cells we used total spleen cells from OT-1 mice. CD8⁺ T cells from these mice have a TCR that recognize OVA-derived peptide SIINFEKL. The number of IFN-γ producing cells in response to stimulation to the specific or control peptides (10 μg/ml) was evaluated in an ELISPOT assay and performed as described earlier (28 (link)). The numbers of spots were counted in triplicates and calculated using an automatic ELISPOT counter (Cellular Technology, Ltd). Cell proliferation induced by antigen specific or CD3 (0.5 μg/ml)/CD28 (5 μg/ml) stimulation was evaluated using ³H-thymidine incorporation as described previously (29 (link)). For experiments which examined the effect of NO, arginase, or ROS inhibitor, L-NMMA (0.5 mM; Calbiochem, San Diego, CA), nor-NOHA (0.5 mM; Calbiochem, San Diego, CA), or catalase (1000 U/mL; Sigma-Aldrich) were added at the beginning of the culture.

Youn J.I., Nagaraj S., Collazo M, & Gabrilovich D.I. (2008). Subsets of Myeloid-Derived Suppressor Cells in Tumor Bearing Mice. Journal of immunology (Baltimore, Md. : 1950), 181(8), 5791-5802.

Publication 2008

Antigens Arginase Biological Assay Catalase CD8-Positive T-Lymphocytes Cell Proliferation Cells Enzyme-Linked Immunospot Assay Exanthema Interferon Type II Mus Myeloid-Derived Suppressor Cells omega-N-Methylarginine Peptides Population Group Spleen Splenic Neoplasms Thymidine

Generation and Characterization of Regulatory B Cells

Cited 8 times

Murine splenic B cells were isolated by negative selection using the RoboSep magnetic purification system (StemCell Technologies, Vancouver, Canada). For tBreg generation, B cells were incubated with 50% cancer CM for two days in cRPMI. Control B cells were treated with PBS, or 100 ng/ml BAFF, or 5 μg/ml LPS. Cancer CM was collected from confluent cancer cells, and for some experiments, to generate serum-free CM, cRMPI was replaced and the cells cultured for 72 hours in serum-free media (Life Sciences). Mouse CD3⁺ T cells were isolated from naïve mouse spleen using T cell enrichment columns (R&D Systems, Minneapolis, MN). To generate non-Tregs (purity >99.5 %), CD4⁺ T cells were isolated by mouse T cell CD4 Subset Column Kit and separated from CD25⁺ cells using CD25 Microbead kit (Miltenyi Biotec, Auburn, CA). The CD25⁺CD4⁺ cells were used as Tregs. To test the suppressive effects of B cells, B cells were cultured together with carboxyfluorescein succinimidyl ester (CFSE, Invitrogen, Carlsbad, CA) -labeled non-Tregs or Tregs (1×10⁵) in the presence of anti-CD3/CD28-coupled beads and IL-2 (500 U/ml) for 5 days. Decrease in CFSE expression of T cells correlates with the proportion of cells that underwent divisions. B cells were also isolated from spleens of tumor-bearing mice using anti-CD19 Ab beads after three rounds of depletion of MSCs using anti-Gr1 Ab beads (Miltenyi Biotec).
To generate Tregs, tBregs were incubated with non-Treg cells (CD25⁻CD4⁺ from BALB/C mice or GFP⁻CD4⁺ cells from FoxP3-GFP mice, purity >99.5%) at a 1:1 ratio and cultured for 5 days in the presence of bead-conjugated anti-CD3/CD28 Abs and 500 U/ml IL-2 in the absence or presence of DMSO or SB431542 (Tocris bioscience, Ellisville, MO). To test their activity, Tregs were re-isolated by two rounds of B cell depletion with FITC-CD19 and PE-B220 Abs (BD Pharmingen) and anti-FITC and anti-PE beads (Miltenyi Biotec) and mixed with naïve CFSE-labeled CD8⁺ T cells in the presence of bead-conjugated anti-CD3/CD28 Abs and 500 U/ml IL-2 for 5 days. TGFβ1 secretion was quantified by ELISA following manufacturer’s protocol (R&D systems, Inc., Minneapolis, MN).

