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Potential Role of the Fragile Histidine Triad in Cancer Evo-Dev

CANCERS (2023)

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Article Biochemistry & Molecular Biology

Spatiotemporal view of malignant histogenesis and macroevolution via formation of polyploid giant cancer cells

Xiaoran Li et al.

Summary: By studying the dynamics of different cellular components during the formation of high-grade serous carcinoma organoids, we discovered that polyploid giant cancer cells (PGCCs) can develop through various modes of nuclear replication. PGCCs undergo processes like asymmetric mitosis, endoreplication, multipolar endomitosis, nuclear fusion, and karyokinesis without cytokinesis. This leads to an increase in nuclear contents and heterogeneity, resulting in the formation of complex tissue structures. These findings suggest that PGCCs play a central role in malignant histogenesis, intratumoral heterogeneity, immune escape, and macroevolution.

ONCOGENE (2023)

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Article Oncology

Transcriptional repression and apoptosis influence the effect of APOBEC3A/3B functional polymorphisms on biliary tract cancer risk

Wenbin Liu et al.

Summary: APOBEC3-related mutations are associated with biliary tract cancers. The functional polymorphisms of APOBEC3A and APOBEC3B play important roles in the development of cholangiocarcinoma and gallbladder cancer. TNF-alpha regulates the levels of APOBEC3A and APOBEC3B by affecting transcriptional repressors and promoter accessibility.

INTERNATIONAL JOURNAL OF CANCER (2022)

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Article Multidisciplinary Sciences

Mapping clustered mutations in cancer reveals APOBEC3 mutagenesis of ecDNA

Erik N. Bergstrom et al.

Summary: This study provides a comprehensive characterization of clustered mutations and small insertions and deletions in cancer genomes. The results show that clustered mutations are enriched in driver genes and associated with differential gene expression and overall survival. Different mutational processes contribute to clustered insertions and deletions, including specific signatures in tobacco smokers and homologous-recombination-deficient cancers. APOBEC3 plays a significant role in clustered substitutions, although only a small percentage matches APOBEC3 patterns. The study also reveals the associations between the activation-induced deaminase (AID) and APOBEC3 family of deaminases with kataegis (longer strand-coordinated events).

NATURE (2022)

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Article Oncology

The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma

Rui Pu et al.

Summary: The study aimed to explore the mechanism by which hepatitis B virus X mutations increase the occurrence of hepatocellular carcinoma (HCC) and identify potential therapeutic targets. The results showed that M3-HBx and Ct-HBx mutants had a higher HCC incidence compared to wild-type HBx. M3-HBx had a stronger capacity to upregulate inflammatory cytokines and promote cell proliferation in HepG2 and HeLa cells. Plasminogen activator inhibitor-1 (PAI1) and cell division cycle 20 (CDC20) were identified as novel effectors, and their expression was significantly upregulated by M3-HBx and Ct-HBx in both cells and mouse livers. Silencing PAI1 attenuated the effects of M3-HBx and Ct-HBx on cell growth. PAI1 could be a promising prognostic biomarker and therapeutic target in HBV-related HCC.

FRONTIERS IN ONCOLOGY (2022)

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Review Cell Biology

Review DNA replication: the recombination connection

Esther A. Epum et al.

Summary: Failure to complete DNA replication can lead to genome instability and cancer. Recent studies have shown that replication at common fragile sites occurs late in the cell cycle, particularly during mitosis, which is closely related to other cancer-promoting phenomena.

TRENDS IN CELL BIOLOGY (2022)

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Article Oncology

Genome chaos: Creating new genomic information essential for cancer macroevolution

Julie Heng et al.

Summary: Traditional cancer research has focused on studying individual molecular mechanisms that contribute to the development of cancer. However, due to the genomic and non-genomic heterogeneity at multiple levels, many molecular mechanisms have been identified with limited clinical predictability. Therefore, it is important to find new concepts that can unify these diverse mechanisms and develop better strategies for understanding and treating cancer.

SEMINARS IN CANCER BIOLOGY (2022)

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Article Multidisciplinary Sciences

Mechanisms of APOBEC3 mutagenesis in human cancer cells

Mia Petljak et al.

