Institution
Memorial Sloan Kettering Cancer Center
Healthcare•New York, New York, United States•
About: Memorial Sloan Kettering Cancer Center is a healthcare organization based out in New York, New York, United States. It is known for research contribution in the topics: Cancer & Population. The organization has 30293 authors who have published 65381 publications receiving 4462534 citations. The organization is also known as: MSKCC & New York Cancer Hospital.
Topics: Cancer, Population, Breast cancer, Radiation therapy, Prostate cancer
Papers published on a yearly basis
Papers
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TL;DR: Tumor size predicts disease-specific survival in patients with primary disease who undergo complete gross resection and investigational protocols are indicated to reduce the rate of recurrence after resections and to improve the outcome for patients with GIST.
Abstract: ObjectiveTo analyze the outcome of 200 patients with gastrointestinal stromal tumor (GIST) who were treated at a single institution and followed up prospectively.Summary Background DataA GIST is a visceral sarcoma that arises from the gastrointestinal tract. Surgical resection is the mainstay of tre
2,532 citations
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2,505 citations
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TL;DR: It is shown that miR-10b is highly expressed in metastatic breast cancer cells and positively regulates cell migration and invasion, and the workings of an undescribed regulatory pathway, in which a pleiotropic transcription factor induces expression of a specific microRNA, which suppresses its direct target and in turn activates another pro-metastatic gene, leading to tumour cell invasion and metastasis.
Abstract: MicroRNAs have been implicated in regulating diverse cellular pathways. Although there is emerging evidence that some microRNAs can function as oncogenes or tumour suppressors, the role of microRNAs in mediating cancer metastasis remains unexplored. Here we show, using a combination of mouse and human cells, that microRNA-10b (miR-10b) is highly expressed in metastatic breast cancer cells and positively regulates cell migration and invasion. Overexpression of miR-10b in otherwise non-metastatic breast tumours initiates robust invasion and metastasis. Expression of miR-10b is induced by the transcription factor Twist, which binds directly to the putative promoter of mir-10b (MIRN10B). The miR-10b induced by Twist proceeds to inhibit translation of the messenger RNA encoding homeobox D10, resulting in increased expression of a well-characterized pro-metastatic gene, RHOC. Significantly, the level of miR-10b expression in primary breast carcinomas correlates with clinical progression. These findings suggest the workings of an undescribed regulatory pathway, in which a pleiotropic transcription factor induces expression of a specific microRNA, which suppresses its direct target and in turn activates another pro-metastatic gene, leading to tumour cell invasion and metastasis.
2,502 citations
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TL;DR: Clonal hematopoiesis with somatic mutations is readily detected by means of DNA sequencing, is increasingly common as people age, and is associated with increased risks of hematologic cancer and death.
Abstract: Cancers arise from multiple acquired mutations, which presumably occur over many years. Early stages in cancer development might be present years before cancers become clinically apparent. Methods We analyzed data from whole-exome sequencing of DNA in peripheral-blood cells from 12,380 persons, unselected for cancer or hematologic phenotypes. We identified somatic mutations on the basis of unusual allelic fractions. We used data from Swedish national patient registers to follow health outcomes for 2 to 7 years after DNA sampling. Results Clonal hematopoiesis with somatic mutations was observed in 10% of persons older than 65 years of age but in only 1% of those younger than 50 years of age. Detectable clonal expansions most frequently involved somatic mutations in three genes (DNMT3A, ASXL1, and TET2) that have previously been implicated in hematologic cancers. Clonal hematopoiesis was a strong risk factor for subsequent hematologic cancer (hazard ratio, 12.9; 95% confidence interval, 5.8 to 28.7). Approximately 42% of hematologic cancers in this cohort arose in persons who had clonality at the time of DNA sampling, more than 6 months before a first diagnosis of cancer. Analysis of bone marrow–biopsy specimens obtained from two patients at the time of diagnosis of acute myeloid leukemia revealed that their cancers arose from the earlier clones. Conclusions Clonal hematopoiesis with somatic mutations is readily detected by means of DNA sequencing, is increasingly common as people age, and is associated with increased risks of hematologic cancer and death. A subset of the genes that are mutated in patients with myeloid cancers is frequently mutated in apparently healthy persons; these mutations may represent characteristic early events in the development of hematologic cancers. (Funded by the National Human Genome Research Institute and others.)
2,497 citations
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TL;DR: Overexpression of this bone metastasis gene set is superimposed on a poor-prognosis gene expression signature already present in the parental breast cancer population, suggesting that metastasis requires a set of functions beyond those underlying the emergence of the primary tumor.
2,493 citations
Authors
Showing all 30708 results
Name | H-index | Papers | Citations |
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Gordon H. Guyatt | 231 | 1620 | 228631 |
Edward Giovannucci | 206 | 1671 | 179875 |
Irving L. Weissman | 201 | 1141 | 172504 |
Craig B. Thompson | 195 | 557 | 173172 |
Joan Massagué | 189 | 408 | 149951 |
Gad Getz | 189 | 520 | 247560 |
Chris Sander | 178 | 713 | 233287 |
Richard B. Lipton | 176 | 2110 | 140776 |
Richard K. Wilson | 173 | 463 | 260000 |
George P. Chrousos | 169 | 1612 | 120752 |
Stephen J. Elledge | 162 | 406 | 112878 |
Murray F. Brennan | 161 | 925 | 97087 |
Lewis L. Lanier | 159 | 554 | 86677 |
David W. Bates | 159 | 1239 | 116698 |
Dan R. Littman | 157 | 426 | 107164 |