Review
Cell Biology
Tala Tayoun, Marianne Oulhen, Agathe Aberlenc, Francoise Farace, Patrycja Pawlikowska
Summary: CTCs provide a tool for studying tumor heterogeneity and metastatic potential, with recent progress in single-cell analysis shedding light on genomic instability and its impact on tumor evolution and resistant clones emergence. Evaluating CIN and CNA in CTCs reveals their role in metastatic progression and resistance, despite technical obstacles in single CTC analysis, but showing potential predictive value for genotoxic treatment response.
Editorial Material
Multidisciplinary Sciences
Craig M. Bielski, Barry S. Taylor
Summary: Genomic instability is a characteristic of cancer, but exploiting this feature to selectively target cancer cells remains a major challenge in cancer biology with significant implications for drug development.
NATURE COMMUNICATIONS
(2021)
Review
Pharmacology & Pharmacy
Arash Salmaninejad, Khandan Ilkhani, Havva Marzban, Jamshid G. Navashenaq, Samira Rahimirad, Fatemeh Radnia, Meysam Yousefi, Zahra Bahmanpour, Sara Azhdari, Amirhossein Sahebkar
Summary: DNA damage can come from both internal and external sources, with potentially serious consequences if not repaired, such as cell death or genetic mutations. DNA repair is crucial in addressing these damages, but aberrations in the process can lead to genomic instability and the onset of cancer.
CURRENT PHARMACEUTICAL DESIGN
(2021)
Review
Biochemistry & Molecular Biology
Jana Yasser Hafez Ali, Amira Mohammed Fitieh, Ismail Hassan Ismail
Summary: This review discusses how the dysregulation of DNA repair pathways in multiple myeloma exacerbates genomic instability and chromosomal abnormalities, leading to disease progression and drug resistance.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Biochemistry & Molecular Biology
Stefano Amente, Giovanni Scala, Barbara Majello, Somaiyeh Azmoun, Helen G. Tempest, Sanjay Premi, Marcus S. Cooke
Summary: Exposure from external and internal environments leads to modifications in genomic DNA, contributing to various diseases. Understanding the impact of damage on cellular function and pathogenesis remains unclear, but mapping DNA adductomics may provide valuable insights.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2021)
Review
Biochemistry & Molecular Biology
Rabia Rasool, Inam Ullah, Bismillah Mubeen, Sultan Alshehri, Syed Sarim Imam, Mohammed M. Ghoneim, Sami I. Alzarea, Fahad A. Al-Abbasi, Bibi Nazia Murtaza, Imran Kazmi, Muhammad Shahid Nadeem
Summary: Breast cancer is a diverse disease caused by mutations and epigenetic aberrations, and studying genomic instability is crucial for personalized treatment and the identification of prognostic markers.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Biochemistry & Molecular Biology
Mengting Chen, Renske Linstra, Marcel A. T. M. van Vugt
Summary: Genomic and chromosomal instability are characteristics of cancer that affect the genetic composition of cancer cells, influencing their behavior and response to treatment. This instability can lead to DNA leakage into the cytoplasm, triggering inflammatory signaling pathways that have pleiotropic effects, including enhanced anti-tumor immunity and potential sensitization of cancer cells to immune checkpoint inhibitors.
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
(2022)
Review
Medicine, Research & Experimental
Adria Hasan, Suroor Fatima Rizvi, Sana Parveen, Snober S. Mir
Summary: Cells may undergo DNA damage due to various stressors, leading to altered cell function and diseases such as cancer. DNA repair mechanisms play a crucial role in maintaining genome stability, with heat shock proteins (HSPs) being key players in this adaptive response. Modulating protein quality control systems like the HSPs network could be a promising strategy for targeting diseases associated with genomic instability, such as cancer.