Summary: The study reveals that endogenous APOBEC3 deaminases generate prevalent mutational signatures in human cancer cells, with APOBEC3A identified as the main driver of these mutations. APOBEC3B can restrain APOBEC3A-dependent mutagenesis to some extent while contributing its own smaller mutation burdens, and the mechanisms translating APOBEC3 activities into distinct mutational signatures are dissected.

NATURE (2022)

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Article Oncology

HBV preS Mutations Promote Hepatocarcinogenesis by Inducing Endoplasmic Reticulum Stress and Upregulating Inflammatory Signaling

Wenbin Liu et al.

Summary: Mutations in the preS region of hepatitis B virus (HBV) are associated with an increased risk of hepatocellular carcinoma (HCC). In this study, several specific preS mutations were found to significantly increase the risk of HCC by promoting inflammation and altering gene expression in inflammation- and metabolism-related pathways. These findings highlight the importance of monitoring these mutations for HCC prevention.

CANCERS (2022)

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APOBEC-Induced Mutagenesis in Cancer

Tony M. Mertz et al.

Summary: The occurrence and development of cancer are closely related to mutations, and dysregulated activity of APOBECs can lead to mutations. The study of mutation signatures helps us understand the patterns and processes of mutations. In humans, APOBEC-generated genetic heterogeneity plays an important role in cancer development, metastasis, and resistance to therapy.

ANNUAL REVIEW OF GENETICS (2022)

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Article Immunology

Transcriptomic FHITlow/pHER2high signature as a predictive factor of outcome and immunotherapy response in non-small cell lung cancer

Audrey Brisebarre et al.

Summary: In recent decades, the development of immunotherapy and targeted therapies has greatly improved the outcome of non-small cell lung cancer (NSCLC) patients. However, new biomarkers are still needed for accurate stratification and personalized management of NSCLC patients. This study identified the transcriptomic signature of NSCLC patients with FHITlow/pHER2high phenotype, which was associated with cell proliferation, metabolism, metastasis, and decreased immune response. This signature was also found to be associated with larger tumor size, lymph node involvement, and late TNM stages. Additionally, it was an independent predictor of overall survival and poor response to immune checkpoint inhibitors in NSCLC patients.

FRONTIERS IN IMMUNOLOGY (2022)

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Article Oncology

Questions to guide cancer evolution as a framework for furthering progress in cancer research and sustainable patient outcomes

Jason A. Somarelli et al.

Summary: In the field of cancer, there are major advances and successes, but also remaining short-comings and significant challenges. Despite progress in cancer research, most patients with metastatic cancer still suffer and have poor outcomes. There have been staggering scientific discoveries, but translating these into improved diagnostic, prognostic, and therapeutic interventions is frustratingly slow.

MEDICAL ONCOLOGY (2022)

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Glycosylase base editors enable C-to-A and C-to-G base changes

Dongdong Zhao et al.

Summary: The study introduces novel glycosylase base editors (GBEs) that can induce C-to-A and C-to-G transversions in Escherichia coli and mammalian cells, respectively. The new editors exhibit high editing specificity and efficiency, making them potential tools for targeting G/C disease-causing mutations.

NATURE BIOTECHNOLOGY (2021)

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Review Medicine, Research & Experimental

EMT, cancer stem cells and autophagy; The three main axes of metastasis

Ghader Babaei et al.

Summary: Epithelial-mesenchymal transition (EMT) and Cancer stem-like cells (CSCs) are major factors contributing to cancer cell metastasis. Autophagy has recently gained attention, playing a dual role in cancer cell development depending on cancer type, tissue, and stage. Studies show different signaling pathways are involved in cancer stem cells, autophagy, and EMT. Investigating effective signaling pathways in all three processes could help determine appropriate therapeutic goals.

BIOMEDICINE & PHARMACOTHERAPY (2021)

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A Positive Feedback Loop of AKR1C3-Mediated Activation of NF-κB and STAT3 Facilitates Proliferation and Metastasis in Hepatocellular Carcinoma

Qingqing Zhou et al.

Summary: AKR1C3 is significantly upregulated in hepatocellular carcinoma (HCC) and associated with poor survival. Through the NF-kappa B/STAT3 signaling loop, AKR1C3 promotes cell proliferation and metastasis, suggesting it could be a promising therapeutic target in HCC.

