Mind-body medicine epigenetic technique (MET) and TP53AIP1 gene expression.

e292 Background: This is a pilot study update on the potential of MET to up-regulate TP53AIP1 gene expression correlated with the up-regulation TP53 gene expression in patients diagnosed with breast cancer. Methods: The selection process for the study participants was nonrandom. The following was the eligibility criteria. 1.) Inclusion Criteria: Breast Cancer, Stages II, III. 2.) Exclusion Criteria: Cognitively impaired, weak or ill. The study utilized two groups. Each group was assigned two research participants. Group One received one session of MET. Group Two received two sessions of MET. Each MET session was approximately 25-35 minutes in duration. Blood samples were taken at baseline and post-MET sessions to provide evidence in gene expression changes. For Group Two, the post-MET session blood draw was done 7 days after baseline. 1.) Primary Endpoint: To determine whether MET can up-regulate TP53AIP1 gene expression. 2.) Secondary Endpoint:To determine whether there is a correlation between up-regulated TP53AIP1 gene expression and up-regulated TP53 gene expression. The blood samples were sent to genomics labs at the Childrens Hospital of Los Angeles and the University of Nevada Las Vegas for mRNA extraction and microarray analysis. The gene expression was measured by DNA microarray results using the “PrimeView gene chip” and “Partek Genomics Suite” statistical software. Results: For three participants, there was no statistical or biologically significant up-regulation in TP53AIP1 gene expression. However, one participant from Group 1 evidenced a biologically significant up-regulation of TP53AIP1 gene expression along with a biologically significant up-regulation of TP53 gene expression. One major limitation of these findings is the statistical insignificance of the results due to the small number of participants. Conclusions: This pilot study evidenced the up-regulation of TP53AIP1 gene expression potentially due to MET and provided evidence supporting the established correlation between TP53 and TP53AIP1 gene expression that could induce apoptosis. This study also provided a foundation for a larger study with more participants.

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Mind-body medicine epigenetic technique (MET) and EGR1 (zif268) gene expression.

Journal of Clinical Oncology ◽

10.1200/jco.2015.33.29_suppl.4 ◽

2015 ◽

Vol 33 (29_suppl) ◽

pp. 4-4

Author(s):

Francisco Ventura Munoz

Keyword(s):

Breast Cancer ◽

Gene Expression ◽

Pilot Study ◽

Los Angeles ◽

Selection Process ◽

Blood Draw ◽

Eligibility Criteria ◽

Blood Samples ◽

Mrna Extraction ◽

Group 1

4 Background: This is a pilot study update on the potential of MET to up-regulate EGR1 gene expression in patients diagnosed with breast cancer. EGR1 gene expression is associated with learning and memory. Methods: The selection process for the study participants was nonrandom. The following was the eligibility criteria. 1. Inclusion Criteria: Breast Cancer, Stages II, III 2. Exclusion Criteria: Cognitively impaired, weak or ill. The study utilized two groups. Each group was assigned two research participants. Group One received one session of MET. Group Two received two sessions of MET. Each MET session was approximately 25-35 minutes in duration. Blood samples were taken at baseline and post-MET sessions to provide evidence in gene expression changes. For Group Two, the post-MET session blood draw was done 7 days after baseline. 1. Primary Endpoint: To determine whether MET can up-regulate EGR1 gene expression. 2. Secondary Endpoint: To determine whether there is a correlation between up-regulated EGR1 gene expression with up-regulated TP53 and TP53AIP1 gene expression. The blood samples were sent to genomics labs at the Childrens Hospital of Los Angeles and the University of Nevada Las Vegas for mRNA extraction and microarray analysis. The gene expression was measured by DNA microarray results using the “PrimeView gene chip” and “Partek Genomics Suite” statistical software. Results: For two participants in Group 1 and one participant in Group 2, there was biologically significant up-regulation in EGR1 gene expression. However, only one participant from Group 1 evidenced a biologically significant up-regulation of EGR1 gene expression along with a biologically significant up-regulation of TP53 and TP53AIP1 gene expression. One major limitation of these findings is the statistical insignificance of the results due to the small number of participants. Conclusions: This pilot study evidenced the up-regulation of EGR1 gene expression potentially due to MET and provided evidence for potential correlation between EGR1, TP53 and TP53AIP1 gene expression. TP53 and TP53AIP1 gene expression are known to induce apoptosis. This study also provided a foundation for a larger study with more participants.

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Mind-body medicine epigenetic technique (MET), cognitive flexibility, and brain-derived neurotrophic factor (BDNF) gene expression.

