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Molecular & Cellular Oncology

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[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
Clément Chevalier, Serge Roche, Christine Bénistant
ERBB2 (v-erb-b2 avian erythroblastic leukemia viral oncogene homolog 2) amplification is associated with invasive breast cancer. We discovered that TOM1L1 (target of myb1-like 1) and ERBB2 co-amplification defines a novel mechanism involved in breast cancer metastatic progression. Upregulation of the vesicular trafficking protein TOM1L1 enhances plasma membrane delivery of membrane-type 1 matrix metalloprotease (MT1-MMP) for efficient extracellular matrix degradation and tumor cell dissemination.
July 2016: Molecular & Cellular Oncology
Lawrence W Wu, Gao Zhang, Meenhard Herlyn
The acquisition of resistance to current mitogen activated protein kinase (MAPK) inhibitors in B-Raf proto-oncogene, serine/threonine kinase (BRAF) mutant melanoma is almost inevitable. Our recent findings identify therapy-induced mitochondrial biogenesis (MitoBiogenesis) and aberrant tumor bioenergetics as therapeutic escape mechanisms and offer a rational combinatorial strategy to further improve the efficacy of MAPK inhibitors.
July 2016: Molecular & Cellular Oncology
Caroline P Le, Erica K Sloan
Chronic stress drives cancer progression, but the routes of metastasis are unclear. We recently demonstrated that chronic stress activates a neural-inflammatory signaling axis to remodel lymphatic vasculature and increase lymph flow. This unanticipated crosstalk between stress and the lymphatic system provides pathways of tumor cell dissemination and accelerates metastasis.
July 2016: Molecular & Cellular Oncology
Adelheid Cerwenka, Jürgen Kopitz, Peter Schirmacher, Wilfried Roth, Georg Gdynia
Targeting tumor glycolysis would hit the main energy source of cancer. We show that natural killer (NK) cells pursue this strategy by employing high mobility group box 1 (HMGB1) protein-a well-known proinflammatory cytokine-to specifically target glycolysis in cancer cells. This opens up new perspectives for cancer immunotherapy.
July 2016: Molecular & Cellular Oncology
Che-Pei Kung, Subhasree Basu, Maureen E Murphy
Besides being a critical tumor suppressor, the TP53 gene also plays a role in metabolism and recent studies in humans have implicated the codon 72 polymorphism of TP53 in this role. Using a humanized knock-in mouse model for these TP53 variants, we show that this polymorphism has a significant impact on the metabolic response to a high-fat diet.
July 2016: Molecular & Cellular Oncology
Tomas Aparicio, Jean Gautier
DNA termini at double-strand breaks are often chemically heterogeneous and require processing before initiation of repair. In a recent report, we demonstrated that CtIP and the MRE11-RAD50-NBS1 (MRN) nuclease complex cooperate with BRCA1 to specifically repair topoisomerase II-DNA adducted breaks. In contrast, BRCA1 is dispensable for repair of restriction endonuclease-generated double-strand breaks.
July 2016: Molecular & Cellular Oncology
Roxana S Redis, George A Calin
Long non-coding RNAs (lncRNAs) exert most of their functions through protein interactions. A better understanding of these interactions will facilitate the development of novel therapeutics. Recently, we described how the lncRNA CCAT2 located at the 8q24 cancer amplicon reprograms cancer metabolism by directly interacting in an allele-specific manner with a protein complex.
July 2016: Molecular & Cellular Oncology
Edouard Mullarky, Luke L Lairson, Lewis C Cantley, Costas A Lyssiotis
Serine metabolism is likely to play a critical role in cancer cell growth. A recent study reports the identification of a novel small-molecule inhibitor of serine synthesis that targets 3-phosphoglycerate dehydrogenase (PHGDH), the first enzyme of the serine synthesis pathway, and selectively abrogates the proliferation of PHGDH overexpressing breast cancer cells.
July 2016: Molecular & Cellular Oncology
Lihua Wang, Pengcheng Bu, Xiling Shen
miR-34a-mediated asymmetric cell division reins in excessive stem cell expansion during tissue regeneration in the intestine and colon. Loss of miR-34a switches asymmetric division to symmetric division and enhances stem cell proliferation. Asymmetric division also occurs in the early stages of colon cancer stem cells. Mechanistically, miR-34a, Numb, and Notch form a feed-forward loop that specifies cell fate when stem cells divide.
July 2016: Molecular & Cellular Oncology
Manja Idorn, Per Thor Straten
We recently demonstrated that voluntary exercise leads to an influx of immune cells in tumors and a greater than 60% reduction in tumor incidence and growth across several mouse models. Improved immunological control of tumor progression may have important clinical implications in the prevention and treatment of cancer in humans.
July 2016: Molecular & Cellular Oncology
Marc J Williams, Benjamin Werner, Trevor A Graham, Andrea Sottoriva
Next-generation sequencing data from human cancers are often difficult to interpret within the context of tumor evolution. We developed a mathematical model describing the accumulation of mutations under neutral evolutionary dynamics and showed that 323/904 cancers (∼30%) from multiple types were consistent with the neutral model of tumor evolution.
July 2016: Molecular & Cellular Oncology
Clara Correia-Melo, João F Passos
In a study published in The EMBO Journal, we demonstrated that mitochondria are necessary for the proinflammatory phenotype of senescence. Furthermore, we identified a new senescence-regulatory pathway involving mTOR-dependent mitochondrial biogenesis. These data highlight mitochondria as targets for interventions that counteract the pro-aging effects of senescence while preserving tumor suppression.
July 2016: Molecular & Cellular Oncology
Susana Llanos, Juana M García-Pedrero
We have identified a novel mechanism of regulation of the protein CDKN1A (also known as p21) by the serine/threonine kinase complex mammalian target of rapamycin complex 1 (mTORC1). Our results demonstrate that the mTORC1 substrate EIF4E-binding protein 1 (4E-BP1) in its non-phosphorylated state interacts with p21 and promotes p21 degradation. In addition, we demonstrate the prevalence of this mechanism in head and neck squamous cell carcinomas and show that it strongly and significantly associates with improved disease-specific survival, providing evidence for its clinical relevance...
July 2016: Molecular & Cellular Oncology
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