scholarly journals Identification of specific microRNA–messenger RNA regulation pairs in four subtypes of breast cancer

2020 ◽  
Vol 14 (3) ◽  
pp. 120-126
Author(s):  
Ling Guo ◽  
Aihua Zhang ◽  
Jie Xiong
Keyword(s):  
Breast Cancer ◽  
Messenger Rna ◽  
Rna Regulation

scholarly journals DCC is differentially expressed in the tumors of breast cancer patients treated with trastuzumab.

2020 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Breast Cancer ◽  
Cancer Patients ◽  
Messenger Rna ◽  
Growth Factor Receptor ◽  
Metastatic Breast ◽  
The United States ◽  
Differentially Expressed ◽  
Breast Cancer Patients ◽  
Primary Tumors ◽  
Deleted In Colorectal Cancer

Trastuzumab (Herceptin) is a monoclonal antibody targeting the extracellular domain of the human epidermal growth factor receptor 2 (HER2) (1) utilized for the treatment of adjuvant and metastatic breast cancer (2) in the United States and worldwide. We mined published microarray and gene expression data (3, 4) to discover in an unbiased manner the most striking transcriptional features of trastuzumab treatment. We identified the deleted in colorectal cancer locus DCC (5, 6) as among the genes most differentially expressed in the primary tumors of patients with breast cancer treated with trastuzumab. The primary tumors of breast cancer patients treated with trastuzumab expressed higher levels of DCC messenger RNA than did patients not treated with trastuzumab, and a single administration of trastuzumab was sufficient to result in differential expression of DCC in primary tumors of the breast, demonstrating that a gene encoding for a netrin receptor, cellular machinery utilized for axon guidance in the central nervous system (5-9), is transcriptionally induced in primary tumors of the breast following treatment with trastuzumab.

scholarly journals Myelin transcription factor 1 (MYT1) is differentially expressed in the tumors of breast cancer patients treated with trastuzumab.

2020 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Cancer Patients ◽  
Messenger Rna ◽  
Metastatic Breast ◽  
The United States ◽  
Differentially Expressed ◽  
Breast Cancer Patients ◽  
Primary Tumors ◽  
Transcription Factor 1

Trastuzumab (Herceptin) is a monoclonal antibody targeting the extracellular domain of the human epidermal growth factor receptor 2 (HER2) (1) utilized for the treatment of adjuvant and metastatic breast cancer (2) in the United States and worldwide. We mined published microarray and gene expression data (3, 4) to discover in an unbiased manner the most significant transcriptional changes associated with trastuzumab treatment. We identified myelin transcription factor 1, encoded by MYT1 among the genes most differentially expressed in the primary tumors of patients with breast cancer treated with trastuzumab. The primary tumors of breast cancer patients treated with trastuzumab expressed higher levels of MYT1 messenger RNA than did patients not treated with trastuzumab, and a single administration of trastuzumab was sufficient to result in differential expression of MYT1 in primary tumors of the breast, demonstrating increased expression of a zinc finger DNA-binding protein and neuronal-specific members of the LSD1 complex with the capacity to interact with Sin3B and with functions in neurogenesis (5-9) as a direct transcriptional consequence of treatment with trastuzumab.

scholarly journals Retinoic Acids Increase 17β-Hydroxysteroid Dehydrogenase Type 1 Expression in JEG-3 and T47D Cells, but the Stimulation Is Potentiated by Epidermal Growth Factor, 12-O-Tetradecanoylphorbol-13-Acetate, and Cyclic Adenosine 3′,5′-Monophosphate Only in JEG-3 Cells*

Endocrinology ◽  
1997 ◽  
Vol 138 (3) ◽  
pp. 898-904 ◽  
Author(s):  
Yun-shang Piao ◽  
Hellevi Peltoketo ◽  
Annukka Jouppila ◽  
Reijo Vihko
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Messenger Rna ◽  
Hydroxysteroid Dehydrogenase ◽  
Rna Expression ◽  
T47d Cells ◽  
Retinoic Acids ◽  
Epidermal Growth ◽  
Choriocarcinoma Cells

