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delineating the molecular pathogenesis of MTC through identification of genetic alterations and dysregulated signaling pathways ( Fig. 1 ). Key therapeutic molecular targets have been identified that allowed the evaluation of a series of multitargeted kinase
Biomedical Research Institute, Pusan National University Hospital, Busan, Korea
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Biomedical Research Institute, Pusan National University Hospital, Busan, Korea
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( Kim et al. 2021 ). Other studies utilizing targeted next-generation sequencing have also suggested a limited role of genetic alterations in LLNM of PTMC ( Jeon et al. 2019 , Perera et al. 2019 ). However, in this study, using RNA sequencing, we
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Division of Endocrinology and Metabolism, Department of Surgery, Department of Hospital Pathology, Medical Life Sciences, Department of Internal Medicine
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Introduction The V600E BRAF mutation is the most common genetic alteration in papillary thyroid carcinoma (PTC). The prevalence of the BRAF V600E mutation varies according to the histological subtype; the mutation is frequent in the tall cell
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Current development in molecular techniques has extended the opportunities to explore genetic alterations in malignant tissue. There is a need to improve prognostication and, in particular, to understand the mechanisms of treatment resistance in different tumours. Gene analyses by microarrays allow concomitant analyses of several genes in concert, providing new opportunities for tumour classification and understanding of key biological disturbances. This paper outlines our continuing studies exploring prognostic and, we hope, predictive factors in breast cancer therapy.
Université Paris-Sud Orsay, Île-de-France, France
Gustave Roussy, Villejuif, France
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Gustave Roussy, Villejuif, France
UMR 8200 CNRS, Villejuif, France
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Gustave Roussy, Villejuif, France
UMR 8200 CNRS, Villejuif, France
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Université Paris-Sud Orsay, Île-de-France, France
Gustave Roussy, Villejuif, France
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PSL Research University, Paris, France
INSERM, U900, Paris, France
Mines Paris Tech, Fontainebleau, France
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Université Paris-Sud Orsay, Île-de-France, France
Gustave Roussy, Villejuif, France
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question of an individual genetic susceptibility to radiation-related DTC may be raised. However, while at the somatic level (i.e. in the tumor tissue), molecular signature of radiation-related thyroid tumors was the subject of several studies ( Detours et
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This review is focused on mouse models for prostate cancer that have been designed on the basis of genetic alterations that are frequently found in human prostate cancer. It begins with an analysis of the similarities and differences in the gross and microscopic anatomy of the mouse and human prostate glands, and extends to the pathologies induced in the genetically manipulated mouse prostate in comparison with the sporadic development of the disease in humans. Major achievements have been made in modeling human prostate cancer in mice in recent years. There are models which display slow, temporal development of increasingly severe preneoplastic lesions, which are remarkably restricted to the prostate gland, a property similar to the aging-related progression of these lesions in humans. Other models rapidly progress to local invasive adenocarcinoma, and, in some of them metastasis is manifested subsequently with defined kinetics. Global assessment of molecular changes in the prostate of the genetically manipulated mice is increasingly underscoring the validity of the models through identification of 'signature' genes which are associated with the organ-confined primary or distant metastases of human prostate cancer. Taken together, various 'natural' models depicting stages of the disease, ranging from the early preneoplastic lesions to metastatic prostate cancer, now provide new tools both for exploring the molecular mechanism underlying prostate cancer and for development or testing of new targeted therapies.
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Most human invasive breast cancers (IBCs) appear to develop over long periods of time from certain pre-existing benign lesions. Of the many types of benign lesions in the human breast, only a few appear to have significant premalignant potential. The best characterized of these include atypical hyperplasias and in situ carcinomas and both categories are probably well on along the evolutionary pathway to IBC. Very little is known about earlier premalignant alterations. All types of premalignant breast lesions are relatively common but only a small proportion appear to progress to IBC. They are currently defined by their histological features and their prognosis is imprecisely estimated from indirect epidemiological evidence. Although lesions within specific categories look alike, they must possess underlying biological differences causing some to remain stable and others to progress. Recent studies suggest that they evolve by highly diverse genetic mechanisms and research into these altered pathways may identify specific early defects that can be targeted to prevent premalignant lesions from developing or becoming cancerous. It is far more rational to think that breast cancer can be prevented than cured once it has developed fully. This review discusses histological models of human premalignant breast disease that provide the framework for scientific investigations into the biological alterations behind them and examples of specific biological alterations that appear to be particularly important.
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Like all cancers, breast cancer is considered to result in part from the accumulation of multiple genetic alterations leading to oncogene overexpression and tumor suppressor loss. More recently, the role of epigenetic change as a distinct and crucial mechanism to silence a variety of methylated tissue-specific and imprinted genes has emerged in many cancer types. This review will briefly discuss basic aspects of DNA methylation, recent advances in DNA methyltransferases, the role of altered chromatin organization and the concept of gene transcriptional regulation built on methylated CpGs. In particular, we discuss epigenetic regulation of certain critical tumor suppressor and growth regulatory genes implicated in breast cancer, and its relevance to breast cancer diagnosis, prognosis, progression and therapy.
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Abstract
Most human prostate tumors are adenocarcinomas which arise from the epithelial cells that line the glands and ducts of the prostate. Consequently, the malignant epithelial cell, or more specifically genetic damage suffered by that malignant epithelial cell, has been the major focus of prostate cancer research to date. There is, however, increasing evidence to suggest that alterations in the stromal microenvironment associated with a malignant epithelium may be necessary for progression of carcinogenesis.
We have recently hypothesized that interactions between the stroma and epithelium become altered as a result of genetic damage to the prostatic epithelial cell. During prostatic carcinogenesis, this abnormal signaling may lead to changes in both the prostatic epithelium and smooth muscle with concomitant loss of growth control. In this way, both a malignant epithelium and an abnormal or ‘tumor stroma’ evolve.
The purpose of this article is to describe interactions between the stroma and epithelium of the normal prostate, and then to summarize evidence suggesting that stromal cells derived from benign versus malignant sources may exert differential effects on epithelial cell growth and differentiation.
Acknowledgements
This work was supported by NIH grants DK52721, CA 59831, DK 45861, CA 64872, DK 52708 and DK 47517, and by an AFUD/Pfizer USPG Research Scholarship to GDG.