CANCER RESEARCH (2021)

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STAT3 phosphorylation at Ser727 and Tyr705 differentially regulates the EMT-MET switch and cancer metastasis

Wei-Hsin Lin et al.

Summary: The research suggests that BM-MSC plays a crucial role in cancer cell dissemination and metastasis in lung cancer models. BM-MSC-induced signaling triggers early dissemination of cancer stem cells and promotes proliferation at secondary sites. Additionally, intercellular signaling regulates the switch between migration and proliferation.

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Genomic Instability and Cancer Risk Associated with Erroneous DNA Repair

Ken-ichi Yoshioka et al.

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.

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Single-stranded DNA binding proteins influence APOBEC3A substrate preference

Amber L. Brown et al.

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Cancer Evo-Dev: A Theory of Inflammation-Induced Oncogenesis

Wenbin Liu et al.

Summary: Chronic inflammation plays a key role in cancer development by interacting with genetic predispositions, environmental exposures, and inflammation-related carcinogenic factors. Interventions that reduce inflammation levels, such as exercising and anti-inflammatory medications, can lower the risk of cancer occurrence and recurrence. The Cancer Evo-Dev theory helps understand how inflammation promotes cancer development and provides a foundation for effective prophylaxis and targeted therapy of various cancers.

FRONTIERS IN IMMUNOLOGY (2021)

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Review Biochemistry & Molecular Biology

Cancer as a form of life: Musings of the cancer and evolution symposium

Doru Paul

Summary: Advanced cancer remains a major challenge in oncology, with high mortality rates despite technological advancements. Funding and efforts towards cancer prevention and early detection are lacking, contributing to the high incidence and mortality of advanced cancer. Viewing cancer as a form of life may provide a fresh perspective on the complex process.

PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY (2021)

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Article Oncology

Induction of APOBEC3 Exacerbates DNA Replication Stress and Chromosomal Instability in Early Breast and Lung Cancer Evolution

Subramanian Venkatesan et al.

Summary: The study reveals that APOBEC3 genes are upregulated in breast and lung preinvasive lesions, and APOBEC3B exacerbates DNA replication stress to promote cellular diversity and chromosomal instability for early selection in cancer evolution.

CANCER DISCOVERY (2021)

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Article Biochemistry & Molecular Biology

Locus-specific transcription silencing at the FHIT gene suppresses replication stress-induced copy number variant formation and associated replication delay

So Hae Park et al.

Summary: The impaired replication progression leads to the formation of de novo copy number variants (CNVs) at common fragile sites (CFSs). The study showed that large gene transcription is a determining factor in replication stress-induced genomic instability, supporting the model that CNV hotspots mainly result from the transcription-dependent passage of unreplicated DNA into mitosis.

NUCLEIC ACIDS RESEARCH (2021)

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Review Cell Biology

The Replication Stress Response on a Narrow Path Between Genomic Instability and Inflammation

Herve Techer et al.

Summary: The replication process in eukaryotic cells is crucial for generating two identical copies of the genome during the S phase, involving the action of replisomes at replication forks. New findings suggest a connection between stalled fork processing and the activation of the cGAS-STING pathway, potentially leading to an inflammatory response with both positive and negative impacts on stressed cells. These discoveries have significant implications for interferonopathies and cancer treatment.

FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY (2021)

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Article Biotechnology & Applied Microbiology

Glycosylase base editors enable C-to-A and C-to-G base changes

Dongdong Zhao et al.

Summary: This study presents new glycosylase base editors (GBEs) that can induce C-to-A and C-to-G transversions in bacteria and mammalian cells, respectively. The GBEs can serve as a complement to existing adenine and cytidine base editors (ABE and CBE) and have the potential to target G/C disease-causing mutations.

NATURE BIOTECHNOLOGY (2021)

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Article Biochemistry & Molecular Biology

The epicenter of chromosomal fragility of Fra14A2, the mouse ortholog of human FRA3B common fragile site, is largely attached to the nuclear matrix in lymphocytes but not in other cell types that do not express such a fragility

Rolando Guadarrama-Ponce et al.

JOURNAL OF CELLULAR BIOCHEMISTRY (2020)

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CA-A CANCER JOURNAL FOR CLINICIANS (2020)

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Esther Rheinbay et al.

NATURE (2020)

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The repertoire of mutational signatures in human cancer

Ludmil B. Alexandrov et al.

