Apobec3b breast cancer. called this into question by showing that breast cancer samples from...

Apobec3b breast cancer. called this into question by showing that breast cancer samples from individuals with germline APOBEC3B deletions showed high levels of mutations consistent with APOBEC-dependent mutagensis. Breast cancer cells can also be exposed to anticancer chemotherapy drugs, such as DNA-damaging platinum-based drugs cisplatin and its analogs (22). Nov 30, 2023 · This is significant because most APOBEC3-positive breast tumors exhibit an intermediate percentage of signature mutations in these broader tetranucleotide motifs, which supports the idea that both APOBEC3A and APOBEC3B contribute in a combinatorial manner to the overall mutation landscape in these tumors. Here, A3B mRNA and May 16, 2025 · Herein, we report that APOBEC3 mutagenesis driven by APOBEC3A (A3A) and APOBEC3B (A3B) facilitates breast cancer evolution independent of treatment exposure, leading to resistance against a Mar 5, 2026 · The study, led by scientists at The Institute of Cancer Research, London, and predominantly funded by Cancer Research UK, but also in collaboration with colleagues in China, uncovers how an enzyme known for generating mutations in cancer, APOBEC3B (A3B), plays a direct role in promoting the growth and survival of a common type of breast cancer Apr 8, 2024 · Initially observed in breast cancers and subsequently found in numerous cancer types including but not limited to bladder, breast, cervical, esophagus, myeloma, head/neck and lung, C>T/G/A mutations resulting from APOBEC3 polynucleotide deoxycytidine deaminases targeting of T C W motifs (corresponding to Sanger mutational signatures SBS2 and Mar 28, 2023 · In breast cancer, for example, PTEN depletion and HER2 amplification have been shown to induce replication stress and increase APOBEC3B activity in vitro [90]. Second, APOBEC3B depletion in an ER + breast cancer cell line results in prolonged tamoxifen responses in murine xenograft experiments. We observe evidence of APOBEC3-mediated subclonal mutagenesis Its expression is up-regulated by - interferon. APOBEC3B has been implicated in the development of several diseases. In lung cancer, the loss of FHIT1 —a common genetic alteration that causes replication stress—was associated with a higher APOBEC3-induced mutation burden [53]. To investigate mechanisms of endogenous APOBEC3 mutagenesis, we deleted APOBEC3A and APOBEC3B from a panel of cancer cell lines that acquire APOBEC3-associated mutations over time 4 (Extended Data Mar 5, 2026 · The study, led by scientists at The Institute of Cancer Research, London, and predominantly funded by Cancer Research UK, but also in collaboration with colleagues in China, uncovers how an enzyme known for generating mutations in cancer, APOBEC3B (A3B), plays a direct role in promoting the growth and survival of a common type of breast cancer Aug 10, 2015 · However, results of a recent paper by Serena Nik-Zainal et al. As a potential continuous source of genetic aberrations in breast cancer, we hypothesized that APOBEC3B overexpression may accelerate cancer progression and lead to poor clinical outcomes. Oct 7, 2016 · First, APOBEC3B levels in primary estrogen receptor–positive (ER +) breast tumors inversely correlate with the clinical benefit of tamoxifen in the treatment of metastatic ER + disease. . It has been associated with carcinogenesis, particularly in breast cancer. A3B gene expression is increased in many cancers, but its upstream dr … We would like to show you a description here but the site won’t allow us. Overall, the results of the present study demonstrated that APOBEC3B mRNA and protein expression levels presented different prognostic values in the survival of patients with breast cancer. Its expression is up-regulated by - interferon. APOBEC3B (A3B) is aberrantly overexpressed in a subset of breast cancers, where it associates with advanced disease, poor prognosis, and treatment resistance, yet the causes of A3B dysregulation in breast cancer remain unclear. Elevated expression of APOBEC3B in cancer cells can lead to increased mutagenesis and genomic instability. However, multiple recent independent studies instead point to APOBEC3A as the primary driver of APOBEC3 mutagenesis. Precisely when APOBEC3 expression is induced during cancer development remains to be defined. Feb 6, 2013 · The DNA cytosine deaminase APOBEC3B is shown to be overexpressed and highly active in most breast cancers; deamination by APOBEC3B could serve as an endogenous, continual source of DNA damage High APOBEC3B mRNA expression was associated with poor relapse-free survival rate, overall survival rate and distant metastasis-free survival rate in patients with breast cancer, particularly for the Luminal A subtype. Here we show that specific APOBEC3 genes are upregulated in breast ductal carcinoma in situ, and in preinvasive lung cancer lesions coincident with cellular proliferation. To evaluate the effects of these exposures, we measured A3A and A3B expression in ER+ and ER− breast cancer cell lines treated with estradiol and/or cisplatin. APOBEC3 enzymes are cytosine deaminases implicated in cancer. APOBEC3B is frequently highly expressed in tumors, and its expression correlates with APOBEC3-linked mutational signature burdens in certain cancer types, leading to its initial designation as the predominant APOBEC3 mutator5,8. APOBEC3B mRNA expression was also indicated to be associated with the immune status of patients with breast cancer. Mar 3, 2015 · Genomic sequencing studies of breast and other cancers have identified patterns of mutations that have been attributed to the endogenous mutator activity of APOBEC3B (A3B), a member of the AID/APOBEC family of cytidine deaminases. csqgp cytwqc nphhq zzmhxpk amj eipxxnz bdjzs xfqx lviijd aexoe