Review
Oncology
Elisa Taiana, Maria Eugenia Gallo Cantafio, Vanessa Katia Favasuli, Cecilia Bandini, Giuseppe Viglietto, Roberto Piva, Antonino Neri, Nicola Amodio
Summary: Genomic instability (GI) plays a critical role in the pathobiology of multiple myeloma (MM) by promoting the acquisition of tumor hallmarks. Non-coding RNA molecules are emerging as key players in GI pathways in MM, providing new opportunities for therapeutic interventions. The dysregulation of non-coding RNAs in MM adds another layer of complexity to understanding the molecular determinants of GI in this disease.
Article
Cell Biology
Han Bai, Shilin Xia, Lei Zhu, Yan Dong, Chao Liu, Nan Li, Han Liu, Jing Xiao
Summary: Research has found that overexpression of polymerase theta (POLQ) is related to the progression and poor prognosis of salivary adenoid cystic carcinoma (SACC). POLQ plays a role in increasing chromosomal instability and enhancing sensitivity to etoposide. This is achieved by promoting the expression of error-prone alt-NHEJ-related protein PARP1 and downregulating c-NHEJ- and HR-related proteins KU70 and RAD51. The PARP inhibitor olaparib has been shown to suppress SACC growth in the presence of etoposide-induced DNA damage.
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
(2022)
Review
Oncology
Feifei Guo, Lingyu Li, Wang Yang, Ji-fan Hu, Jiuwei Cui
Summary: Genomic instability is a key feature of cancer, potentially promoting tumorigenesis by increasing gene destruction and loss of genome integrity. Studies have shown that long noncoding RNAs play a significant role in regulating genomic stability.
Article
Multidisciplinary Sciences
Franklin Mayca Pozo, Xinran Geng, Ilaria Tamagno, Mark W. Jackson, Ernest G. Heimsath, John A. Hammer, Richard E. Cheney, Youwei Zhang
Summary: MYO10 overexpression in tumors increases genomic instability, induces an inflammatory response, and accelerates tumor growth, while depletion of MYO10 reduces genomic instability and inflammation signaling, slowing down tumor progression. MYO10 promotes tumor progression by inducing genomic instability, which creates an immunogenic environment for immune checkpoint blockades.
Review
Biochemistry & Molecular Biology
Ken-ichi Yoshioka, Rika Kusumoto-Matsuo, Yusuke Matsuno, Masamichi Ishiai
Summary: Genomic instability contributes to cancer development, with repair defects increasing cancer risk. While many cancers develop independently of DNA repair defects, DNA repair systems are crucial for cell survival. Some cancers may compensate for deficiencies in one repair pathway by upregulating other pathways.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Cell Biology
Ming Tang, Emma Bolderson, Kenneth J. O'Byrne, Derek J. Richard
Summary: Hypoxia is associated with poor prognosis in cancer due to enhanced tumor malignancy and therapeutic resistance. The aggressiveness of tumors partially stems from hypoxia-induced genomic instability. Understanding how tumor hypoxia induces genomic instability is crucial for improving cancer therapeutics.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Review
Cell Biology
Francesca Marcon, Simona Giunta, Margherita Bignami
Summary: Satellite DNA sequences are a crucial part of centromeres, which are essential for the accurate segregation of chromosomes during cell division. Due to their complex repetitive structure, satellite DNA can hinder DNA replication and other DNA-based processes, potentially leading to chromosome breakage. In recent years, several DNA repair proteins have been found to interact with and function at centromeres, contributing to the maintenance of their structure and function. While the importance of these repair factors has been demonstrated by chromosome aberrations resulting from their inactivation, their roles in satellite DNA replication and repair are still being explored. Recent studies have also linked specific DNA repair factors at centromeres to age-related increase in chromosomal instability under physiological and pathological conditions.
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
(2024)
Article
Toxicology
Sweta Ghosh, Mayukh Banerjee, Bodduluri Haribabu, Venkatakrishna Rao Jala
Summary: Environmental chemicals like iAs can increase oxidative stress in the body, disrupting gut homeostasis, but gut microbiota are essential to protect against its toxicity, with microbial metabolites such as UroA potentially providing protection against environmental hazards by reducing oxidative stress and enhancing gut barrier function.