Olkhanud P.B., Damdinsuren B., Bodogai M., Gress R.E., Sen R., Wejksza K., Malchinkhuu E., Wersto R.P, & Biragyn A. (2011). Tumor-evoked regulatory B cells promote breast cancer metastasis by converting resting CD4+ T cells to T regulatory cells. Cancer research, 71(10), 3505-3515.

Publication 2011

4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide 5-(6)-carboxyfluorescein diacetate succinimidyl ester B-Lymphocytes carboxyfluorescein CD4 Positive T Lymphocytes CD8-Positive T-Lymphocytes Cells Culture Media, Serum-Free Enzyme-Linked Immunosorbent Assay Esters Fluorescein-5-isothiocyanate IL2RA protein, human Malignant Neoplasms Mice, Inbred BALB C Microspheres Muromonab-CD3 Mus Regulatory T-Lymphocytes secretion Serum Spleen Splenic Neoplasms Stem Cells Sulfoxide, Dimethyl T-Lymphocyte TGF-beta1 TNFSF13B protein, human

Modulating Tumor Immunity by Cell Depletion and Adoptive Transfer

Cited 5 times

B16F10, B16-SIY, LLC1, LLC1-OVA, MC38 or EG7 cells (1 × 10⁶) in suspension were injected s.c. For MDSC depletion, 3 d after tumor cell injection mice were injected i.p. by 5-FU (50 mg/kg) or anti-Gr1 antibodies (RB6-8C5, 200 µg) once every 4 d. Depletion of CD4⁺ T cells, CD8⁺ T cells or NK cells was achieved by twice a week i.p. injection of depleting mAb clone GK1.5 (anti-CD4, 200 µg), clone 53.6.7 (anti-CD8α, 200 µg) or clone PK136 (anti-NK1.1, 200 µg) starting one day prior to tumor challenge. Flow cytometry confirmed depletion efficiency of target cells for 3 d following injections. For adoptive transfer of MDSCs, splenic Gr1⁺CD11b⁺ MDSCs from tumor-bearing WT or miR-155^−/− mice were injected i.v. at 5 × 10⁶ per mouse into LLC1-bearing mice at d7 and d14. For adoptive transfer of Tregs (33 (link)), splenic CD4⁺CD25⁺ Treg cells were selected with a CD4⁺CD25⁺ regulatory T cell isolation kit (Miltenyi Biotec) from WT or miR-155^−/− mice, and i.v. injected at 2 × 10⁶ per mouse into LLC1-bearing mice on d7, d14 and d20. The size of tumor was determined at 2–3-day intervals. Tumor volumes were measured along 3 orthogonal axes (a, b, and c) and calculated as abc/2.

Chen S., Wang L., Fan J., Ye C., Dominguez D., Zhang Y., Curiel T.J., Fang D., Kuzel T.M, & Zhang B. (2014). Host miR-155 promotes tumor growth through a myeloid-derived suppressor cell-dependent mechanism. Cancer research, 75(3), 519-531.

Publication 2014

Adoptive Transfer Anti-Antibodies CD4 Positive T Lymphocytes CD8-Positive T-Lymphocytes Cells Clone Cells Epistropheus Flow Cytometry IL2RA protein, human isolation ITGAM protein, human monoclonal antibody GK1.5 Mus Myeloid-Derived Suppressor Cells Natural Killer Cells Neoplasms Regulatory T-Lymphocytes Somatostatin-Secreting Cells Spleen Splenic Neoplasms

Immune Checkpoint Modulation in Tumor Microenvironment

Cited 5 times

Fig. S1 shows the Tim-3 and PD-1 expression on CD8 and CD4 cells in the spleen of tumor-bearing mice. Fig. S2 shows the expression of PD-L1, Tim-3, and Galectin-9 on CT26 tumor cells. Fig. S3 shows the effects of anti–PD-L1 antibody on the growth of CT26 tumor in vitro. Fig. S4 shows the effect of in vivo targeting of the Tim-3 and PD-1 signaling pathways in tumor-bearing mice on peripheral T cell responses. Online supplemental material is available at http://www.jem.org/cgi/content/full/jem.20100637/DC1.