Abstract Human 17β-hydroxysteroid dehydrogenase type 1 (17HSD type 1) primarily catalyzes the reduction of low activity estrone to high activity estradiol in ovarian granulosa cells and placental trophoblasts. 17HSD type 1 is also present in certain peripheral tissues, such as breast tissue. In the present study we investigated the effects of retinoic acids (RAs) together with other stimuli known to modulate estradiol production and/or cell growth on expression of 17HSD type 1 in JEG-3 choriocarcinoma cells and estrogen-responsive T47D breast cancer cells. Treatment of cultured JEG-3 and T47D cells with all-trans-RA and 9-cis-RA increased reductive 17HSD activity and 17HSD type 1 messenger RNA expression severalfold in both cell lines. On the other hand, epidermal growth factor (EGF), Ca ionophore, the protein kinase C activator 12-O-tetradecanoylphorbol-13-acetate (TPA), and cAMP elevated 17HSD type 1 expression only in JEG-3 cells. Correspondingly, the effects of RAs were potentiated by EGF, TPA, and cAMP in JEG-3 cells, whereas no such phenomenon was observed in T47D cells. In JEG-3 cells, simultaneous administration of RAs with TPA and EGF maximally resulted in approximately 40- and 20-fold increases in 17HSD type 1 messenger RNA expression, respectively. The present data indicate that RAs may stimulate estradiol biosynthesis by regulating 17HSD type 1 expression in certain breast cancer and choriocarcinoma cells. The results suggest that interaction of multiple regulatory pathways is involved in maintaining high 17HSD type 1 expression in the placenta. In addition, regulation of 17HSD type 1 expression may be different in trophoblast cells from that in breast epithelial cells.

Identifying treatment options for triple negative breast cancer patients using RNA-sequencing.

2017 ◽  
Vol 35 (7_suppl) ◽  
pp. 31-31
Author(s):  
Gitte Pedersen
Keyword(s):  
Breast Cancer ◽  
Dna Repair ◽  
Cancer Patients ◽  
Messenger Rna ◽  
Dna Analysis ◽  
Triple Negative ◽  
Tumor Antigens ◽  
Standard Of Care ◽  
Breast Cancer Patients ◽  
Number Of Patients

31 Background: In the context of diagnostics, RNA is proxy for proteins and proteins are typically targets for drugs; e.g. breast cancer is typically driven by over-expression of various hormone receptors and Her2. In the current standard-of-care setting there is no measurement of mutations. Furthermore, all the markers for response to the new immune therapies are expressed as mRNA. Approximately 15% of the breast cancer patients are triple negative. Due to the poor outcome of chemo, standard-of-care guidelines (NCCN) suggests doctors encourage the patient to enroll in clinical trials. However, with more than 2000 ongoing trials in breast, which trial could potentially benefit the patient? Methods: Using the RNA-seq data from the TCGA study, we analyzed more than 120 triple negative datasets. Results: We found at least one over-expressed checkpoint inhibitor target in almost all the patients, suggesting that if you analyzed for all of the checkpoint targets, it would be possible to find a clinical study for these patients. Furthermore, when we analyzed over-expressed tumor antigens, we realized that it would be possible to design sophisticated combination trials with this information. In addition, we identified patients that were BRCAwt with an impaired DNA repair pathway; e.g. some had BRCA silencing and could potentially benefit from PARP inhibitors. Finally, a small number of patients overexpressed the androgen receptor for which there is a drug approved for prostate cancer. Conclusions: Compared to DNA analysis, tumor RNA profiling has the potential to guide a much broader set of drugs and treatment approaches including immunotherapy and chemotherapy. Messenger RNA (mRNA) analysis can reveal tumor antigens and drug targets expressed by cancer cells, as well as the vital status of the tumor microenvironment including immune response, the integrity of DNA repair mechanisms, and the engagement of angiogenesis and other cancer-related pathways.

scholarly journals ZDHHC3 as a Risk and Mortality Marker for Breast Cancer in African American Women

2017 ◽  
Vol 16 ◽  
pp. 117693511774664 ◽  
Author(s):  
Nick Kinney ◽  
Robin T Varghese ◽  
Ramu Anandakrishnan ◽  
Harold R “Skip” Garner
Keyword(s):  
Breast Cancer ◽  
African American ◽  
African American Women ◽  
Messenger Rna ◽  
White Women ◽  
African American Woman ◽  
Breast Cancer Mortality ◽  
American Woman ◽  
Ribosomal Gene ◽  
American Women