ARCHIVES OF TOXICOLOGY
(2022)
Article
Environmental Sciences
Ana P. Ferragut Cardoso, Mayukh Banerjee, Laila Al-Eryani, Mohammed Sayed, Daniel W. Wilkey, Michael L. Merchant, Juw W. Park, J. Christopher States
Summary: Chronic arsenic exposure is linked to increased cancer risk. This study aimed to profile alternative splicing events in human keratinocytes induced by arsenic. Results suggest arsenic exposure may disrupt an alternative splice factor network and induce genome-wide alternative splicing contributing to arsenic-induced carcinogenesis.
ENVIRONMENTAL HEALTH PERSPECTIVES
(2022)
Article
Toxicology
Mayukh Banerjee, Laila Al-Eryani, Sudhir Srivastava, Shesh N. Rai, Jianmin Pan, Theodore S. Kalbfleisch, J. Christopher States
Summary: This study performed longitudinal differential expression analysis of miRNA and mRNA in a HaCaT cell line model of arsenic-induced cutaneous squamous cell carcinoma (cSCC). The results showed differential expression of miRNA and mRNA molecules depending on the time points, with some pathways predicted to be modulated as a function of time or arsenic exposure. The HaCaT model can distinguish between the effects of passaging and chronic arsenic exposure individually.
TOXICOLOGICAL SCIENCES
(2022)
Meeting Abstract
Biochemistry & Molecular Biology
Sweta Ghosh, Mayukh Banerjee, Haribabu Bodduluri, Venkatakrishna Rao Jala
Editorial Material
Toxicology
J. Christopher States, Jeffrey M. Peters
TOXICOLOGICAL SCIENCES
(2022)
Article
Environmental Sciences
Jonathan C. Bastick, Mayukh Banerjee, J. Christopher States
Summary: Inorganic arsenic exposure can displace zinc from zinc fingers of the splice regulator ZRANB2, disrupting its role in the splicing of its target TRA2B. However, zinc supplementation can prevent the disruption of ZRANB2 splice function caused by iAs, suggesting a potential preventive measure against iAs-mediated diseases.
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
(2022)
Article
Pharmacology & Pharmacy
Alexandra N. Nail, Lakynkalina M. McCaffrey, Mayukh Banerjee, Ana P. Ferragut Cardoso, J. Christopher States
Summary: An estimated 220 million people worldwide are chronically exposed to inorganic arsenic (iAs), which can lead to skin lesions and multi-organ cancers. This study suggests that chronic iAs exposure inhibits DNA repair and damage response signaling, leading to error-prone repair pathways and chromosomal instability.
TOXICOLOGY AND APPLIED PHARMACOLOGY
(2022)
Article
Pharmacology & Pharmacy
Mayukh Banerjee, Kavitha Yaddanapudi, J. Christopher States
Summary: This study demonstrates that environmentally relevant exposure to inorganic arsenic (iAs) can disrupt the cell cycle and induce mitotic accumulation of cells. This effect may be mediated by the displacement of zinc from the RING finger subunit of the anaphase promoting complex/cyclosome (ANAPC11), leading to the stabilization of cyclin B1 and securin. Zinc supplementation can prevent this cell cycle disruption caused by iAs exposure.
TOXICOLOGY AND APPLIED PHARMACOLOGY
(2022)
Article
Oncology
David Schweer, Namrata Anand, Abigail Anderson, J. Robert McCorkle, Khaga Neupane, Alexandra N. Nail, Brock Harvey, Kristen S. Hill, Frederick Ueland, Christopher Richards, Jill Kolesar
Summary: Ovarian cancer is a deadly female malignancy characterized by high rates of recurrence and chemotherapy resistance. Tumor-associated macrophages (TAMs) play a significant role in the tumor microenvironment and consist of mostly M2 protumor macrophages that promote chemo-resistance and metastasis. Vesicles engineered from M1 macrophages (MEVs) represent a novel therapeutic approach for converting M2 macrophages to M1-like phenotype macrophages.
FRONTIERS IN ONCOLOGY
(2023)
