p ret y905 (Cell Signaling Technology Inc)
Structured Review

P Ret Y905, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 103 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ret+tyr905+p+ret/Phospho-Ret+(Tyr905)+Antibody/bio_rxiv__2025__10__07__680986-57-5-7
Average 94 stars, based on 103 article reviews
Images
1) Product Images from "RET Receptor Tyrosine Kinase Promotes Breast Cancer Metastasis to the Brain and RET Inhibitors Pralsetinib and Selpercatinib Suppress Breast Cancer Brain Metastases"
Article Title: RET Receptor Tyrosine Kinase Promotes Breast Cancer Metastasis to the Brain and RET Inhibitors Pralsetinib and Selpercatinib Suppress Breast Cancer Brain Metastases
Journal: bioRxiv
doi: 10.1101/2025.10.07.680986
Figure Legend Snippet: (A) RET pathway activation scores between breast cancer patients with no metastases vs. brain metastases using GEO breast cancer datasets (GSE2034, GSE2603, GSE5327, GSE12276, GSE14020). An unpaired, two-tailed t-test was used in panel (A). (B) Pearson correlation analysis using GEO correlating RET activation signatures to a breast-to-brain metastasis signature. (C) Using the Kaplan-Meier analysis, log-rank analyses, GEO datasets, and the RET activation signatures, 672 breast cancer patients were stratified into two groups, either a high or low RET pathway activation for overall metastasis-free survival. Median of overall metastasis-free survival times are indicated in months (N=672). (D) High versus low RET activation scores were analyzed for brain metastasis-free survival (N = 318). (E) IHC staining of p-RET (Y905) expression levels in 15 matched pairs of primary breast tumors and their corresponding BCBM samples either luminal, HER2-enriched, or TNBC subtypes (20X images presented). (F) H-score quantification of p-RET (Y905) positivity, presented as a ladder plot (N=15). A paired, two-tailed t-test was used.
Techniques Used: Activation Assay, Two Tailed Test, Immunohistochemistry, Expressing
Figure Legend Snippet: (A) Schematic of intracranial mouse model. 6–7-week-old athymic nude mice were intracranially inoculated with luciferase-expressing MDA-MB-231-RET cells (N=12) or MDA-MB-231-Ctrl cells (N=11). Mice were imaged twice weekly to monitor tumor formation and growth. At the study endpoint (Day 28), mice were euthanized, and organs were collected for ex vivo analyses. (B) Bi-weekly average brain tumor burden per group throughout the study, assessed by BLI (top). Representative BLI images from Day 28 (bottom). (C) Quantification of ex vivo BLI of brains (top). Representative BLI images of ex vivo brain (bottom). (D) IHC staining of p-RET (Y905) and Ki-67 expression levels in brain tumors (scale bar 100µm). (E) H-score quantification of p-RET (Y905) positivity and Ki-67 positivity. (F) Tumor retention rate following inoculation. (H) Average weight of mice in each group. Two-way ANOVAs were used to calculate p-values with a mixed-effects analysis for panels (B and G). An unpaired, two-tailed t-test was used in panels (C and E).
Techniques Used: Luciferase, Expressing, Ex Vivo, Immunohistochemistry, Two Tailed Test
Figure Legend Snippet: RET inhibitors reduce cell viability, suppress downstream RET signaling, and induce apoptosis in brain-tropic breast cancer cells in vitro . The effect of treatment with (A) pralsetinib or (B) selpercatinib on cell viability of brain-tropic breast cancer cell lines (N=5). (C) Western blot analysis to determine protein expression of p-RET (Y905), p-STAT3 (Y705), total RET, total STAT3, p-ERK (T202/Y204), and total ERK ½ following treatment with prasetinib (left) or selpercatinib (right). Vinculin serves as high molecular weight loading control, and β-actin serves as a low molecular weight loading control. Annexin V/PI flow cytometry co-staining of (D) SKBRM cells, (E) CN34-BrM cells, and (F) MDA-MB-231-BrM cells treated with pralsetinib or selpercatinib (quantification on the left and representative images on the right) (N=5). Western blot analysis of cleaved PARP and full-length PARP in brain-tropic breast cancer cells following treatment with (G) pralsetinib, or (H) selpercatinib. An unpaired, two-tailed t-test between vehicle and treatment was used in panels (A,B,D,E and F).
Techniques Used: In Vitro, Western Blot, Expressing, High Molecular Weight, Control, Molecular Weight, Flow Cytometry, Staining, Two Tailed Test
Figure Legend Snippet: Systemic administration of pralsetinib selectively reduces established brain metastatic tumor growth and proliferation in vivo . (A) Schematic of intracranial inoculation mouse model. 6–7-week-old athymic nude mice (N=10/group) were inoculated with luciferase-expressing MDA-MB-231-BrM cells. Mice received their first treatment 2 days after inoculation and were treated 5 times a week and imaged twice a week to monitor tumor growth. At the study endpoint (Day 24), mice were euthanized, and brains were collected for ex vivo analyses. (B) Weekly average metastatic burden per group throughout the study, assessed by BLI (bottom), and representative BLI images from Day 25(top), vehicle N = 9 and Pralsetinib N = 10. (C) Representative BLI images of ex vivo brain (top). Quantification of ex vivo BLI of brains (bottom). (D) Circulating ALT levels between treatment groups. (E) The average weight of mice throughout the study. (F) IHC staining of p-RET (Y905) and Ki-67 expression levels in brain tumors (left) (scale bar = 100µm), and H-score quantification of p-RET (Y905) positivity and Ki-67 positivity (right). (G) Fluorescent TUNEL assay on mouse brain tumors. Images of representative fields show nuclei from control and treated tumors (left) (scale bar = 100µm). Two-way ANOVAs were used to calculate p-values with a mixed-effects analysis for panels (B and E). An unpaired, two-tailed t-test was used in panels (C, D, F and G).
Techniques Used: In Vivo, Luciferase, Expressing, Ex Vivo, Immunohistochemistry, TUNEL Assay, Control, Two Tailed Test
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