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Change in HER2 (ERBB2) gene status after taxane-based chemotherapy for breast cancer: polyploidization can lead to diagnostic pitfalls with potential impact for clinical management.

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TLDR
A HER2 genetic examination by fluorescence in situ hybridization (FISH) of invasive breast cancers before and after taxane treatment found Thirty of 344 patients whose tumors were initially HER2-negative were found by FISH to have supernumerary HER2 gene copies after neoadjuvant chemotherapy.
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This article is published in Cancer Genetics and Cytogenetics.The article was published on 2013-01-01. It has received 30 citations till now. The article focuses on the topics: Breast cancer & Primary tumor.

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Immunological Effects of Conventional Chemotherapy and Targeted Anticancer Agents.

TL;DR: The tremendous clinical success of checkpoint blockers illustrates the potential of reestablishing latent immunosurveillance for cancer therapy, and their in-depth comprehension will facilitate the design of novel combinatorial regimens with improved clinical efficacy.
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Linking cellular stress responses to systemic homeostasis

TL;DR: Cellular stress responses primarily serve to rectify stress-associated damage, but these responses are also coupled with the generation of various signals that are transmitted to the cellular microenvironments or even across tissues, which generally supports the maintenance of systemic homeostasis but can also result in pathology.
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Releasing Pressure in Tumors: What Do We Know So Far and Where Do We Go from Here? A Review

TL;DR: The methods to reduce tumor pressure that may open up new avenues in cancer treatment are explored, including irradiation, hyperbaric oxygen therapy, hyper- or hypothermic therapy, and photodynamic therapy.
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Pertuzumab plus Trastuzumab plus Docetaxel for Metastatic Breast Cancer

TL;DR: The combination of pertuzumab plus trastuzumAB plus docetaxel, when used as first-line treatment for HER2-positive metastatic breast cancer, significantly prolonged progression-free survival, with no increase in cardiac toxic effects.
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Mitotic catastrophe: a mechanism for avoiding genomic instability

TL;DR: The disruption of mitotic catastrophe precipitates tumorigenesis and cancer progression, and its induction constitutes a therapeutic endpoint.
Journal ArticleDOI

Evidence for Replicative Repair of DNA Double-Strand Breaks Leading to Oncogenic Translocation and Gene Amplification

TL;DR: Mice deficient in both a nonhomologous end joining (NHEJ) DNA repair protein and the p53 tumor suppressor develop lymphomas at an early age harboring amplification of an IgH/c-myc fusion, report that these chromosomal rearrangements are initiated by a recombination activating gene (RAG)-induced DNA cleavage.
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