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Molecular & Cellular Oncology

Valentina Palermo, Sara Rinalducci, Massimo Sanchez, Francesca Grillini, Annapaola Franchitto, Pietro Pichierri
Replication-dependent double-strand breaks (DSBs) are the main source of genomic instability as their inaccurate repair stimulates chromosomal rearrangements. In a recent work, we uncover a novel regulatory circuit that involves the Werner's syndrome helicase and CDK1, and that is essential for repair pathway choice at replication-dependent DSBs.
2017: Molecular & Cellular Oncology
Manel Joaquin, Eulàlia de Nadal, Francesc Posas
The N-term phosphorylation of Retinoblastoma (RB) by the p38 stress-activated protein kinase (SAPK) makes RB insensitive to cyclin-dependent kinase (CDK)-Cyclin inhibition, which enhances the transcriptional repression of E2F-driven promoters and delays tumor cell growth. This novel mechanism of RB regulation opens up a window for developing new cancer drug treatments for tumors harboring high CDK-Cyclin activity and a wild-type RB gene.
2017: Molecular & Cellular Oncology
Veenu Tripathi, Ying E Zhang
Transforming growth factor β (TGF-β) is a well-known growth inhibitor of normal epithelial cells, but it is also secreted by solid tumors to promote cancer progression. Our recent discovery of SMAD3-PCBP1 complex with direct RNA-binding properties has shed light on how this conversion is implemented by controlling pre-mRNA splicing patterns.
2017: Molecular & Cellular Oncology
Thomas J Bartosh
Relapse in cancer patients following an apparent cure and a prolonged latency period, known as tumor dormancy, remains an unrelenting clinical crisis. Here, I expand on our recent findings that potentially link cancer cell cannibalism of bone marrow-derived mesenchymal stem/stromal cells (BM-MSCs) to the senescence-associated secretory phenotype (SASP) and tumor dormancy.
2017: Molecular & Cellular Oncology
Zhongqiu Xie, Hui Li
Biological samples can be grouped into separate clusters based on their gene expression profiles. This approach has yielded meaningful biological insights and facilitated biomarker discoveries. Recently, we developed another approach to study connections between biological samples based on their fusion RNA expression. We have used this approach to provide insights into the cell of origin for a mysterious tumor, alveolar rhabdomyosarcoma.
2017: Molecular & Cellular Oncology
Markus Räschle
Stalling of the DNA replication machinery activates the ATR checkpoint kinase, which coordinates the cellular responses to replication stress. New studies identify a novel ATR activator, ETAA1, which is indispensable for the maintenance of genome integrity. Dysregulation of ETAA1 may contribute to the development of pancreatic cancer.
2017: Molecular & Cellular Oncology
Anitha K Shenoy, Jianrong Lu
The relevance of epithelial-to-mesenchymal transition (EMT) in cancer is still under debate. Recently, we reported that EMT bestows key pericyte properties on cancer cells and may thus represent epithelial-to-pericyte transition (EPT). Carcinoma cells undergo EPT to stabilize blood vessels and fuel primary tumor growth. Association of EPT cancer cells with vascular niches may also promote resistance to therapy.
2017: Molecular & Cellular Oncology
M Diefenbacher, A Orian
RNF4, a SUMO-targeted ubiquitin ligase, stabilizes a selected group of oncoproteins. It potentiates oncoprotein activity and serves as a positive feedback agonist of Wnt and Notch pathways. RNF4 is essential for cancer cell survival and its levels are elevated in human cancers, correlating with poor outcome in a subset of cancer patients.
2017: Molecular & Cellular Oncology
Alan J Simmons, Ken S Lau
An impediment to the understanding of cancer is the heterogeneous nature of cell populations within a tumor microenvironment. We reported a method to query protein signaling in single epithelial cells from formalin-fixed paraffin-embedded (FFPE) colorectal cancer tissues. Here, we discuss the feasibility and limitations of this approach for investigating signaling state heterogeneity.
2017: Molecular & Cellular Oncology
Zachary Hothem, Andrew Bayci, Bryan J Thibodeau, Billie E Ketelsen, Laura E Fortier, Alison F Uzieblo, Diane Cosner, Kristin Totoraitis, Richard D Keidan, George D Wilson
Most melanomas present as thin lesions (≤1.0 mm) with a good prognosis; however, a small percentage of patients with thin lesions experience recurrence or metastasis. The aim of our study was to identify a distinct pattern of gene expression within thin melanomas known to have eventually metastasized to regional lymph nodes or distant sites compared with those that followed the typical course with good response to wide local excision alone. Patients who were disease-free for a minimum of 10 y served as controls (n = 10) to the experimental group who developed metastasis (n = 9)...