Sakuishi K., Apetoh L., Sullivan J.M., Blazar B.R., Kuchroo V.K, & Anderson A.C. (2010). Targeting Tim-3 and PD-1 pathways to reverse T cell exhaustion and restore anti-tumor immunity. The Journal of Experimental Medicine, 207(10), 2187-2194.

Publication 2010

Antibodies, Anti-Idiotypic CD4 Positive T Lymphocytes CD274 protein, human Cells HAVCR2 protein, human LGALS9 protein, human Mus Neoplasms Signal Transduction Pathways Splenic Neoplasms T-Lymphocyte

Identifying molecular features of cancer-associated MDSCs

Cited 4 times

The aim of this study is to define the molecular features of cancer-associated MDSCs using unbiased single-cell transcriptomics. To this end, we analzyed the most commonly used mouse model for breast cancer (i.e., MMTV-PyMT), which was previously shown to lead to MDSC generation in tumor-bearing animals. We first characterized various tissues for the presence of MDSCs by isolating CD11b+/Gr1+ cells and subjecting them to T cell suppression assays in vivo, which showed robust presence of MDSC capacity in the spleen of tumor-bearing mice. We performed single-cell transcriptomics on in total 14,646 FACS-isolated CD11b+/Gr1+ cells harvested from spleens of three tumor-bearing and three control mice. We then performed computational analyses for cell type clustering to identify cells of neutrophilic and monocytic origin, and focused our analyses on those clusters that were predominantly present in tumor-bearing mice. We performed orthogonal validation of MDSC-related expression changes using qPCR in additional tumor-bearing and control mice. Subset analysis for cell surface markers allowed us to identify MDSC-specific cell surface molecules (CD84, Jaml), which were validated and integrated with known cell surface markers for granulocytic (Ly6g or CD15) and monocytic (Ly6c or CD14) cells by flow cytometry in samples from control and tumor-bearing mice, as well as in primary in vitro generated MDSCs from mouse bone marrow or human peripheral blood samples. Because of the retrospective and observational nature, no prior sample size calculation was performed.

Alshetaiwi H., Pervolarakis N., McIntyre L.L., Ma D., Nguyen Q., Rath J.A., Nee K., Hernandez G., Evans K., Torosian L., Silva A., Walsh C, & Kessenbrock K. (2020). Defining the emergence of myeloid-derived suppressor cells in breast cancer using single-cell transcriptomics. Science immunology, 5(44), eaay6017.

Publication 2020

Animals Biological Assay BLOOD Bone Marrow Breast Carcinoma Cells Flow Cytometry Gene Expression Profiling Granulocyte Homo sapiens ITGAM protein, human Malignant Neoplasms Mouse mammary tumor virus Mus Myeloid-Derived Suppressor Cells Neoplasms Neutrophil Reproduction Splenic Neoplasms T-Lymphocyte Tissues

Most recents protocols related to «Splenic Neoplasms»

