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Breast Carcinoma

Breast Carcinoma is a malignant neoplastic disease originating in the breast tissue.
It is the most common type of breast cancer, accounting for the majority of breast cancer cases.
Breast carcinoma can arise from various cell types within the breast, including ductal, lobular, and other epithelial cells.
Subtypes of breast carcinoma include invasive ductal carcinoma, invasive lobular carcinoma, and other histological variants.
Breast carcinoma is a significant public health concern, with incidence and mortality rates varying by geographic region and demographic factors.
Early detection, accurate diagnosis, and advancements in treatment strategies are crucial for improving outcomes for individuals affected by this disease.

Most cited protocols related to «Breast Carcinoma»

MCF-7, ZR75-1, T-47D and BT-474 human cell lines were obtained from ATCC and grown in the relevant media. TAM-R cells13 (link) were a kind gift from Dr Iain Hutcheson and Prof. Robert Nicholson (Cardiff). The ER+ breast cancer tumours were obtained from the Nottingham Tenovus primary breast cancer series, Addenbrooke’s Hospital and Imperial College Healthcare NHS Trust, London, UK with appropriate ethical approval from the repositories. The malignant pericardial effusion and the two distant metastases were obtained from Imperial College Healthcare NHS Trust, London, UK. For ChIP in the tumours and metastases, the frozen sample was cut into smaller pieces prior to ChIP, which was then performed as previously described16 . For the malignant pericardial effusion, epithelial cells were first enriched using Dynabeads conjugated with Epcam17 (link). For ChIPs from cell line material, proliferating cells were cross-linked and processed for ChIP as previously described16 . The antibodies used were anti-ER (sc-543) from Santa Cruz Biotechnologies and anti-FoxA1 (ab5089) from Abcam. Sequences generated by the Illumina Genome Analyzer were processed by the Illumina analysis pipeline version 1.6.1, and aligned to the Human Reference Genome (assembly hg18, NCBI Build 36.1, March 2008) using BWA version 0.5.518 . Differential binding analysis was performed using the DiffBind package19 . For immunohistochemical analyses, ER staining was conducted using the 6F11/2 mouse monoclonal antibody (Novocastra, Leica Microsystems, Bucks, UK) and FoxA1 staining was conducted using a rabbit polyclonal antibody (ab23738) from Abcam. An Allred scoring system was used to assess staining accounting for both staining intensity and the proportion of cells stained.
Publication 2011
Antibodies Breast Carcinoma Breast Neoplasm Cell Lines DNA Chips Effusion, Pericardial Epithelial Cells FOXA1 protein, human Freezing Genome Genome, Human Homo sapiens Immunoglobulins Malignant Neoplasms Monoclonal Antibodies Mus Neoplasm Metastasis Neoplasms Rabbits
Articles were selected for inclusion in the systematic review of the evidence if they met the following criteria: (1) the study compared, prospectively or retrospectively, fluorescent ISH (FISH) and immunohistochemistry (IHC) results or other tests; described technical comparisons across various assay platforms; examined potential testing algorithms for HER2 testing; or examined the correlation of HER2 status in primary versus metastatic tumors from the same patients; (2) the study population consisted of patients with a diagnosis of invasive breast cancer; or (3) the primary outcomes included the negative predictive value (NPV) or positive predictive value (PPV) of ISH and IHC assays used to determine HER2 status, alone and in combination; negative and positive concordance across platforms; and accuracy in determining HER2 status and benefit from anti-HER2 therapy and in determining sensitivity and specificity of individual tests. Consideration was given to studies that directly compared results across assay platforms.
Studies were not limited to randomized controlled trials but also included other study types, including cohort designs, case series, evaluation studies, and comparative studies. The Update Committee also reviewed other testing guidelines and proficiency strategies of various US and international organizations, including unpublished data. Letters, commentaries, and editorials were reviewed for any new information. Case reports were excluded. The clinical questions addressed in the update are available in Data Supplement 5.
This information was used to help the Update Committee develop new algorithms (for pathologists and oncologists) for testing, specify testing requirements and exclusions, and facilitate the necessary quality assurance monitoring that will make HER2 testing less variable and ensure more analytic consistency between laboratories. The term ratio, as used in the guideline recommendations and algorithms, always applies to the HER2/CEP17 ratio, which means the ratio of HER2 signals per cell (numerator) over CEP17 signals per cell (denominator).
Publication 2013
Biological Assay Breast Carcinoma Dietary Supplements ERBB2 protein, human Immunohistochemistry Neoplasm Metastasis Oncologists Pathologists Patients Signal Transduction Therapeutics