Journal of Clinical Oncology ◽

10.1200/jco.2017.35.5_suppl.172 ◽

2017 ◽

Vol 35 (5_suppl) ◽

pp. 172-172

Author(s):

Francisco Ventura Munoz

Keyword(s):

Breast Cancer ◽

Gene Expression ◽

Pilot Study ◽

Los Angeles ◽

Cognitive Flexibility ◽

Selection Process ◽

Breast Cancer Patients ◽

Bdnf Gene ◽

Blood Draw ◽

Blood Samples

172 Background: This is a pilot study update on the potential of MET to up-regulate BDNF gene expression with breast cancer patients assessed with high cognitive flexibility. MET is a technique developed to manage chronic stress and anxiety. BDNF gene expression is associated with learning and memory. Cognitively flexibility is defined as the ability to focus and sustain attention. It also implies vivid imagination and holistic thinking. Methods: The selection process for the study participants was nonrandom. The following was the eligibility criteria. 1. Inclusion Criteria: Breast Cancer, Stages II, III 2. Exclusion Criteria: Cognitively impaired, weak or ill. The study utilized two groups. Each group was assigned two research participants. Group One received one session of MET. Group Two received two sessions of MET. Each MET session was approximately 25-35 minutes in duration. Blood samples were taken at baseline and post-MET sessions to provide evidence in gene expression changes. For Group Two, the post-MET session blood draw was done 7 days after baseline. 1. Primary Endpoint: To determine whether MET can up-regulate BDNF gene expression. 2. Secondary Endpoint:To determine whether there is a correlation between up-regulated BDNF gene expression and cognitive flexibility. The blood samples were sent to genomics labs at the Children’s Hospital of Los Angeles and the University of Nevada Las Vegas for mRNA extraction and microarray analysis. The gene expression was measured by DNA microarray results using the “PrimeView gene chip” and “Partek Genomics Suite” statistical software. Results: One participant from Group 1 evidenced a biologically significant up-regulation of BDNF gene expression. This participant was assessed with high cognitive flexibility. One major limitation of these findings is the statistical insignificance of the results due to the small number of participants. Conclusions: This pilot study evidenced the up-regulation of BDNF gene expression potentially due to MET and provided evidence for the potential correlation of BDNF gene expression and cognitive flexibility. This study also provided a foundation for a larger study with more participants.

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An open-label, pilot study of veliparib and lapatinib in patients with metastatic, triple-negative breast cancer

Breast Cancer Research ◽

10.1186/s13058-021-01408-9 ◽

2021 ◽

Vol 23 (1) ◽

Author(s):

Erica M. Stringer-Reasor ◽

Jori E. May ◽

Eva Olariu ◽

Valerie Caterinicchia ◽

Yufeng Li ◽

...

Keyword(s):

Breast Cancer ◽

Gene Expression ◽

Dna Repair ◽

Pilot Study ◽

Expression Analysis ◽

Triple Negative Breast Cancer ◽

Gene Expression Analysis ◽

Triple Negative ◽

Egfr Inhibition ◽

Link Type

Abstract Background Poly (ADP-ribose)-polymerase inhibitors (PARPi) have been approved for cancer patients with germline BRCA1/2 (gBRCA1/2) mutations, and efforts to expand the utility of PARPi beyond BRCA1/2 are ongoing. In preclinical models of triple-negative breast cancer (TNBC) with intact DNA repair, we have previously shown an induced synthetic lethality with combined EGFR inhibition and PARPi. Here, we report the safety and clinical activity of lapatinib and veliparib in patients with metastatic TNBC. Methods A first-in-human, pilot study of lapatinib and veliparib was conducted in metastatic TNBC (NCT02158507). The primary endpoint was safety and tolerability. Secondary endpoints were objective response rates and pharmacokinetic evaluation. Gene expression analysis of pre-treatment tumor biopsies was performed. Key eligibility included TNBC patients with measurable disease and prior anthracycline-based and taxane chemotherapy. Patients with gBRCA1/2 mutations were excluded. Results Twenty patients were enrolled, of which 17 were evaluable for response. The median number of prior therapies in the metastatic setting was 1 (range 0–2). Fifty percent of patients were Caucasian, 45% African–American, and 5% Hispanic. Of evaluable patients, 4 demonstrated a partial response and 2 had stable disease. There were no dose-limiting toxicities. Most AEs were limited to grade 1 or 2 and no drug–drug interactions noted. Exploratory gene expression analysis suggested baseline DNA repair pathway score was lower and baseline immunogenicity was higher in the responders compared to non-responders. Conclusions Lapatinib plus veliparib therapy has a manageable safety profile and promising antitumor activity in advanced TNBC. Further investigation of dual therapy with EGFR inhibition and PARP inhibition is needed. Trial registration ClinicalTrials.gov, NCT02158507. Registered on 12 September 2014

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Gene expression profiling in clinical blood samples: The statin pilot study

Atherosclerosis Supplements ◽

10.1016/s1567-5688(02)80781-4 ◽

2002 ◽

Vol 3 (2) ◽

pp. 235

Keyword(s):

Gene Expression ◽

Pilot Study ◽

Gene Expression Profiling ◽

Expression Profiling ◽

Blood Samples

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Using cfRNA as a tool to evaluate clinical treatment outcomes in patients with metastatic lung cancers and other tumors

Cancer Drug Resistance ◽

10.20517/cdr.2021.78 ◽

2021 ◽

Author(s):

Luis E. Raez ◽

Kathleen Danenberg ◽

Daniel Sumarriva ◽

Joshua Usher ◽

Jacob Sands ◽

...