Tumor and Spleen Cell Isolation Protocol

Pieces of tumors were collected and digested overnight in digestion buffer (2.1 mg/mL collagenase type I (Worthington), 75 µg/mL DNAase I (Worthington), 5 mM CaCl₂ and 1% P/S in RPMI). The following day, samples were incubated for 15 min at 37°C and filtered through a 70 µm nylon cell strainer and erythrocytes lysed using the red blood cells (RBC) lysing buffer (Sigma) for 1–2 min. Splenocytes (isolated from spleens of female mice) were instead generated by forcing freshly isolated spleens through 70 µm cell strainers and erythrocytes lysed using RBC lysing buffer for 1 min. Following centrifugation, cells (tumor/splenocytes) were washed and eventually resuspended in PBS. Single-cell suspensions from tumors/spleens were stained for 30 min (4°C in the dark) for relevant cell-surface markers in Fluorescence-activated cell sorter (FACS) staining buffer (PBS with 7% FBS). Next, cells were washed, resuspended in PBS and stored at 4°C until flow cytometric analyses were performed on the same day. All samples were acquired on Cytek Aurora equipped with four lasers (Cytek Biosciences) or by FACSCanto II cell Analyzer BD and analyzed with FlowJo V.10.6.1 or V.10.8 software. Viable cells were determined as a fraction of single cells negative for staining with Zombie Aqua Fixable Viability Dye. The immune cell populations were analyzed in three different panels: Panel 1 (general panel), Panel 2 (myeloid panel) and Panel 3 (lymphoid panel), which are described in online supplemental materials and methods. All cells were gated on singlets, living cells and the corresponding gating strategy for each cell population.

Frias A., Di Leo L., Antoranz A., Nazerai L., Carretta M., Bodemeyer V., Pagliuca C., Dahl C., Claps G., Mandelli G.E., Andhari M.D., Pacheco M.P., Sauter T., Robert C., Guldberg P., Madsen D.H., Cecconi F., Bosisio F.M, & De Zio D. (2023). Ambra1 modulates the tumor immune microenvironment and response to PD-1 blockade in melanoma. Journal for Immunotherapy of Cancer, 11(3), e006389.

Publication 2023

Buffers Centrifugation Collagenase Deoxyribonucleases Digestion Erythrocytes Females Flow Cytometry Fluorescence Lymph Mus Neoplasms Nylons Splenic Neoplasms

RNA-Seq of Splenic Tumor Cells and Cell Lines

Protocol full text hidden due to copyright restrictions

Open the protocol to access the free full text link

Publication 2023

Cell Lines Cells DNA, Complementary DNA Library Genome Homo sapiens Mus olaparib Oligonucleotide Primers Oligonucleotides Poly T RNA, Messenger RNA, Neoplasm RNA-Seq Splenic Neoplasms THP-1 Cells

Modulation of CD8+ T Cells and NK Cells by Myeloid Erythroid Progenitors in Pancreatic Cancer

CD8 + T cells and NK cells were isolated from the spleens of Panc02 tumor-bearing mice using negative selection MojoSort™ Mouse CD8 + T Cell Isolation Kit (BioLegend, Sand Diego, CA), and positive selection NKp46-biotin antibodies (BioLegend), respectively. For immune cell activation, 50,000 CD8 + T cells or NK cells were cultured in full DMEM medium for 96 h at 37 °C in the presence or absence of 25,000 MEPs (ratio of 2:1), or in the presence of 50 μL MEP CM (reaching 1:1 volume ratio). Subsequently, cells were centrifuged at 470 × g for 5 min at room temperature. Cell pellets were re-suspended in recommended medium (2% fetal calf serum, 0.1 mM EDTA in PBS), and the levels of total CD8 + T cells, NK cells and activated cells (CD8 + CD25 + or NKp46 + CD107 + ) were quantified by flow cytometry. In parallel, the cells, as above, were permeabilized, fixed and evaluated for granzyme B expression by flow cytometry using FITC anti-human/mouse granzyme B recombinant antibody (BioLegend), in accordance with the manufacturer’s instructions.
For the Panc02 tumor killing assay, CD8 + T cells and NK cells (5 × 10⁵/ml) were co-cultured with Panc02 cells (4 × 10⁴/ml) in full DMEM medium for 24 h at 37 °C in the presence or absence of MEPs (25 × 10⁴/ml) or MEP CM (1:1 ratio with full medium). Propidium iodide (PI, 500 nM) was added to cultures in order to identify dead cells. T-cell killing effect was monitored using Incucyte Zoom HD/2CLR system (Essen BioScience, Ann Arbor, MI) and dead cells were quantified by flow cytometry. All experiments were performed in at least five biological replicates.

