PubMed:24121271 JSONTXT 13 Projects

Annnotations TAB TSV DIC JSON TextAE Lectin_function IAV-Glycan

Id Subject Object Predicate Lexical cue
T1 0-103 DRI_Unspecified denotes The retinoblastoma tumor suppressor pathway modulates the invasiveness of ErbB2-positive breast cancer.
T2 104-233 DRI_Background denotes The processes that control the progression of ductal carcinoma in situ (DCIS) to invasive breast cancer remain poorly understood.
T3 234-380 DRI_Outcome denotes Epidermal growth factor receptor 2 (ErbB2) overexpression is common in DCIS, as is disruption of the retinoblastoma tumor suppressor (RB) pathway.
T4 381-484 DRI_Approach denotes Here, we examined the cooperative impact of ErbB2 and RB deregulation on facets of disease progression.
T5 485-721 DRI_Outcome denotes Our studies demonstrate that RB deficiency altered the expression of key molecules needed for proper cellular organization and epithelial cell-cell adhesion as part of a program related to the epithelial-to-mesenchymal transition (EMT).
T6 722-821 DRI_Outcome denotes An increase in the invasive potential of ErbB2-overexpressing cells was observed upon RB depletion.
T7 822-983 DRI_Outcome denotes Further, stable knockdown of RB resulted in invasive lesions in orthotopic xenograft assays, compared with DCIS-like lesions developing from RB-proficient cells.
T8 984-1126 DRI_Outcome denotes Conversely, the invasive phenotype observed in ErbB2-positive cancer models was inhibited through CDK4/6 inhibition in an RB-dependent manner.
T9 1127-1337 DRI_Unspecified denotes Finally, in a cohort of DCIS cases, we show that, although elevated levels of ErbB2 are associated with increased risk of a subsequent DCIS recurrence, it is not associated with progression to invasive disease.
T10 1338-1450 DRI_Background denotes In contrast, RB loss in ErbB2-positive DCIS cases was associated with increased risk for invasive breast cancer.
T11 1451-1674 DRI_Approach denotes Taken together, these data demonstrate a key role for the RB pathway in invasion associated with breast tumor progression, and shed light on the key molecular events that promote the progression of DCIS to invasive disease.