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Carcinogenesis

About: Carcinogenesis is a research topic. Over the lifetime, 60368 publications have been published within this topic receiving 3192599 citations. The topic is also known as: oncogenesis & tumorigenesis.


Papers
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Journal ArticleDOI
TL;DR: It is demonstrated that pathologic elevation of a single proinflammatory cytokine may be sufficient to induce neoplasia and provide a direct link between IL-1beta, MDSCs, and carcinogenesis.

754 citations

Journal ArticleDOI
05 Feb 2014-Nature
TL;DR: There is a switch after birth, when AT2 cells function as stem cells that contribute to alveolar renewal, repair and cancer, and it is proposed that local signals regulate AT2 stem-cell activity.
Abstract: Alveoli are gas-exchange sacs lined by squamous alveolar type (AT) 1 cells and cuboidal, surfactant-secreting AT2 cells. Classical studies suggested that AT1 arise from AT2 cells, but recent studies propose other sources. Here we use molecular markers, lineage tracing and clonal analysis to map alveolar progenitors throughout the mouse lifespan. We show that, during development, AT1 and AT2 cells arise directly from a bipotent progenitor, whereas after birth new AT1 cells derive from rare, self-renewing, long-lived, mature AT2 cells that produce slowly expanding clonal foci of alveolar renewal. This stem-cell function is broadly activated by AT1 injury, and AT2 self-renewal is selectively induced by EGFR (epidermal growth factor receptor) ligands in vitro and oncogenic Kras(G12D) in vivo, efficiently generating multifocal, clonal adenomas. Thus, there is a switch after birth, when AT2 cells function as stem cells that contribute to alveolar renewal, repair and cancer. We propose that local signals regulate AT2 stem-cell activity: a signal transduced by EGFR-KRAS controls self-renewal and is hijacked during oncogenesis, whereas another signal controls reprogramming to AT1 fate.

754 citations

Journal ArticleDOI
15 Mar 1991-Science
TL;DR: A gene, MCC, which encodes an 829-amino acid protein with a short region of similarity to the G protein-coupled m3 muscarinic acetylcholine receptor is identified and is a candidate for the putative colorectal tumor suppressor gene located at chromosome region 5q21.
Abstract: Recent studies have suggested the existence of a tumor suppressor gene located at chromosome region 5q21. DNA probes from this region were used to study a panel of sporadic colorectal carcinomas. One of these probes, cosmid 5.71, detected a somatically rearranged restriction fragment in the DNA from a single tumor. Further analysis of the 5.71 cosmid revealed two regions that were highly conserved in rodent DNA. These sequences were used to identify a gene, MCC (mutated in colorectal cancer), which encodes an 829-amino acid protein with a short region of similarity to the G protein-coupled m3 muscarinic acetylcholine receptor. The rearrangement in the tumor disrupted the coding region of the MCC gene. Moreover, two colorectal tumors were found with somatically acquired point mutations in MCC that resulted in amino acid substitutions. MCC is thus a candidate for the putative colorectal tumor suppressor gene located at 5q21. Further studies will be required to determine whether the gene is mutated in other sporadic tumors or in the germ line of patients with an inherited predisposition to colonic tumorigenesis.

753 citations

Journal ArticleDOI
TL;DR: The possible role of epigenetic abnormalities as well as genetic alterations in such dynamics and in the creation of cellular heterogeneity in cancers of all types are discussed.

752 citations

Book
30 May 1985
TL;DR: Malignant Transformation Growth and Spread of Cancer Molecular Abnormalities in Specific Malignancies, Molecular Basis of Cancer Therapy, Molecular Transformation, and spread of cancer molecular abnormalities in specific malignancies as mentioned in this paper.
Abstract: Malignant Transformation Growth and Spread of Cancer Molecular Abnormalities in Specific Malignancies, Molecular Basis of Cancer Therapy.

752 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20239,028
20227,271
20213,536
20203,486
20193,433
20183,073