Vorontsova A., Cooper T.J., Haj-Shomaly J., Benguigui M., Levin S., Manobla B., Menachem R., Timaner M., Raviv Z, & Shaked Y. (2023). Chemotherapy-induced tumor immunogenicity is mediated in part by megakaryocyte-erythroid progenitors. Oncogene, 42(10), 771-781.

Publication 2023

Antibodies Antibodies, Anti-Idiotypic Biological Assay Biopharmaceuticals Biotin CD8-Positive T-Lymphocytes Cells Cultured Cells Edetic Acid Fetal Bovine Serum Flow Cytometry Fluorescein-5-isothiocyanate GZMB protein, human Homo sapiens IL2RA protein, human isolation Mus Natural Killer Cells NCR1 protein, human Neoplasms Pellets, Drug Propidium Iodide Splenic Neoplasms T-Lymphocyte

Modeling Spontaneous Esophageal Squamous Cell Carcinoma in Mice

Female C57BL/6 J mice of 6–7 weeks aged were purchased from the Vital River Laboratory Animal Technology Co. Ltd (Beijing, China). Mice were housed in SPF animal facility at room temperature with humidity of 40–60% and light and dark cycle for 12 h. Ethical consent and experimental procedures were approved by the Ethics Committee Zhengzhou University (ethical approval code: ZZUIRB2021-32).
For the induction of spontaneous ESCC, the mice were fed with drinking water containing 100 μg/mL 4-nitroquinoline-1-oxide (4-NQO) for 16 weeks. Thereafter, the mice were fed with sterilized pure water to allow the formation of ESCC. During the whole experiment, the activity status, food and water intake behaviors, body weight, and survival status of mice were observed and recorded every 2 days. The whole esophageal tissues of mice fed for 16, 28 and 32 weeks were performed the H&E staining for the detection of the ESCC induction process. Besides, the total RNA of the esophageal tissues of mice fed for 28 weeks were extracted and used to determine the expression of CCL3, CCR1 and CCR5. Also, the esophageal tissues were subjected to immunofluorescence staining for DAPI, CCL3 and the macrophages (F4/80). At week 31, the 4-NQO induced ESCC mice were randomly divided into two groups, and were intraperitoneally injected with 200 μL of normal saline or 10 mg/kg Pep3 daily for 8 days. At the end of treatment, the esophageal tissues of mice were harvested and photographed by an anatomical microscope, and the number and length diameter of tumor lesions were recorded.
The spleen of the ESCC tumor bearing mice treated with NS or Pep3 were grinded and filtered into a single cell suspension. For the detection of the CD8⁺ T cells, CD4⁺ T cells and macrophages, the splenocyte was stained with the following antibodies purchased from eBioscience, anti-CD45 (30-F11), anti-CD3 (17A2), anti-CD8 (53–6.7), anti-CD11b (M1/70), anti-CD11c (N418), anti-F4/80 (BM8) and anti-CD206 (MR6F3). The mouse esophageal tissues were subjected to H&E staining and immunofluorescence staining for DAPI, Ki67, F4/80, and immunohistochemistry staining for PITPNM3 (Novus Biologicals, Littleton, USA, NBP2-33,894) by Servicebio (Wuhan, China).

Sui X., Chen C., Zhou X., Wen X., Shi C., Chen G., Liu J., He Z., Yao Y., Li Y, & Gao Y. (2023). Integrative analysis of bulk and single-cell gene expression profiles to identify tumor-associated macrophage-derived CCL18 as a therapeutic target of esophageal squamous cell carcinoma. Journal of Experimental & Clinical Cancer Research : CR, 42, 51.

