scholarly journals A non-functional retinoblastoma tumor suppressor (RB) pathway in premenopausal breast cancer is associated with resistance to tamoxifen

Cell Cycle ◽  
2011 ◽  
Vol 10 (6) ◽  
pp. 956-962 ◽  
Author(s):  
Sophie Lehn ◽  
Mårten Fernö ◽  
Karin Jirström ◽  
Lisa Rydén ◽  
Göran Landberg
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Premenopausal Breast Cancer ◽  
Retinoblastoma Tumor Suppressor ◽  
Rb Pathway ◽  
Retinoblastoma Tumor

scholarly journals The retinoblastoma tumor suppressor modifies the therapeutic response of breast cancer

2007 ◽  
Vol 117 (1) ◽  
pp. 218-228 ◽  
Author(s):  
Emily E. Bosco ◽  
Ying Wang ◽  
Huan Xu ◽  
Jack T. Zilfou ◽  
Karen E. Knudsen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Therapeutic Response ◽  
Retinoblastoma Tumor Suppressor ◽  
Retinoblastoma Tumor

scholarly journals The retinoblastoma tumor suppressor pathway modulates the invasiveness of ErbB2-positive breast cancer

Oncogene ◽  
2013 ◽  
Vol 33 (30) ◽  
pp. 3980-3991 ◽  
Author(s):  
A K Witkiewicz ◽  
D W Cox ◽  
D Rivadeneira ◽  
A E Ertel ◽  
P Fortina ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Retinoblastoma Tumor Suppressor ◽  
Retinoblastoma Tumor ◽  
Positive Breast Cancer

scholarly journals Pan-cancer molecular analysis of the RB tumor suppressor pathway

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Erik S. Knudsen ◽  
Ram Nambiar ◽  
Spencer R. Rosario ◽  
Dominic J. Smiraglia ◽  
David W. Goodrich ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Critical Role ◽  
Single Copy ◽  
Suppressor Gene ◽  
Molecular Features ◽  
Retinoblastoma Tumor Suppressor ◽  
Rb Pathway ◽  
Retinoblastoma Tumor ◽  
Tumor Types ◽  
Chromosome 13Q

AbstractThe retinoblastoma tumor suppressor gene (RB1) plays a critical role in coordinating multiple pathways that impact cancer initiation, disease progression, and therapeutic responses. Here we probed molecular features associated with the RB-pathway across 31 tumor-types. While the RB-pathway has been purported to exhibit multiple mutually exclusive genetic events, only RB1 alteration is mutually exclusive with deregulation of CDK4/6 activity. An ER+ breast cancer model with targeted RB1 deletion was used to identify signatures of CDK4/6 activity and RB-dependency (CDK4/6-RB integrated signature). This signature was prognostic in tumor-types with gene expression features indicative of slower growth. Single copy loss on chromosome 13q encompassing the RB1 locus is prevalent in many cancers, yielding reduced expression of multiple genes in cis, and is inversely related to the CDK4/6-RB integrated signature supporting a cause-effect relationship. Genes that are positively and inversely correlated with the CDK4/6-RB integrated signature define new tumor-specific pathways associated with RB-pathway activity.

scholarly journals The retinoblastoma tumor suppressor limits ribosomal readthrough during oncogene induced senescence

2019 ◽  
Author(s):  
Neylen del Toro ◽  
Frédéric Lessard ◽  
Sarah Tardif ◽  
Jacob Bouchard ◽  
Véronique Bourdeau ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Ribosomal Proteins ◽  
Cancer Biology ◽  
Viral Oncoprotein ◽  
Origin And Evolution ◽  
Retinoblastoma Tumor Suppressor ◽  
Dna Mutations ◽  
Rb Pathway ◽  
Normal Human ◽  
Retinoblastoma Tumor

AbstractThe origin and evolution of cancer cells is considered to be mainly fueled by mutations affecting the DNA sequence. Although errors in translation could also expand the cellular proteome, their role in cancer biology remains poorly understood. Tumor suppressors called “caretakers” block cancer initiation and progression by preventing DNA mutations and/or stimulating DNA repair. If translational errors contribute to tumorigenesis, then caretakers genes will prevent such errors in normal cells in response to oncogenic stimuli. Here, we show that the retinoblastoma protein (RB) acts as caretaker tumor suppressor by preventing the readthrough of termination codons, a process that allows proteins to be synthetized with additional domains. In particular, we show that expression of oncogenic ras in normal human cells triggers a cellular senescence response characterized by a significant reduction of basal ribosomal readthrough. However, inactivation of the RB tumor suppressor pathway in these cells, using the viral oncoprotein E7 or the oncogenic kinase CDK4 increased readthrough. Conversely, activation of the RB pathway by the tumor suppressor PML, the ribosomal proteins RPS14/uS11 and RPL22/eL22 or the CDK4/6 inhibitor palbociclib reduced readthrough. We thus reveal a novel function for the RB pathway as a caretaker of translational errors with implications for tumor suppression and cancer treatment.

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