Institution
Johns Hopkins University School of Medicine
Healthcare•Baltimore, Maryland, United States•
About: Johns Hopkins University School of Medicine is a healthcare organization based out in Baltimore, Maryland, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 44277 authors who have published 79222 publications receiving 4788882 citations.
Topics: Population, Cancer, Transplantation, Prostate cancer, Poison control
Papers published on a yearly basis
Papers
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TL;DR: There have been important advances in understanding of the molecular pathogenesis and progression of head and neck cancer and also in approaches to therapy, which include innovations in surgery, radiation therapy, and cytotoxic-drug therapy.
Abstract: Head and neck cancers include neoplasms of the oral cavity, pharynx, and larynx. The risk of these cancers is strongly associated with smoking and alcohol ingestion. There have been important advances in understanding of the molecular pathogenesis and progression of head and neck cancer and also in approaches to therapy, which include innovations in surgery, radiation therapy, and cytotoxic-drug therapy.
1,239 citations
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TL;DR: It is shown that the microRNA miR-34a regulates silent information regulator 1 (SIRT1) expression, which functions as a tumor suppressor, in part, through a SIRT1-p53 pathway.
Abstract: MicroRNA 34a (miR-34a) is a tumor suppressor gene, but how it regulates cell proliferation is not completely understood. We now show that the microRNA miR-34a regulates silent information regulator 1 (SIRT1) expression. MiR-34a inhibits SIRT1 expression through a miR-34a-binding site within the 3′ UTR of SIRT1. MiR-34 inhibition of SIRT1 leads to an increase in acetylated p53 and expression of p21 and PUMA, transcriptional targets of p53 that regulate the cell cycle and apoptosis, respectively. Furthermore, miR-34 suppression of SIRT1 ultimately leads to apoptosis in WT human colon cancer cells but not in human colon cancer cells lacking p53. Finally, miR-34a itself is a transcriptional target of p53, suggesting a positive feedback loop between p53 and miR-34a. Thus, miR-34a functions as a tumor suppressor, in part, through a SIRT1-p53 pathway.
1,238 citations
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TL;DR: From these analyses probability plots and nomograms have been constructed to assist urologists in the preoperative prediction of final pathological stage for patients with clinically localized prostate cancer.
1,232 citations
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TL;DR: It is demonstrated that two enzymes cooperatively maintain DNA methylation and gene silencing in human cancer cells, and compelling evidence that such methylation is essential for optimal neoplastic proliferation is provided.
Abstract: Inactivation of tumour suppressor genes is central to the development of all common forms of human cancer. This inactivation often results from epigenetic silencing associated with hypermethylation rather than intragenic mutations. In human cells, the mechanisms underlying locus-specific or global methylation patterns remain unclear. The prototypic DNA methyltransferase, Dnmt1, accounts for most methylation in mouse cells, but human cancer cells lacking DNMT1 retain significant genomic methylation and associated gene silencing. We disrupted the human DNMT3b gene in a colorectal cancer cell line. This deletion reduced global DNA methylation by less than 3%. Surprisingly, however, genetic disruption of both DNMT1 and DNMT3b nearly eliminated methyltransferase activity, and reduced genomic DNA methylation by greater than 95%. These marked changes resulted in demethylation of repeated sequences, loss of insulin-like growth factor II (IGF2) imprinting, abrogation of silencing of the tumour suppressor gene p16INK4a, and growth suppression. Here we demonstrate that two enzymes cooperatively maintain DNA methylation and gene silencing in human cancer cells, and provide compelling evidence that such methylation is essential for optimal neoplastic proliferation.
1,228 citations
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TL;DR: How miRNAs influence tumorigenesis by acting as oncogenes and tumour suppressors is discussed.
Abstract: MicroRNAs (miRNAs) are a recently discovered class of approximately 18-24 nucleotide RNA molecules that negatively regulate target mRNAs. All studied multicellular eukaryotes utilise miRNAs to regulate basic cellular functions including proliferation, differentiation, and death. It is now apparent that abnormal miRNA expression is a common feature of human malignancies. In this review, we will discuss how miRNAs influence tumorigenesis by acting as oncogenes and tumour suppressors.
1,226 citations
Authors
Showing all 44754 results
Name | H-index | Papers | Citations |
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Robert Langer | 281 | 2324 | 326306 |
Bert Vogelstein | 247 | 757 | 332094 |
Solomon H. Snyder | 232 | 1222 | 200444 |
Steven A. Rosenberg | 218 | 1204 | 199262 |
Kenneth W. Kinzler | 215 | 640 | 243944 |
Hagop M. Kantarjian | 204 | 3708 | 210208 |
Mark P. Mattson | 200 | 980 | 138033 |
Stuart H. Orkin | 186 | 715 | 112182 |
Paul G. Richardson | 183 | 1533 | 155912 |
Aaron R. Folsom | 181 | 1118 | 134044 |
Gonçalo R. Abecasis | 179 | 595 | 230323 |
Jie Zhang | 178 | 4857 | 221720 |
Daniel R. Weinberger | 177 | 879 | 128450 |
David Baker | 173 | 1226 | 109377 |
Eliezer Masliah | 170 | 982 | 127818 |