Publication 2023

Animals Animals, Laboratory Antibodies Biological Factors Body Weight CCL3 protein, human CCR1 protein, human CCR5 protein, human CD4 Positive T Lymphocytes CD8-Positive T-Lymphocytes DAPI Ethics Committees Females Fluorescent Antibody Technique Food Humidity ITGAM protein, human Light Macrophage Mice, Inbred C57BL Microscopy Muromonab-CD3 Mus Neoplasms Normal Saline Novus Oxides Rivers Splenic Neoplasms Tissues Water Consumption

MRI Imaging of Liver Metastasis Rabbit Model

According to the pre-experimental results and the experience of other relevant literatures, liver metastatic tumors will grow to 1.5–2 cm in 2–3 weeks^{7 ,7}. Therefore, we performed Magnetic Resonance Imaging (MRI) scanning at 2–3 weeks after implantation. Both groups A and B underwent MRI scanning (SIEMENS AG, Aero) to confirm tumor growth in the spleen and metastasis to the liver. A 15-channel knee phase-controlled front coil was used. After general anesthesia, rabbit liver metastasis models were placed in the channel coil for a conventional MRI scan, and the scan sequence included 3D-Vibe-T1WI, FS-TSE-T2WI, diffusion-weighted imaging (DWI), and 3D-Vibe-T1WI gadodiamide-enhanced MRI scan (Table 1). If no lesion was found on MRI scanning, the last scanning was performed at the 4th week after operation. MRI findings were interpreted by a senior radiologist (Yong Du, with 36 years experience).Table 1

MR scanning and sequence parameters.

MR sequence	Patient position	TE(ms)	TR(ms)	Slice thickness (mm)	Matrix	FA	FoV(mm)
fs-tse-T2WI	axial	110.0	3000.0	3.0	256 × 256	140.0	180 × 180
3D-Vibe-T1WI	axial	5.0	10.0	1.2	320 × 195	10.0	260 × 211
DWI	axial	77.0	6000.0	3.0	112 × 112	90.0	230 × 230
3D-Vibe-T1WI + C	axial	5.0	10.0	1.2	320 × 195	10.0	260 × 211

TE echo time; TR repetition time; FA flip angle; FoV field of view.

Li B., Feng G., Feng L., Feng X., Zhang Q., Zhang C., Yang H, & Du Y. (2023). Establishment of a rabbit liver metastasis model by percutaneous puncture of the spleen and implantation of the VX2 tumor strain under CT guidance. Scientific Reports, 13, 2802.

Publication 2023

Diffusion ECHO protocol Forehead gadodiamide General Anesthesia Liver Neoplasm Metastasis Neoplasms, Liver Nuclear Magnetic Resonance Ovum Implantation Rabbits Radiologist Splenic Neoplasms

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More about "Splenic Neoplasms"

Splenic tumors, spleen cancers, and spleen growths are a diverse group of neoplasms (abnormal cell growths) that originate within the spleen, a vital organ of the lymphatic system.
These include both benign (non-cancerous) and malignant (cancerous) growths, such as hemangiomas, lymphomas, and sarcomas.
Accurate identification and characterization of these splenic neoplasms is crucial for effective treatment planning and improving patient outcomes.
PubCompare.ai's AI-driven protocol optimization can help streamline the research process by effortlessly locating the best experimental protocols from literature, preprints, and patents using intelligent comparisons.
This powerfull AI-fueled tool supports informed decision-making by researchers studying splenic tumors, spleen cancers, and other spleen-related conditions.
For example, techniques like FACSCalibur flow cytometry, CFSE cell proliferation assays, and EasySep™ Mouse MDSC (CD11b+Gr1+) Isolation Kits can be used to analyze immune cell populations in splenic neoplasms.
CD11b MicroBeads, DNase, IL-2, and MACS sorting can further enrich and characterize these cells.
Liberase enzyme treatments and β-mercaptoethanol can also be employed to isolate and culture splenic tumor cells for in-depth analysis.
By leveraging PubCompare.ai's AI-powered protocol optimization, researchers can quickly identify the most effective experimental approaches from the literature to advance their studies of spleen cancers and other splenic neoplasms.