HiTIN: Hierarchy-aware Tree Isomorphism Network for Hierarchical Text Classification

Hierarchical text classification (HTC) is a challenging subtask of multi-label classification as the labels form a complex hierarchical structure. Existing dual-encoder methods in HTC achieve weak performance gains with huge memory overheads and their structure encoders heavily rely on domain knowledge. Under such observation, we tend to investigate the feasibility of a memory-friendly model with strong generalization capability that could boost the performance of HTC without prior statistics or label semantics. In this paper, we propose Hierarchy-aware Tree Isomorphism Network (HiTIN) to enhance the text representations with only syntactic information of the label hierarchy. Specifically, we convert the label hierarchy into an unweighted tree structure, termed coding tree, with the guidance of structural entropy. Then we design a structure encoder to incorporate hierarchy-aware information in the coding tree into text representations. Besides the text encoder, HiTIN only contains a few multi-layer perceptions and linear transformations, which greatly saves memory. We conduct experiments on three commonly used datasets and the results demonstrate that HiTIN could achieve better test performance and less memory consumption than state-of-the-art (SOTA) methods.Comment: Accepted by ACL'2

BACH1 is critical for homologous recombination and appears to be the Fanconi anemia gene product FANCJ

SummaryWe showed in this study that cells deficient of the BRCA1-associated BACH1 helicase, also known as BRIP1, failed to elicit homologous recombination (HR) after DNA double-stranded breaks (DSBs). BACH1-deficient cells were also sensitive to mitomycin C (MMC) and underwent MMC-induced chromosome instability. Moreover, we identified a homozygous nonsense mutation in BACH1 in a FA-J patient-derived cell line and could not detect BACH1 protein in this cell line. Expression of wild-type BACH1 in this cell line reduced the accumulation of cells at G2/M phases following exposure to DNA crosslinkers, a characteristic of Fanconi anemia (FA) cells. These results support the conclusion that BACH1 is FANCJ

Interface magnetic and electrical properties of CoFeB /InAs heterostructures

Amorphous magnetic CoFeB ultrathin films have been synthesized on the narrow band gap semiconductor InAs(100) surface, and the nature of the interface magnetic anisotropy and electrical contact has been studied. Angle-dependent hysteresis loops reveal that the films have an in-plane uniaxial magnetic anisotropy (UMA) with the easy axis along the InAs [0-11] crystal direction. The UMA was found to be dependent on the annealing temperatures of the substrates, which indicates the significant role of the Fe, Co-As bonding at the interface related to the surface condition of the InAs(100). I-V measurements show an ohmic contact interface between the CoFeB films and the InAs substrates, which is not affected by the surface condition of the InAs (100)

Targeting Radioresistant Breast Cancer Cells by Single Agent CHK1 Inhibitor via Enhancing Replication Stress

Radiotherapy (RT) remains a standard therapeutic modality for breast cancer patients. However, intrinsic or acquired resistance limits the efficacy of RT. Here, we demonstrate that CHK1 inhibitor AZD7762 alone significantly inhibited the growth of radioresistant breast cancer cells (RBCC). Given the critical role of ATR/CHK1 signaling in suppressing oncogene-induced replication stress (RS), we hypothesize that CHK1 inhibition leads to the specific killing for RBCC due to its abrogation in the suppression of RS induced by oncogenes. In agreement, the expression of oncogenes c-Myc/CDC25A/c-Src/H-ras/E2F1 and DNA damage response (DDR) proteins ATR/CHK1/BRCA1/CtIP were elevated in RBCC. AZD7762 exposure led to significantly higher levels of RS in RBCC, compared to the parental cells. The mechanisms by which CHK1 inhibition led to specific increase of RS in RBCC were related to the interruptions in the replication fork dynamics and the homologous recombination (HR). In summary, RBCC activate oncogenic pathways and thus depend upon mechanisms controlled by CHK1 signaling to maintain RS under control for survival. Our study provided the first example where upregulating RS by CHK1 inhibitor contributes to the specific killing of RBCC, and highlight the importance of the CHK1 as a potential target for treatment of radioresistant cancer cells

Targeting Radioresistant Breast Cancer Cells by Single Agent CHK1 Inhibitor via Enhancing Replication Stress

Radiotherapy (RT) remains a standard therapeutic modality for breast cancer patients. However, intrinsic or acquired resistance limits the efficacy of RT. Here, we demonstrate that CHK1 inhibitor AZD7762 alone significantly inhibited the growth of radioresistant breast cancer cells (RBCC). Given the critical role of ATR/CHK1 signaling in suppressing oncogene-induced replication stress (RS), we hypothesize that CHK1 inhibition leads to the specific killing for RBCC due to its abrogation in the suppression of RS induced by oncogenes. In agreement, the expression of oncogenes c-Myc/CDC25A/c-Src/H-ras/E2F1 and DNA damage response (DDR) proteins ATR/CHK1/BRCA1/CtIP were elevated in RBCC. AZD7762 exposure led to significantly higher levels of RS in RBCC, compared to the parental cells. The mechanisms by which CHK1 inhibition led to specific increase of RS in RBCC were related to the interruptions in the replication fork dynamics and the homologous recombination (HR). In summary, RBCC activate oncogenic pathways and thus depend upon mechanisms controlled by CHK1 signaling to maintain RS under control for survival. Our study provided the first example where upregulating RS by CHK1 inhibitor contributes to the specific killing of RBCC, and highlight the importance of the CHK1 as a potential target for treatment of radioresistant cancer cells