RESUMEN
Small-animal imaging with positron emission tomography (PET) has become a valuable tool for evaluating preclinical models of breast cancer and other diseases. In this review, we examine a number of issues related to preclinical imaging studies with PET, using transgenic models of ductal carcinoma in situ and metastasis as specific examples. We discuss imaging components such as reconstruction, normalization, and extraction of quantitative parameters. We also analyze the effect of longitudinal correlations on cohort size and present some simple statistical techniques for determining cohort sizes that may be helpful in designing preclinical imaging studies. We describe studies that are greatly facilitated by access to non-invasive imaging data including a study involving multiple endpoints and another investigating metastasis. We conclude with a brief survey of emerging approaches in small-animal PET imaging.
Asunto(s)
Carcinoma in Situ/diagnóstico por imagen , Carcinoma Ductal de Mama/diagnóstico por imagen , Carcinoma Ductal de Mama/secundario , Fluorodesoxiglucosa F18 , Neoplasias Mamarias Experimentales/diagnóstico por imagen , Tomografía de Emisión de Positrones/métodos , Tomografía de Emisión de Positrones/tendencias , Animales , Modelos Animales de Enfermedad , Progresión de la Enfermedad , Estudios Longitudinales , Metástasis Linfática , Glándulas Mamarias Animales/diagnóstico por imagen , Glándulas Mamarias Animales/patología , Neoplasias Mamarias Experimentales/patología , Ratones , Recuento Corporal Total/instrumentación , Recuento Corporal Total/tendenciasAsunto(s)
Neoplasias/patología , Animales , Biomarcadores de Tumor , Dieta , Humanos , Neoplasias/prevención & controlRESUMEN
Recent studies have shown that several loss-of-function mouse models of prostate carcinogenesis can develop a spectrum of precancerous lesions that resemble human prostatic intraepithelial neoplasia (PIN). Here, we have investigated the malignant potential of the high-grade PIN lesions that form in Nkx3.1(+/-); Pten(+/-) compound mutant mice and demonstrate their neoplastic progression in a serial transplantation/tissue recombination assay. Furthermore, we find that a majority of Nkx3.1(+/-); Pten(+/-) mice greater than 1 year of age develop invasive adenocarcinoma, which is frequently accompanied by metastases to lymph nodes. Finally, we observe androgen independence of high-grade PIN lesions after androgen ablation of Nkx3.1(+/-); Pten(+/-) mice. We conclude that Nkx3.1(+/-); Pten(+/-) mice recapitulate key features of advanced prostate cancer and represent a useful model for investigating associated molecular mechanisms and for evaluating therapeutic approaches.