African American woman are 43% more likely to die from breast cancer than white women and have increased the risk of tumor recurrence despite lower incidence. We investigate variations in microsatellite genomic regions—a type of repetitive DNA—and possible links to the breast cancer mortality gap. We screen 33 854 microsatellites in germline DNA of African American women with and without breast cancer: 4 are statistically significant. These are located in the 3′ UTR (untranslated region) of gene ZDHHC3, an intron of transcribed pseudogene INTS4L1, an intron of ribosomal gene RNA5-8S5, and an intergenic region of chromosome 16. The marker in ZDHHC3 is interesting for 3 reasons: (a) the ZDHHC3 gene is located in region 3p21 which has already been linked to early invasive breast cancer, (b) the Kaplan-Meier estimator demonstrates that ZDHHC3 alterations are associated with poor breast cancer survival in all racial/ethnic groups combined, and (c) data from cBioPortal suggest that ZDHHC3 messenger RNA expression is significantly lower in African Americans compared with whites. These independent lines of evidence make ZDHHC3 a candidate for further investigation.

Messenger RNA regulation in human diploid fibroblasts

1977 ◽  
Vol 90 (2) ◽  
pp. 211-224 ◽  
Author(s):  
Thomas H. Meedel ◽  
Elliot M. Levine
Keyword(s):  
Messenger Rna ◽  
Rna Regulation ◽  
Diploid Fibroblasts ◽  
Human Diploid Fibroblasts

scholarly journals MATK is differentially expressed in the tumors of breast cancer patients treated with trastuzumab.

2020 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Breast Cancer ◽  
Tyrosine Kinase ◽  
Cancer Patients ◽  
Messenger Rna ◽  
Growth Factor Receptor ◽  
Metastatic Breast ◽  
The United States ◽  
Differentially Expressed ◽  
Breast Cancer Patients ◽  
Primary Tumors

Trastuzumab (Herceptin) is a monoclonal antibody targeting the extracellular domain of the human epidermal growth factor receptor 2 (HER2) (1) utilized for the treatment of adjuvant and metastatic breast cancer (2) in the United States and worldwide. We mined published microarray and gene expression data (3, 4) to discover in an unbiased manner the most striking transcriptional features of trastuzumab treatment. We identified the megakaryocyte-associated tyrosine kinase MATK (5, 6) as among the genes most differentially expressed in the primary tumors of patients with breast cancer treated with trastuzumab. The primary tumors of breast cancer patients treated with trastuzumab expressed higher levels of MATK messenger RNA than did patients not treated with trastuzumab, and a single administration of trastuzumab was sufficient to result in differential expression of MATK in primary tumors of the breast, demonstrating that a platelet-expressed tyrosine kinase (5, 6) that interacts with the receptor for the stem cell factor (7) is likely transcriptionally induced in primary tumors of the breast by trastuzumab.

scholarly journals Regulatory roles of RNA modifications in breast cancer

NAR Cancer ◽  
2021 ◽  
Vol 3 (3) ◽  
Author(s):  
Kanchan Kumari ◽  
Paula Groza ◽  
Francesca Aguilo
Keyword(s):  
Breast Cancer ◽  
Messenger Rna ◽  
Therapeutic Strategies ◽  
Rna Modifications ◽  
Breast Tumorigenesis ◽  
Cellular Processes ◽  
Trna Modifications ◽  
Expression Control ◽  
Gene Expression Control ◽  
Ribosomal Rrna

Abstract Collectively referred to as the epitranscriptome, RNA modifications play important roles in gene expression control regulating relevant cellular processes. In the last few decades, growing numbers of RNA modifications have been identified not only in abundant ribosomal (rRNA) and transfer RNA (tRNA) but also in messenger RNA (mRNA). In addition, many writers, erasers and readers that dynamically regulate the chemical marks have also been characterized. Correct deposition of RNA modifications is prerequisite for cellular homeostasis, and its alteration results in aberrant transcriptional programs that dictate human disease, including breast cancer, the most frequent female malignancy, and the leading cause of cancer-related death in women. In this review, we emphasize the major RNA modifications that are present in tRNA, rRNA and mRNA. We have categorized breast cancer-associated chemical marks and summarize their contribution to breast tumorigenesis. In addition, we describe less abundant tRNA modifications with related pathways implicated in breast cancer. Finally, we discuss current limitations and perspectives on epitranscriptomics for use in therapeutic strategies against breast and other cancers.

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