CN34 tumour cells were isolated from the pleural effusion of a breast cancer patient treated at our institution, after written consent in accordance with Institutional Review Board (IRB) regulations. Brain metastatic populations from these cells and MDA-MB-231cells were obtained by consecutive rounds of in vivo selection in 6–7-week-old beige nude and athymic mice, respectively. All animal work was done in accordance with the MSKCC Institutional Animal Care and Use Committee. Methods for RNA extraction, labelling and hybridization for DNA microarray analysis have been described previously17 (link). Bioinformatics analyses with detailed descriptions can be found in the Methods. Knockdown and overexpression of candidate genes, and cetuximab inhibitor studies were performed as previously described6 (link). The in vitro BBB model was set up as previously described25 (link), and modified to enable tumour cell counting. Sambucus nigra lectin staining was performed using standard histochemical techniques, and quantified using Metamorph software analysis. The Methods section provides further information, including malignant cell isolation from pleural fluids, tumour cell extraction and cell culture protocols, animal inoculation and bioluminescence imaging, generation of retroviral gene knockdown and overexpression vectors, transfections and infections, RNA and protein expression, in vitro BBB transmigration assay, endothelial cell adhesion assay, and metastatic tissue staining and quantification.
Publication 2009
Animals Biological Assay Brain Breast Carcinoma Cell Adhesion Cell Culture Techniques Cells Cell Separation Cetuximab Cloning Vectors Crossbreeding DNA Chips Endothelial Cells Endothelium Ethics Committees, Research Gene Knockdown Techniques Genes Infection Institutional Animal Care and Use Committees Lectin Mice, Nude Microarray Analysis Neoplasms Patients Pleura Pleural Effusion Population Group Proteins Retroviridae Sambucus nigra Tissues Transfection Vaccination
All tumor samples for the current study were obtained through the TCGA Biospecimen Core Resource (BCR) as described previously6 (link). No other selection criteria other than availability were applied for this study. Patient-derived xenograft tumors from established Basal and Luminal-B breast cancer intrinsic subtypes 37 (link), 38 (link) were raised subcutaneously in 8 week old NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ mice (Jackson Labs, Bar Harbor, Maine) as previously described39 (link), 40 (link). Normal colon biopsies were obtained from screening colonoscopies performed between July 2006 and October 2010 under Vanderbilt University IRB approval #061096.
Tissue proteins were extracted and tryptic peptide digests were analyzed by multidimensional liquid chromatography-tandem mass spectrometry. Xenograft QC samples were run after every 5 colorectal tumor samples. Raw data were processed for peptide identification by database and spectral library searching and identified peptides were assembled as proteins and mapped to gene identifiers for proteogenomic comparisons. Quantitative proteomic comparisons were based on spectral count data. Detailed descriptions of the samples, LC-MS/MS analysis, and data analysis methods can be found in Supplementary Methods. All of the primary mass spectrometry data on TCGA tumor samples are deposited at the CPTAC Data Coordinating Center as raw and mzML files and complete protein assembly datasets for public access (https://cptac-data-portal.georgetown.edu).
Publication 2014
Biopsy Breast Carcinoma cDNA Library Colon Colonoscopy Colorectal Neoplasms Heterografts Liquid Chromatography Mass Spectrometry Mice, Inbred NOD Neoplasms Patients Peptides Phenobarbital Proteins Tandem Mass Spectrometry Tissues Trypsin
Results are based in part upon data generated by TCGA Research Network (http://cancergenome.nih.gov/). We aggregated TCGA transcriptomic and RPPA data from public repositories, listed in the “Data availability” section. RNA-seq expression data were processed by TCGA at the gene level, rather than at the transcript level. Tumors spanned 32 different TCGA projects, each project representing a specific cancer type, listed as follows: LAML, acute myeloid leukemia; ACC, adrenocortical carcinoma; BLCA, bladder urothelial carcinoma; LGG, lower grade glioma; BRCA, breast invasive carcinoma; CESC, cervical squamous cell carcinoma and endocervical adenocarcinoma; CHOL, cholangiocarcinoma; CRC, colorectal adenocarcinoma (combining COAD and READ projects); ESCA, esophageal carcinoma; GBM, glioblastoma multiforme; HNSC, head and neck squamous cell carcinoma; KICH, kidney chromophobe; KIRC, kidney renal clear cell carcinoma; KIRP, kidney renal papillary cell carcinoma; LIHC, liver hepatocellular carcinoma; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; DLBC, lymphoid neoplasm diffuse large B-cell lymphoma; MESO, mesothelioma; OV, ovarian serous cystadenocarcinoma; PAAD, pancreatic adenocarcinoma; PCPG, pheochromocytoma and paraganglioma; PRAD, prostate adenocarcinoma; SARC, sarcoma; SKCM, skin cutaneous melanoma; STAD, stomach adenocarcinoma; TGCT, testicular germ cell tumors; THYM, thymoma; THCA, thyroid carcinoma; UCS, uterine carcinosarcoma; UCEC, uterine corpus endometrial carcinoma; UVM, uveal melanoma. Cancer molecular profiling data were generated through informed consent as part of previously published studies and analyzed per each original study’s data use guidelines and restrictions.
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Publication 2019
4-carboxyphenylglyoxal Adenocarcinoma Adenocarcinoma of Lung Adrenocortical Carcinoma Breast Carcinoma Carcinoma, Thyroid Carcinoma, Transitional Cell Carcinosarcoma Cells Cholangiocarcinoma Chromophobia Chronic Obstructive Airway Disease Diffuse Large B-Cell Lymphoma Endocervix Endometrial Carcinoma Esophageal Cancer Familial Atypical Mole-Malignant Melanoma Syndrome Gene Expression Profiling Genes Glioblastoma Multiforme Glioma Hepatocellular Carcinomas Hypernephroid Carcinomas Kidney Leukemia, Myelocytic, Acute Lung Lymph Malignant Neoplasms Mesothelioma Neck Neoplasms Ovary Pancreas Paraganglioma Pheochromocytoma Prostate Renal Cell Carcinoma RNA-Seq Sarcoma Serous Cystadenocarcinoma Squamous Cell Carcinoma Squamous Cell Carcinoma of the Head and Neck Stomach Testicular Germ Cell Tumor Thymoma Urinary Bladder Uterus Uveal melanoma X-Ray Photoelectron Spectroscopy

