Synthesis of the first 2-hydroxyanthraquinone substituted cyclotriphosphazenes and their cytotoxic properties

2020 ◽  
Vol 44 (39) ◽  
pp. 16733-16740
Author(s):  
Gönül Yenilmez Çiftçi ◽  
Nagihan Bayık ◽  
Esra Tanrıverdi Eçik ◽  
Elif Şenkuytu ◽  
Maşuk Akşahin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Colon Cancer ◽  
Cell Lines ◽  
Normal Breast ◽  
Normal Colon ◽  
Breast Epithelium ◽  
Normal Breast Epithelium ◽  
Cytotoxic Effects ◽  
Epithelium Cell ◽  
Mcf 7

New 2-hydroxyanthraquinone based cyclotriphosphazenes were prepared and their cytotoxic effects were investigated in MCF-7 (breast cancer), MCF-12A (normal breast epithelium), DLD-1 (colon cancer), and CD-18Co (normal colon epithelium) cell lines.

Melatonin and Associated Signaling Pathways that Control Normal Breast Epithelium and Breast Cancer

2011 ◽  
Vol 16 (3) ◽  
pp. 235-245 ◽  
Author(s):  
Steven M. Hill ◽  
David E. Blask ◽  
Shulin Xiang ◽  
Lin Yuan ◽  
Lulu Mao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathways ◽  
Normal Breast ◽  
Breast Epithelium ◽  
Normal Breast Epithelium

scholarly journals DNA Methylation and Breast Cancer Risk: An Epigenome-Wide Study of Normal Breast Tissue and Blood

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3088 ◽  
Author(s):  
Kaoutar Ennour-Idrissi ◽  
Dzevka Dragic ◽  
Elissar Issa ◽  
Annick Michaud ◽  
Sue-Ling Chang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Breast Tissue ◽  
Normal Breast Tissue ◽  
Normal Breast ◽  
Breast Epithelium ◽  
Normal Breast Epithelium ◽  
Differentially Methylated Genes

Differential DNA methylation is a potential marker of breast cancer risk. Few studies have investigated DNA methylation changes in normal breast tissue and were largely confounded by cancer field effects. To detect methylation changes in normal breast epithelium that are causally associated with breast cancer occurrence, we used a nested case–control study design based on a prospective cohort of patients diagnosed with a primary invasive hormone receptor-positive breast cancer. Twenty patients diagnosed with a contralateral breast cancer (CBC) were matched (1:1) with 20 patients who did not develop a CBC on relevant risk factors. Differentially methylated Cytosine-phosphate-Guanines (CpGs) and regions in normal breast epithelium were identified using an epigenome-wide DNA methylation assay and robust linear regressions. Analyses were replicated in two independent sets of normal breast tissue and blood. We identified 7315 CpGs (FDR < 0.05), 52 passing strict Bonferroni correction (p < 1.22 × 10−7) and 43 mapping to known genes involved in metabolic diseases with significant enrichment (p < 0.01) of pathways involving fatty acids metabolic processes. Four differentially methylated genes were detected in both site-specific and regions analyses (LHX2, TFAP2B, JAKMIP1, SEPT9), and three genes overlapped all three datasets (POM121L2, KCNQ1, CLEC4C). Once validated, the seven differentially methylated genes distinguishing women who developed and who did not develop a sporadic breast cancer could be used to enhance breast cancer risk-stratification, and allow implementation of targeted screening and preventive strategies that would ultimately improve breast cancer prognosis.

scholarly journals Gene expression abnormalities in histologically normal breast epithelium of breast cancer patients

2007 ◽  
Vol 122 (7) ◽  
pp. 1557-1566 ◽  
Author(s):  
Anusri Tripathi ◽  
Chialin King ◽  
Antonio de la Morenas ◽  
Victoria Kristina Perry ◽  
Bohdana Burke ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Patients ◽  
Normal Breast ◽  
Breast Cancer Patients ◽  
Breast Epithelium ◽  
Normal Breast Epithelium

Gene expression abnormalities in histologically normal breast epithelium from patients with luminal type of breast cancer

2014 ◽  
Vol 42 (5) ◽  
pp. 977-988 ◽  
Author(s):  
Pavol Zubor ◽  
Jozef Hatok ◽  
Petra Moricova ◽  
Karol Kajo ◽  
Ivana Kapustova ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Normal Breast ◽  
Breast Epithelium ◽  
Normal Breast Epithelium ◽  
Luminal Type

scholarly journals Anti-Proliferation Effects of Benzimidazole Derivatives on HCT-116 Colon Cancer and MCF-7 Breast Cancer Cell Lines

2012 ◽  
Vol 13 (8) ◽  
pp. 4075-4079 ◽  
Author(s):  
Mohammed Hadi Al-Douh ◽  
Hayder B. Sahib ◽  
Hasnah Osman ◽  
Shafida Abd Hamid ◽  
Salizawati M. Salhimi
Keyword(s):  
Breast Cancer ◽  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Benzimidazole Derivatives ◽  
Hct 116 ◽  
Mcf 7

scholarly journals Circadian Alterations Increase with Progression in a Patient-Derived Cell Culture Model of Breast Cancer

2021 ◽  
Vol 3 (4) ◽  
pp. 598-608
Author(s):  
Hui-Hsien Lin ◽  
Stephanie R. Taylor ◽  
Michelle E. Farkas
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Progression ◽  
Phase Relationship ◽  
Metastatic Carcinoma ◽  
Normal Breast ◽  
Normal Breast Epithelium ◽  
Clock Proteins ◽  
Ductal Hyperplasia ◽  
Cancerous Cells

Circadian rhythm disruption can elicit the development of various diseases, including breast cancer. While studies have used cell lines to study correlations between altered circadian rhythms and cancer, these models have different genetic backgrounds and do not mirror the changes that occur with disease development. Isogenic cell models can recapitulate changes across cancer progression. Hence, in this study, a patient-derived breast cancer model, the 21T series, was used to evaluate changes to circadian oscillations of core clock protein transcription as cells progress from normal to malignant states. Three cell lines were used: H16N2 (normal breast epithelium), 21PT (atypical ductal hyperplasia), and 21MT-1 (invasive metastatic carcinoma). The cancerous cells are both HER2+. We assessed the transcriptional profiles of two core clock proteins, BMAL1 and PER2, which represent a positive and negative component of the molecular oscillator. In the normal H16N2 cells, both genes possessed rhythmic mRNA oscillations with close to standard periods and phases. However, in the cancerous cells, consistent changes were observed: both genes had periods that deviated farther from normal and did not have an anti-phase relationship. In the future, mechanistic studies should be undertaken to determine the oncogenic changes responsible for the circadian alterations found.

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