NATURE (2020)

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Regulatory R-loops as facilitators of gene expression and genome stability

Christof Niehrs et al.

NATURE REVIEWS MOLECULAR CELL BIOLOGY (2020)

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Suppression of PKC delta/NF-kappa B Signaling and Apoptosis Induction through Extrinsic/Intrinsic Pathways Are Associated with Magnolol-Inhibited Tumor Progression in Colorectal Cancer In Vitro and In Vivo

Chun-Min Su et al.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2020)

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Repair pathway choice for double-strand breaks

Yixi Xu et al.

GUARDIANS OF THE GENOME: DNA DAMAGE AND REPAIR (2020)

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Genome-wide high-resolution mapping of mitotic DNA synthesis sites and common fragile sites by direct sequencing

Fang Ji et al.

CELL RESEARCH (2020)

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3D genome organization contributes to genome instability at fragile sites

Dan Sarni et al.

NATURE COMMUNICATIONS (2020)

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FHIT, a Novel Modifier Gene in Pulmonary Arterial Hypertension

Svenja Dannewitz Prosseda et al.

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2019)

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Mechanisms shaping the mutational landscape of the FRA3B/FHIT-deficient cancer genome

Joshua C. Saldivar et al.

GENES CHROMOSOMES & CANCER (2019)

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High-resolution genomic alterations in Barrett's metaplasia of patients who progress to esophageal dysplasia and adenocarcinoma

Jorge L. Sepulveda et al.

INTERNATIONAL JOURNAL OF CANCER (2019)

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Genetic Polymorphisms Predisposing the Interleukin 6-Induced APOBEC3B-UNG Imbalance Increase HCC Risk via Promoting the Generation of APOBEC-Signature HBV Mutations

Wenbin Liu et al.

CLINICAL CANCER RESEARCH (2019)

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Inflammation and Cancer: Triggers, Mechanisms, and Consequences

Florian R. Greten et al.

IMMUNITY (2019)

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R Loops: From Physiological to Pathological Roles

Tatiana Garcia-Muse et al.

CELL (2019)

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The deaminase APOBEC3B triggers the death of cells lacking uracil DNA glycosylase

Artur A. Serebrenik et al.

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2019)

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State-of-the-art strategies for targeting the DNA damage response in cancer

Patrick G. Pilie et al.

NATURE REVIEWS CLINICAL ONCOLOGY (2019)

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Do FHIT gene alterations play a role in human solid tumors?

Lisiane Silveira Zavalhia et al.

ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2018)

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Lifetime exposure to ambient air pollution and methylation of tumor suppressor genes in breast tumors

Catherine L. Callahan et al.

ENVIRONMENTAL RESEARCH (2018)

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Modeling the Embrace of a Mutator: APOBEC Selection of Nucleic Acid Ligands

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TRENDS IN BIOCHEMICAL SCIENCES (2018)

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The Multifaceted Role of Chromosomal Instability in Cancer and Its Microenvironment

Samuel F. Bakhoum et al.

CELL (2018)

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Myeloid-Derived Suppressor Cells Produce IL-10 to Elicit DNMT3b-Dependent IRF8 Silencing to Promote Colitis-Associated Colon Tumorigenesis

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CELL REPORTS (2018)

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Mutation Signatures Including APOBEC in Cancer Cell Lines

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JNCI CANCER SPECTRUM (2018)

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Correlation of gene expression and associated mutation profiles of APOBEC3A, APOBEC3B, REV1, UNG, and FHIT with chemosensitivity of cancer cell lines to drug treatment

Suleyman Vural et al.

HUMAN GENOMICS (2018)

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Meggy Suarez-Carmona et al.

MOLECULAR ONCOLOGY (2017)

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Fhit down-regulation is an early event in pancreatic carcinogenesis

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VIRCHOWS ARCHIV (2017)

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High expression of PD-1 ligands is associated with kataegis mutational signature and APOBEC3 alterations

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Universal Patterns of Selection in Cancer and Somatic Tissues

Inigo Martincorena et al.