Most recents protocols related to «Breast Carcinoma»

Example 23

We have demonstrated that LXR agonists inhibit in vitro cancer progression phenotypes in breast cancer, pancreatic cancer, and renal cancer. To investigate if LXR agonist treatment inhibits breast cancer primary tumor growth in vivo, mice injected with MDA-468 human breast cancer cells were treated with either a control diet or a diet supplemented with LXR agonist GW3965 2 (FIG. 36).

To determine the effect of orally delivered GW3965 2 on breast cancer tumor growth, 2×106 MDA-468 human breast cancer cells were resuspended in 50 μL PBS and 50 μL matrigel and the cell suspension was injected into both lower memory fat pads of 7-week-old Nod Scid gamma female mice. The mice were assigned to a control diet treatment or a GW3965-supplemented diet treatment (75 mg/kg/day) two days prior to injection of the cancer cells. The GW3965 2 drug compound was formulated in the mouse chow by Research Diets, Inc. Tumor dimensions were measured using digital calipers, and tumor volume was calculated as (small diameter)2×(large diameter)/2.

Treatment with GW3965 resulted in significant reduction in breast cancer tumor size in vivo (FIG. 36).

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Patent 2024
agonists Breast Carcinoma Breast Neoplasm Cancer of Kidney Cardiac Arrest Cells Diet Disease Progression Drug Compounding Fingers Gamma Rays GW 3965 Malignant Neoplasm of Breast Malignant Neoplasms Mammary Carcinoma, Human matrigel Memory Mice, Inbred NOD Mus Neoplasms Pad, Fat Pancreatic Cancer Phenotype SCID Mice Woman

Example 5

In this Example, the lung metastasis-suppressing effects of anti-S100A8/A9 monoclonal antibodies were investigated. Through use of a lung metastasis model of human breast cancer MDA-MB-231 cells, the lung metastasis-suppressing effects of anti-S100A8/A9 monoclonal antibodies were investigated. For the MDA-MB-231 cells, a line stably expressing GFP was generated.

