Ovarian Cancer
Overian cancer is a complex and challenging disease that affects the ovaries, the female reproductive organs responsible for producing eggs and hormones.
This malignant condition arises from the abnormal growth and proliferation of cells within the ovaries, often leading to the formation of tumors.
Research in ovarian cancer is rapidly evolving, with new advancements in diagnostic techniques, treatment strategies, and preventive measures.
PubCompare.ai, an AI-powered platform, can help optimize your ovarian cancer research by enabling you to effortlessly locate the best protocols from literature, pre-prints, and patents, while providing accurate comparisons to enhance reproducibility and accuracy.
Explore the latest developments in ovarian cancer research and gain a deeper understanding of this disease through the use of PubCompare.ai.
Our platform offers a concise, informative overview to help you stay up-to-date with the latest findings and improve the quality and impact of your ovarian cancer research.
Most cited protocols related to «Ovarian Cancer»
We ran CIBERSORT with disabled quantile normalization, as recommended on their website for RNA-seq data. While quanTIseq provides an entire pipeline, starting with read-mapping and estimation of gene expression, we only ran the last part of that pipeline, which estimates the immune cell fractions from gene expression data. We ran TIMER with ‘OV’ on ovarian cancer ascites samples and with ‘SKCM’ on melanoma samples. We ran quanTIseq with the option
The SNP array files were preprocessed using the aroma.affymetrix package [15 (link)] as described [16 (link)], and copy number variations were determined using ASCAT version 2.1 [3 (link)]; sex chromosomes were excluded from the analysis.
The Sequenza results were obtained using version 2.1.0 with default parameters; the input was generated by the python script sequenza-utils.py version 2.1.0 with default binning size of 50 bases for the exome sequencing or 200 bases for the whole-genome sequencing. The absCN-seq results were obtained using version 1.0 with default parameters; the input was the same genomic segments used by Sequenza as well as high-quality somatic mutations calls detected by VarScan2 as described in the software documentation. The ABSOLUTE results were obtained using software version 1.0.6 with default parameters except that the platform was specified as ‘Illumina_WES’; the input was the same genomic segments used with Sequenza and absCN-seq.
Exome sequencing data from 31 of the NCI-60 tumor cell lines, aligned to the genome version hg19, were downloaded in May 2014 in the BAM format [17 (link)].
Whole-genome sequencing, aligned to the hg19 genome in the BAM format at ×30 of coverage, of two cell lines HCC1143 and HCC1954, matching normal blood, and simulated admixtures at tumor cellularity of 20%, 40%, 60%, and 80%, were obtained in March 2014 from the TCGA4 benchmark cohort (
All BAM files were processed to remove PCR duplicates and low-quality mappings with Picard, and then converted to pileup format using SAMtools [12 (link)].
Most recents protocols related to «Ovarian Cancer»
Example 8
The efficacy of CHP20-25 against PARG activity was examined by dot blot assays. PARG was incubated with PAR for 20 min at room temperature with or without inhibitors. PAR-digestion results were analyzed using dot blotting with anti-PAR antibody. IC50 values of CHP20-25 were measured by dot blotting with anti-PAR antibody in a dose course of CHP20-25. Colony formation assays were performed using HCC1937 (BRCA1-mutant breast cancer cells) and PARPi-resistant UWB1.289 (BRCA1-mutant ovarian cancer cells) with 2.5-20 μM PARG inhibitors (CHP20-25,
Example 10
Binding of MSLN-BiTE to membrane-bound target expressed in cells was determined with an on-cell affinity assay. 3×104 cells per well of a microtiter plate were incubated with MSLN-BiTE protein in a dose response for 16-22 h at 4° C. Cells were washed twice with flow buffer (PBS that contained 2% fetal calf serum and 0.01% sodium azide), and then resuspended in flow buffer and incubated with an anti-His Fab labeled with Alexa Fluor-647 for 50 minutes at 4° C. Cells were fixed after incubation to optimize detection of the fluorescent signal. Cells were then washed twice and resuspended in flow buffer that contained propidium iodide at 1 ug/ml. Cells were analyzed by flow cytometry for live cells that were positive for Alexa Fluor-647. EC50 values were determined from the dose response curve of Alexa Fluor-647 positive cells.
