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Molecular Cancer Research
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4.48
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Papers 3726
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#1Nanxiang Xiong (Union Hospital)H-Index: 1
#2Junjun Li (Union Hospital)
Last. Hong-Yang Zhao (HUST: Huazhong University of Science and Technology)H-Index: 9
view all 5 authors...
Glioblastoma (GBM) is the most lethal primary brain tumor and has a complex molecular profile. Hypoxia plays a critical role during tumor progression and in the tumor microenvironment (TME). Exosomes released by tumor cells contain informative nucleic acids, proteins and lipids involved in the interaction between cancer and stromal cells, thus leading to TME remodeling. Accumulating evidence indicates that exosomes play a pivotal role in cell-to-cell communication. However, the mechanism by whic...
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#1Thirupandiyur S. Udayakumar (UM: University of Miami)H-Index: 6
#2Dillon Betancourt (UM: University of Miami)H-Index: 4
Last. Alan Pollack (UM: University of Miami)H-Index: 67
view all 9 authors...
Vesicular Stomatitis Virus (VSV) expressing interferon-β (IFNβ) induces apoptosis in multiple tumor models while maintaining an excellent safety profile. VSV-IFNβ is oncoselective due to permissive replication in cells with an altered IFN pathway. The human VSV-IFNβ (hIFNβ) vector is currently used in clinical trials as a standalone therapy; however, we hypothesized that oncolytic virotherapy might be more effective when used in combination with radiotherapy (RT). We investigated the synergistic...
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#1Mio HarachiH-Index: 1
#2Kenta MasuiH-Index: 17
Last. Noriyuki ShibataH-Index: 29
view all 8 authors...
Epigenetic regulation known for DNA methylation and histone modification is critical for securing proper gene expression and chromosomal function, and its aberration induces various pathological conditions including cancer. Trimethylation of histone H3 on lysine 27 (H3K27me3) is known to suppress various genes related to cancer cell survival and the level of H3K27me3 may have an influence on tumor progression and malignancy. However, it remains unclear how histone methylation is regulated in res...
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#1Nishi Srivastava (Fox Chase Cancer Center)
#2Alison Kurimchak (Fox Chase Cancer Center)H-Index: 8
Last. James S. Duncan (Fox Chase Cancer Center)H-Index: 17
view all 5 authors...
Activating mutations in KRAS occur in about half of colorectal cancers (CRC) and are associated with drug resistance and poor survival. A number of distinct oncogenic mutations in KRAS have been identified in CRC, including mutations in exon 2-producing (G12D, G12V, and G13D) and in exon 4 (A146T and A146V). Importantly, emerging clinical and basic science data indicate that these KRAS mutations are not all equal in their oncogenic properties and sensitivity to targeted therapies. To access and ...
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#1Yi-Jang Lin (BIDMC: Beth Israel Deaconess Medical Center)H-Index: 2
#2Patrick S Dischinger (Van Andel Institute)H-Index: 1
Last. Kevin M. Haigis (BIDMC: Beth Israel Deaconess Medical Center)H-Index: 34
view all 5 authors...
The K-RAS (Kirsten rat sarcoma) oncoprotein is mutationally activated in ~40% of colorectal cancers (CRCs), and K-RAS mutation state is an excellent predictor of the failure of a cancer to respond to conventional chemotherapy or targeted therapy. The colonic epithelium provides a biologically interesting context in which to study the allele-specific characteristics of K-RAS, because CRC displays a broad spectrum of activating mutations that occur at lower frequencies than K-RAS-mutant tumors of ...
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#1Angelina V. Vaseva (University of Texas Health Science Center at San Antonio)
#2Abhik Bandyopadhyay (University of Texas Health Science Center at San Antonio)H-Index: 19
Last. Peter J. Houghton (University of Texas Health Science Center at San Antonio)H-Index: 75
view all 9 authors...
Recent sequencing of childhood rhabdomyosarcoma identified the presence of RAS pathway mutations in nearly 75% of high-risk embryonal rhabdomyosarcoma (ERMS). While RAS oncoproteins (HRAS, NRAS and KRAS) are well-established therapeutic targets for many adult human cancers, still very little is known about the role of RAS mutations in the development and maintenance of ERMS. We sequenced ERMS cell lines and PDX tumors and identified 4 cell lines harboring activating mutations in H- or NRAS and t...
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#1Matthew A. MarxH-Index: 10
#2Brian R. BaerH-Index: 3
Last. Mark Joseph ChicarelliH-Index: 4
view all 20 authors...
The ability to effectively target mutated KRAS has remained elusive despite decades of research. By solving a highly informative set of ligand-complexed co-crystal structures coupled with iterative structure-based drug design, substituted tetrahydropyridopyrimidines were identified as selective, covalent inhibitors of mutant KRAS G12C. Key molecular interactions with the protein were optimized, with the potency of lead compounds evaluated by (a) mass spectrometric quantification of modified KRAS...
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#1Wenting Liao (University of Texas MD Anderson Cancer Center)H-Index: 2
#2Michael J. Overman (University of Texas MD Anderson Cancer Center)H-Index: 37
Last. Xiaoying Shang (University of Texas MD Anderson Cancer Center)H-Index: 5
view all 25 authors...
Oncogenic Kras (Kras*) plays a key role in tumor maintenance and therapeutic resistance in several cancer types, although the precise biologic functions and mechanisms are not completely understood. We had previously shown in pancreatic ductal adenocarcinoma that some tumors underwent spontaneous relapse and were devoid of Kras* expression and downstream canonical MAPK signaling, instead acquiring amplification and overexpression of the transcriptional coactivator Yap1. Functional studies establ...
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#1Kaja Kostyrko (UCSF: University of California, San Francisco)H-Index: 6
#2Marcus R. Kelly (Stanford University)H-Index: 3
Last. Alejandro Sweet-Cordero (UCSF: University of California, San Francisco)H-Index: 1
view all 8 authors...
Synthetic lethal-based approaches to targeting KRAS driven cancers have recently been receiving increasing attention. However, as KRAS activates multiple effector pathways, targeting single genes may not be sufficient to fully inhibit KRAS-driven oncogenesis. In addition, genome-wide screens can be limited by high noise and low signal. Furthermore, it is increasingly clear that standard screens based on 2D proliferation can miss critical phenotypes relevant to cancer biology. Therefore, we devel...
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#1James Chih-Hsin YangH-Index: 104
#2Ken-ichi HanadaH-Index: 13
Last. Steven A. RosenbergH-Index: 175
view all 3 authors...
Durable complete regressions of metastatic cancers can be achieved by the transfer of in vitro expanded tumor-reactive T-cells. In patients with melanoma, this can be done by giving tumor-infiltrating lymphocytes (TIL) reactive with tumor-specific mutated antigens (“neoantigens”). Unfortunately, the vast majority of immunogenic neoantigens have been shown to be totally patient specific. One exception is that T cells recognizing mutated KRAS have been found in the TIL of multiple patients. In one...
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