Keyword(s):

Breast Cancer ◽

Gene Expression ◽

Response To Therapy ◽

Liquid Biopsies ◽

Blood Samples ◽

Lung Cancers ◽

Metastatic Lung ◽

Clinical Responses ◽

Pre Treatment ◽

Actin Expression

Aim: We report an exploratory analysis of cfRNA as a biomarker to monitor clinical responses in non-small cell lung cancer (NSCLC), breast cancer, and colorectal cancer (CRC). An analysis of cfRNA as a method for measuring PD-L1 expression with comparison to clinical responses was also performed in the NSCLC cohort. Methods: Blood samples were collected from 127 patients with metastatic disease that were undergoing therapy, 52 with NSCLC, 50 with breast cancer, and 25 with CRC. cfRNA was purified from fractionated plasma, and following reverse transcription (RT), total cfRNA and gene expression of PD-L1were analyzed by real-time polymerase chain reaction (qPCR) using beta-actin expression as a surrogate for relative amounts of cfDNA and cfRNA. For the concordance study of liquid biopsies and tissue biopsies, the isolated RNA was analyzed by RNAseq for the expressions of 13 genes. We had to close the study early due to a lack of follow-up during the Covid-19 pandemic. Results: We collected a total of 373 blood samples. Mean cfRNA PCR signals after RT were about 50-fold higher than those of cfDNA. cfRNA was detected in all patients, while cfDNA was detected in 88% of them. A high concordance was found for the expression levels of 13 genes between blood and solid tumor tissue. Changes in cfRNA levels followed over the course of treatments were associated with response to therapy, increasing in progressive disease (PD) and falling when a partial response (PR) occurred. The expression of PD-L1 over time in patients treated with immunotherapy decreased with PR but increased with PD. Pre-treatment levels of PD-L1 were predictive of response in patients treated with immunotherapy. Conclusion: Changes in cfRNA correlate with clinical response to the therapy. Total cfRNA may be useful in predicting clinical outcomes. PD-L1 gene expression may provide a biomarker to predict response to PD-L1 inhibition.

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Personalized gene expression profiling-guided (MAGE) therapy in heavily treated metastatic breast cancer (MBC): A pilot study.

Journal of Clinical Oncology ◽

10.1200/jco.2015.33.15_suppl.e22071 ◽

2015 ◽

Vol 33 (15_suppl) ◽

pp. e22071-e22071

Author(s):

Manuel Sureda ◽

Joseba Rebollo ◽

Elena Ma Martínez ◽

Francisco J. Fernández-Morejón ◽

Vicente Munoz ◽

...

Keyword(s):

Breast Cancer ◽

Gene Expression ◽

Metastatic Breast Cancer ◽

Pilot Study ◽

Gene Expression Profiling ◽

Expression Profiling ◽

Metastatic Breast

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The Anti-tumoral Effect of β-D-Mannuronic Acid (M2000) as a Novel NSAID on Treg Cells Frequency and MMP-2, MMP-9, CCL22 and TGFβ1 Gene Expression in Pre-surgical Breast Cancer Patients

Iranian Journal of Allergy Asthma and Immunology ◽

10.18502/ijaai.v18i1.633 ◽

2019 ◽

Author(s):

Sarvenaz Kashefi ◽

Hamid Ahmadi ◽

Ramesh Omranipour ◽

Habibollah Mahmoodzadeh ◽

Fahimeh Jafarnezhad-Ansariha ◽

...

Keyword(s):

Breast Cancer ◽

Gene Expression ◽

Matrix Metalloproteinase ◽

Chronic Inflammation ◽

Transforming Growth Factor ◽

Matrix Metalloproteinase 2 ◽

Therapeutic Effects ◽

Main Role ◽

Blood Samples ◽

Mannuronic Acid

With respect to the role of chronic inflammation in the induction and progression of breast cancer (BC). The relationship between tumor and tumor microenvironment may be a hopeful strategy for BC therapy. According to the effect of β-D-Mannuronic acid (M2000) as a novel non-steroidal anti-inflammatory drug (NSAID) on BC murine model and 4T1 cell line, we started to study that was a phase II, randomized, controlled clinical trial. 24 women with BC were included in this study and were followed by fixed oral doses of M2000, 500 mg two times a day (6-8 weeks). Blood samples were collected at baseline and weeks 6-8. To compare the patterns of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), C-C motif chemokine ligand 22 (CCL22) and The transforming growth factor-beta 1 (TGFβ1) gene expression and T regulatory cells (Tregs) frequency of healthy women normal controls with BC patients, a set of 10 blood samples of women healthy volunteers was collected. The gene expression was evaluated by quantitative Real-time PCR (qRT-PCR) and the frequency of Tregs was assessed by flow cytometry. Our results showed, reduction in MMP-2 (p=0.08), MMP-9 (p=0.03), CCL22 (p=0.003) and TGFβ1 (p=0.1) gene expression and Tregs frequency (p=0.01) which play a main role in the development of chronic inflammation, angiogenesis, tumorigenesis and metastasis. Our findings demonstrated that M2000 therapy as a novel designed NSAID had valuable therapeutic effects on BC. No adverse effects were observed following the use of M2000 after 6-8 weeks.

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