Example 4
Colony formation assay was performed using HCC1937 (BRCA1-deficient breast cancer cells), HCC1937 BRCA1 (BRCA1-reconstituted HCC1937 cells) cells, PEO-1 (BRCA2-deficient ovarian cancer cells), and PEO-4 (BRCA2-reconstituted PEO-1 cells) with indicated concentrations of PARG inhibitor (#34).
Colony formation assay: HCC1937, HCC1937-BRCA1, PEO-1 or PEO-4 (˜1000 cells) were seeded into six-well plates and then treated by various doses of PARG inhibitor (#34). After 14-21 days of culture, the viable cells were fixed by methanol and stained with crystal violet. The number of colonies (>50 cells for each colony) was calculated.
Example 18
Antagonistic TFNR2 polypeptides, such as antibodies, antigen-binding fragments thereof, single-chain polypeptides, and constructs described herein, may exert biological activities on T-reg cells and T effector cells. To investigate these effects, antagonistic TNFR2 antibodies TNFRAB1 and TNFRAB2 were incubated with cultured T-reg cells at ascending concentrations of antibody, and the percentage change in the quantity of T-reg cells in culture was subsequently recorded. The results of these experiments are shown in
Additionally, antagonistic TNFR2 antibodies TNFRAB1 and TNFRAB2 promote the proliferation of T effector cells. To investigate this activity, antagonistic TNFR2 antibodies TNFRAB1 and TNFRAB2 were incubated with cultured CD8+ T cells at ascending concentrations of antibody, and the percentage change in the quantity of CD8+ T cells in culture was subsequently recorded. The results of these experiments are shown in
The antagonistic TNFR2 antibodies TNFRAB1 and TNFRAB2 also directly kill TNFR2-expressing cancer cells. The antagonistic TNFR2 antibody TNFRAB1, was incubated with cultured OVCAR3 cells, a line of TNFR2+ ovarian cancer cells, at ascending concentrations of antibody, and the percentage change in the quantity of CD8+ T cells in culture was subsequently recorded. The results of this experiments are shown in
Taken together, the data shown in
Example 2
For Western blot analysis 20 μg of total protein extracted from cells lyzed with Laemmli-lysis buffer was used. Extracts were diluted in reducing sample buffer (Roth), subjected to SDS-PAGE and subsequently electrotransferred onto PVDF membrane (Pall). Immunostaining was performed with polyclonal antibodies reactive to CLDN6 (ARP) and beta-Actin (Abcam) followed by detection of primary antibodies with horseradish-peroxidase conjugated goat anti-mouse and goat anti-rabbit secondary antibodies (Dako).
Tissue lysates from up to five individuals were tested for each normal tissue type. No CLDN6 protein expression was detected in any of the normal tissues analyzed. In contrast to normal tissues, high expression of CLDN6 protein was detected in samples from ovarian cancer and lung cancer. CLDN6 expression was detected in NIH-OVCAR3 (ovarian cancer), MKN7 (gastric cancer), AGS (gastric cancer), CPC-N (SCLC), HCT-116 (colon cancer), FU97 (gastric cancer), NEC8 (testicular embryonal carcinoma), JAR (placental choriocarcinoma), JEG3 (placental choriocarcinoma), BEWO (placental choriocarcinoma), and PA-1 (ovarian teratocarcinoma).
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More about "Ovarian Cancer"
Ovarian cancer is a complex and challenging disease that affects the ovaries, the female reproductive organs responsible for producing eggs and hormones.
This malignant condition arises from the abnormal growth and proliferation of cells within the ovaries, often leading to the formation of tumors.
Research in ovarian cancer is rapidly evolving, with new advancements in diagnostic techniques, treatment strategies, and preventive measures.
PubCompare.ai, an AI-powered platform, can help optimize your ovarian cancer research by enabling you to effortlessly locate the best protocols from literature, pre-prints, and patents, while providing accurate comparisons to enhance reproducibility and accuracy.
Explore the latest developments in ovarian cancer research and gain a deeper understanding of this disease through the use of PubCompare.ai.
Our platform offers a concise, informative overview to help you stay up-to-date with the latest findings and improve the quality and impact of your ovarian cancer research.