Publications by authors named "Akiko Itaya"
A 68-year-old woman underwent neoadjuvant chemotherapy for left breast cancer(triple negative type), cT2N3cM0, cStage ⅢC, and Bt+Ax(Ⅲ). The pathological diagnosis was ypT1aN2aM0, ypStage ⅢA, ER-, PgR-, HER2 score 1+, Ki- 67 25%. Adjuvant radiotherapy(50 Gy/25 Fr)was then administered, followed by capecitabine as adjuvant chemotherapy.
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- Iliopsoas abscesses (IPAs) linked to bowel obstruction from colon cancer are uncommon, with no established treatment guidelines.
- A 63-year-old man was diagnosed with an IPA and subsequent bowel obstruction after drainage of the abscess; he underwent a hemicolectomy and chemotherapy, but experienced a local recurrence that required further surgical intervention.
- Effective management of IPAs caused by colorectal cancer should employ minimally invasive techniques, considering factors like size and location of the abscess, highlighting the importance of collaboration between gastrointestinal surgeons and oncologists.
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- R-loops, which are structures formed by DNA:RNA hybrids and displaced single-strand DNA, pose a significant risk to genome stability.
- The study reveals that the FANCD2 protein helps lower R-loop levels and interacts with RNA processing factors like hnRNP U and DDX47.
- By facilitating the efficient processing of long RNA transcripts, FANCD2 potentially reduces collisions between transcription and replication, contributing to genome stability during mild replication stress.
The Fanconi anemia (FA) pathway is critically involved in the maintenance of hematopoietic stem cells and the suppression of carcinogenesis. A key FA protein, FANCD2, is monoubiquitinated and accumulates in chromatin in response to DNA interstrand crosslinks (ICLs), where it coordinates DNA repair through mechanisms that are still poorly understood. Here, we report that CtIP protein directly interacts with FANCD2.
View Article and Find Full Text PDFWhen DNA replication is stalled at sites of DNA damage, a cascade of responses is activated in the cell to halt cell cycle progression and promote DNA repair. A pathway initiated by the kinase Ataxia teleangiectasia and Rad3 related (ATR) and its partner ATR interacting protein (ATRIP) plays an important role in this response. The Fanconi anemia (FA) pathway is also activated following genomic stress, and defects in this pathway cause a cancer-prone hematologic disorder in humans.
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