In accordance with a protocol illustrated in FIG. 11, 1×105 human breast cancer MDA-MB-231 cells and 50 μg of each anti-S100A8/A9 monoclonal antibodies (Clone Nos.: 45, 85, 235, 258, and 260) were simultaneously injected into the tail vein of each five Balb/c nu/nu mice per group, and 1 month later, CT scans were performed. FIG. 12 shows the results for comparing typical CT images and the areas of tumor cells calculated from the CT images to those of a negative control group.

As a result, it was recognized that Clone Nos. 85, 258, and 260 showed significant lung metastasis-suppressing effects. For the MDA-MB-231 cells, mouse lung metastasis was hardly found, suggesting a need for a further investigation on the generation of a metastasis model.

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Patent 2024
Breast Breast Carcinoma Clone Cells Homo sapiens Lung Lung Cancer MDA-MB-231 Cells Mice, Inbred BALB C Mice, Nude Monoclonal Antibodies Mus Needs Assessment Neoplasm Metastasis Neoplasms Tail Veins Veins, Pulmonary X-Ray Computed Tomography

Example 11

The present Example describes using activatable antibodies to detect expression and/or activation in tissue microarrays (TMAs). The anti-Jagged antibody 4D11 was used with a non-small cell lung cancer (NSCLC) TMA and a breast cancer (BC) TMA. Most of the NSCLC and BC patient tumor samples were positive for Jagged expression. The same NSCLC and BC TMAs were contacted with the activatable anti-Jagged antibody referred to herein as 5342-1204-4D11. 97% of NSCLC and 100% of BC patient tumor samples were positive for binding and activation of 5342-1204-4D11 activatable anti-Jagged antibody. Furthermore, more than 80% of the tumor samples were characterized by a high activation rate (++or +++) as shown in FIG. 21. The same NSCLC and BC TMAs were contacted with the A11 antibody, which binds to the protease MT-SP1. 77% of the NSCLC and 98% of the BC patient tumor samples were positive for MT-SP1 activity. 8 NSCLC tumors lacked MT-SP1 activity, but demonstrated binding and activation of the 5342-1204-4D11 activatable anti-Jagged antibody, which suggests the participation of proteases in the activation of the 5342-1204-4D11 activatable anti-Jagged antibody.

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Patent 2024
Antibodies Antibodies, Anti-Idiotypic Breast Carcinoma Breast Neoplasm Endopeptidases Immunoglobulins Malignant Neoplasms Microarray Analysis Neoplasms Non-Small Cell Lung Carcinoma Patients Peptide Hydrolases ST14 protein, human Tissues
The cellular uptake of Cy5.5-CNPs was investigated in three types of normal cells, such as breast cancer cells (4T1), rat cardiomyocytes (H9C2), mouse fibroblasts (L929) and macrophages (Raw264.7). Each cell was incubated with Cy5.5-CNPs (100, 225 or 900 μg/ml) for 4 or 24 h. After treatment, cells were fixed with 4% paraformaldehyde for 15 min, and stained with 4′,6-diamidino-2-phenylindole (DAPI) for 10 min. The cellular uptake was observed using a Leica TCS SP8 confocal laser-scanning microscope (CLSM; Leica Microsystems GmbH; Wetzlar, Germany). Quantitative analyses of the fluorescence images were performed using ImageJ software (NIH, Bethesda, MD, USA). The cytotoxicity was assessed by the Cell Counting Kit-8 (CCK-8) assay. Briefly, 5 × 104 4T1, H9C2, L929 and Raw264.7 cells were seeded into 96-well cell culture plates. Then, each cell was treated with different concentration of Cy5.5-CNPs ranging from 0 to 900 μg/ml. After 24 h of incubation, the cells were further incubated with cell culture medium containing 10% of CCK-8 solution for 20 min. Finally, the cell viability was analyzed using a microplate reader (VERSAmaxTM; Molecular Devices Corp., USA) with a wavelength of 450 nm.
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Publication 2023
Biological Assay Breast Carcinoma Cell Culture Techniques Cells Cell Survival Culture Media CY5.5 cyanine dye Cytotoxin Fibroblasts Fluorescence Macrophage Medical Devices Microscopy, Confocal Mus Myocytes, Cardiac paraform RAW 264.7 Cells
The enrolled patients were divided into four cohorts including ER+/PR+, ER+/PR-, ER-/PR+ and ER-/PR- according to HoR status. Then, Pearson’s χ2 test was used to estimate the clinicopathologic difference among these four cohorts. The cancer-specific survival (CSS) and overall survival (OS) were the endpoints of our study. CSS was defined as the interval from the diagnosis of breast cancer to death caused by breast cancer or the final follow-up in censored cases, and OS was defined as the interval from diagnosis of breast cancer to death from all causes or the last follow-up in censored cases. Survival differences were assessed through Kaplan-Meier analysis, followed by a log−rank test. Then, the multivariable Cox proportional hazards model was used and hazard ratios (HR) with the corresponding 95% confidence intervals (CI) were subsequently calculated to estimate the independent prognostic factors. STATA software (Version 13; Stata Corporation) was applied for all statistical analyses. The forest plot was generated by Microsoft Office Excel (Version 2021; Microsoft Corporation). All tests were two sided and p value <0.05 were considered statistically significant.
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Publication 2023
Breast Carcinoma Diagnosis Forests Malignant Neoplasm of Breast Malignant Neoplasms Patients Prognostic Factors