CELL (2017)

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WNT/β-Catenin Directs Self-Renewal Symmetric Cell Division of hTERThigh Prostate Cancer Stem Cells

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CANCER RESEARCH (2017)

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Exome-wide single-base substitutions in tissues and derived cell lines of the constitutive Fhit knockout mouse

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CANCER SCIENCE (2016)

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Fragile Genes That Are Frequently Altered in Cancer: Players Not Passengers

Jenna R. Karras et al.

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FHIT promoter methylation status, low protein and high mRNA levels in patients with non-small cell lung cancer

Karolina H. Czarnecka et al.

INTERNATIONAL JOURNAL OF ONCOLOGY (2016)

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The APOBEC Protein Family: United by Structure, Divergent in Function

Jason D. Salter et al.

TRENDS IN BIOCHEMICAL SCIENCES (2016)

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Kai Ma et al.

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Sheroy Minocherhomji et al.

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An APOBEC3A hypermutation signature is distinguishable from the signature of background mutagenesis by APOBEC3B in human cancers

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Inigo Martincorena et al.

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c-Myc suppresses microRNA-29b to promote tumor aggressiveness and poor outcomes in non-small cell lung cancer by targeting FHIT

D-W Wu et al.

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FHIT loss-induced DNA damage creates optimal APOBEC substrates: Insights into APOBEC-mediated mutagenesis

Catherine E. Waters et al.

ONCOTARGET (2015)

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Effect of functional nuclear factor-kappaB genetic polymorphisms on hepatitis B virus persistence and their interactions with viral mutations on the risk of hepatocellular carcinoma

Q. Zhang et al.

ANNALS OF ONCOLOGY (2014)

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Human cytidine deaminases facilitate hepatitis B virus evolution and link inflammation and hepatocellular carcinoma

Yang Deng et al.

CANCER LETTERS (2014)

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Very large common fragile site genes and their potential role in cancer development

Ge Gao et al.

CELLULAR AND MOLECULAR LIFE SCIENCES (2014)

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The FHIT gene product: tumor suppressor and genome caretaker

Catherine E. Waters et al.

CELLULAR AND MOLECULAR LIFE SCIENCES (2014)

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Fhit Regulates EMT Targets through an EGFR/Src/ERK/Slug Signaling Axis in Human Bronchial Cells

Audrey Joannes et al.

MOLECULAR CANCER RESEARCH (2014)

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Article Genetics & Heredity

FHIT Suppresses Epithelial-Mesenchymal Transition (EMT) and Metastasis in Lung Cancer through Modulation of MicroRNAs

Sung-Suk Suh et al.

PLOS GENETICS (2014)

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FISH comets show that the salvage enzyme TK1 contributes to gene-specific DNA repair

Katherine A. McAllister et al.

FRONTIERS IN GENETICS (2014)

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Replicative Stress and the FHIT Gene: Roles in Tumor Suppression, Genome Stability and Prevention of Carcinogenesis

Jenna Karras et al.

CANCERS (2014)

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Chromosomal instability (CIN): what it is and why it is crucial to cancer evolution

Henry H. Heng et al.

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Karyotype Heterogeneity and Unclassified Chromosomal Abnormalities

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Genetic instability of the tumor suppressor gene FHIT in normal human cells

Elisa Palumbo et al.

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Common Chromosome Fragile Sites in Human and Murine Epithelial Cells and FHIT/FRA3B Loss-Induced Global Genome Instability

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APOBEC3B is an enzymatic source of mutation in breast cancer

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MicroRNA miR-491-5p Targeting both TP53 and Bcl-XL Induces Cell Apoptosis in SW1990 Pancreatic Cancer Cells through Mitochondria Mediated Pathway

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MOLECULES (2012)

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Initiation of Genome Instability and Preneoplastic Processes through Loss of Fhit Expression

Joshua C. Saldivar et al.

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Nucleotide Deficiency Promotes Genomic Instability in Early Stages of Cancer Development

Assaf C. Bester et al.

CELL (2011)

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FHIT Gene and Flanking Region on Chromosome 3p are Subjected to Extensive Allelic Loss in Egyptian Breast Cancer Patients

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Intramitochondrial calcium regulation by the FHIT gene product sensitizes to apoptosis

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Jie Cao et al.

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Stochastic cancer progression driven by non-clonal chromosome aberrations

Henry H. Q. Heng et al.

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Loss of fragile histidine triad gene expression in advanced lung cancer is consequent to allelic loss at 3p14 locus and promoter methylation

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