2017: Molecular & Cellular Oncology
Aldwin Suryo Rahmanto, Fredrik J Swartling, Olle Sangfelt
Cancer cells with stem-like properties are believed to contribute to treatment resistance, dissemination, and recurrence. SOX9 controls stem cell plasticity and its deregulation may provide a basis for tumor progression. Here, we summarize our findings of targeted SOX9 destruction by SCF(FBW7) (Skp1/Cul1/F-box) in medulloblastoma and its potential for therapeutic intervention.
2017: Molecular & Cellular Oncology
Kamil Lisek, Dawid Walerych, Giannino Del Sal
The proteasome machinery is a common target of gain-of-function p53 missense mutants. Upregulation of the proteasome fosters chemoresistance to proteasome inhibitors. In triple negative breast cancer cells this resistance mechanism, namely the Nrf2-regulated "bounce-back" response to proteasome inhibitors, can be overcome by targeting p53 mutant proteins with APR-246/PRIMA-1Met.
2017: Molecular & Cellular Oncology
Veit Goder
The endoplasmic reticulum (ER) is considered a prominent membrane source for the formation of autophagosomes. Recent results from our laboratory revealed a cellular mechanism for the contribution of the ER to autophagosomes in yeast: membranes, together with unconventional membrane fusion machinery, are delivered to sites of autophagosome formation by specific coat protein complex II (COPII) vesicles.
2017: Molecular & Cellular Oncology
(no author information available yet)
[This corrects the article DOI: 10.1080/23723556.2015.1033588.].
July 2016: Molecular & Cellular Oncology
Luis J Schwarz, Justin M Balko
The cornerstone for precision medicine is the development of robust biomarkers that reflect molecular phenotypes and therapeutic vulnerabilities in disease. We recently described Janus kinase-2 (JAK2)-specific inhibition as a therapeutic opportunity in triple negative breast cancers with 9p24 amplification. Here, we comment on this work and discuss the challenges of targeting this amplicon.
July 2016: Molecular & Cellular Oncology
Yohei Niikura, Risa Kitagawa, Katsumi Kitagawa
CENP-A (Centromere protein A) is a histone H3 variant that epigenetically determines the centromere position, but the mechanism of its centromere inheritance is obscure. We propose that CENP-A ubiquitylation, which is inherited through dimerization between rounds of cell division, is a candidate for the epigenetic mark of centromere identity.
July 2016: Molecular & Cellular Oncology
Zhen-Dong Xiao, Xiaowen Liu, Li Zhuang, Boyi Gan
NBR2 (neighbor of BRCA1 gene 2) is a non-protein coding gene that resides adjacent to tumor suppressor gene BRCA1, but its role in cancer biology has remained unknown. Our recent study showed that NBR2 encodes a long non-coding RNA and suppresses tumor development through regulation of adenosine monophosphate-activated protein kinase (AMPK) activation.
July 2016: Molecular & Cellular Oncology
Hisataka Sabe, Ari Hashimoto, Shigeru Hashimoto, Tsukasa Oikawa
The mevalonate pathway results in the prenylation of small GTPases, which are pivotal for oncogenesis and cancer malignancies. However, inhibitors of this pathway, such as statins, have not necessarily produced favorable results in clinical trials. We recently identified properties of statin responders, together with the underlying molecular mechanisms and simple biomarkers to predict these responders.
July 2016: Molecular & Cellular Oncology
Alenka Lovy, J Kevin Foskett, César Cárdenas
Mitochondrial metabolism is essential to fulfill the large demand for macromolecule biosynthesis in cancer. We recently identified low-level InsP3R-mediated Ca(2+) transfer to mitochondria as an unexpected requirement for mitochondrial function. Here we reveal that its absence specifically targets cancer cells and causes necrosis at daughter cell separation during ongoing proliferation.
July 2016: Molecular & Cellular Oncology
Noa Lamm, Batsheva Kerem
Human pluripotent stem cells (hPSCs) frequently acquire chromosomal aberrations, including aneuploidy, during culture. Recently, we identified a replication stress-based mechanism leading to ongoing chromosomal instability in aneuploid hPSCs that may also operate during the initiation of instability in diploid cells.
July 2016: Molecular & Cellular Oncology
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