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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
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MCF-7 is a cell line derived from human breast adenocarcinoma. It is an adherent epithelial cell line that can be used for in vitro studies.
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MDA-MB-231 is a cell line derived from a human breast adenocarcinoma. This cell line is commonly used in cancer research and is known for its aggressive and metastatic properties.
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DMEM (Dulbecco's Modified Eagle's Medium) is a cell culture medium formulated to support the growth and maintenance of a variety of cell types, including mammalian cells. It provides essential nutrients, amino acids, vitamins, and other components necessary for cell proliferation and survival in an in vitro environment.
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Penicillin/streptomycin is a commonly used antibiotic solution for cell culture applications. It contains a combination of penicillin and streptomycin, which are broad-spectrum antibiotics that inhibit the growth of both Gram-positive and Gram-negative bacteria.
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Penicillin is a type of antibiotic used in laboratory settings. It is a broad-spectrum antimicrobial agent effective against a variety of bacteria. Penicillin functions by disrupting the bacterial cell wall, leading to cell death.
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Streptomycin is a broad-spectrum antibiotic used in laboratory settings. It functions as a protein synthesis inhibitor, targeting the 30S subunit of bacterial ribosomes, which plays a crucial role in the translation of genetic information into proteins. Streptomycin is commonly used in microbiological research and applications that require selective inhibition of bacterial growth.
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RPMI 1640 medium is a commonly used cell culture medium developed at Roswell Park Memorial Institute. It is a balanced salt solution that provides essential nutrients, vitamins, and amino acids to support the growth and maintenance of a variety of cell types in vitro.
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RPMI 1640 is a common cell culture medium used for the in vitro cultivation of a variety of cells, including human and animal cells. It provides a balanced salt solution and a source of essential nutrients and growth factors to support cell growth and proliferation.
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FBS, or Fetal Bovine Serum, is a commonly used cell culture supplement. It is derived from the blood of bovine fetuses and provides essential growth factors, hormones, and other nutrients to support the growth and proliferation of a wide range of cell types in vitro.

More about "Breast Carcinoma"

Breast Carcinoma, also known as Breast Cancer, is a malignant neoplastic disease that originates in the breast tissue.
It is the most common type of breast cancer, accounting for the majority of cases.
Breast Carcinoma can arise from various cell types within the breast, including ductal, lobular, and other epithelial cells.
Subtypes of Breast Carcinoma include Invasive Ductal Carcinoma, Invasive Lobular Carcinoma, and other histological variants.
Breast Carcinoma is a significant public health concern, with incidence and mortality rates varying by geographic region and demographic factors.
Early detection, accurate diagnosis, and advancements in treatment strategies are crucial for improving outcomes for individuals affected by this disease.
Researchers often utilize cell lines such as FBS, MCF-7, and MDA-MB-231 to study Breast Carcinoma.
These cell lines are commonly cultured in DMEM or RPMI 1640 medium, supplemented with Penicillin/Streptomycin to prevent bacterial contamination.
Understanding the biology and behavior of these cell lines can provide valuable insights into the development and progression of Breast Carcinoma.
Advances in research, such as those facilitated by the PubCompare.ai platform, can help optimize Breast Carcinoma research by locating protocols from literature, preprints, and patents, and utilizing AI-driven comparisons to identify the best protocols and products.
This can enhance reproducibility and accuracy in Breast Cancer research, ultimately leading to improved outcomes for those affected by this disease.