Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 16420928

[Benign solid liver tumors].

José Manuel Ramia·Karim Muffak·Jesús Villar·Daniel Garrote·José Antonio Ferrón
View original source ↗Export metadata ↓

Abstract

Benign solid liver tumors are a heterogeneous group of lesions (adenoma, focal nodular hyperplasia, hemangioma, etc.) with highly varied epidemiological characteristics. Advances in diagnostic methods have improved preoperative diagnosis. Magnetic resonance imaging has become the key test, but there is still a percentage of cases in which definitive preoperative diagnosis is not feasible. The most frequent symptom is abdominal pain, although patients are frequently asymptomatic. Surgery is indicated when diagnosis is uncertain or there are complications (rupture, hemorrhage, etc.). Because of the risk of malignant transformation, adenomas should always be resected. Morbidity and mortality after resection of these tumors is very low since excision is limited, performed in young people without concomitant disease, and in healthy liver.

Explore related subjects

AdenomaHemangioma, CavernousHumansLiver NeoplasmsEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

José Manuel Ramia, Karim Muffak, Jesús Villar, Daniel Garrote, José Antonio Ferrón. 2005. [Benign solid liver tumors].. https://doi.org/10.1016/s0009-739x(05)70848-4

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2009

HMGA proteins up-regulate CCNB2 gene in mouse and human pituitary adenomas.

The high mobility group As (HMGAs) belong to a family of nonhistone nuclear proteins that orchestrate the assembly of nucleoprotein complexes. Through a complex network of protein-DNA and protein-protein interaction, they play important roles in gene transcription, recombination, and chromatin structure. This protein family is involved, through different mechanisms, in both benign and malignant neoplasias. We have recently reported that transgenic mice carrying the Hmga1 or Hmga2 genes under transcriptional control of the cytomegalovirus promoter develop pituitary adenomas secreting prolactin and growth hormone. We have shown that the mechanism of the HMGA2-induced pituitary adenoma is based on the increased E2F1 activity. The expression profile of mouse normal pituitary glands and adenomas induced in HMGA transgenic mice revealed an increased expression of the ccnb2 gene, coding for the cyclin B2 protein, in the neoplastic tissues compared with the normal pituitary gland. Here, we show, by electrophoretic mobility shift assay and chromatin immunoprecipitation, a direct binding of HMGA proteins to the promoter of ccnb2 gene, whereas luciferase assays showed that HMGAs are able to up-regulate ccnb2 promoter activity. Finally, we report an increased CCNB2 expression in human pituitary adenomas of different histotypes that is directly correlated with HMGA1 and HMGA2 expression. Because cyclin B2 is involved in the regulation of the cell cycle, these results taken together indicate that HMGA-induced cyclin B2 overexpression gives an important contribution to experimental and human pituitary tumorigenesis.

Adenoma↗
PubMed2007

A weighted logistic regression model for estimation of recurrence of adenomas.

In a colorectal polyp prevention trial, some participants might have their follow-up colonoscopy conducted before the scheduled time (i.e. at the end of the trial). This results in variable follow-up lengths for participants and the data of recurrence status at the end of the trial can be considered as current status data. In this paper, we use a weighted logistic regression model to estimate recurrence rate of adenoma data at the end of the trial. The weights are used to adjust for variable follow-up. We show that logistic regression tends to underestimate recurrence rate. In a simulation study, we show that Kaplan-Meier estimator derived from the right endpoint of the current status data tends to overestimate recurrence rate in contrast to logistic regression and the weighted logistic regression method can produce reasonable estimates of recurrence rate even under a high non-compliance rate compared to conventional logistic regression and Kaplan-Meier estimator. The method described here is illustrated with an example from a colon cancer study.

Adenoma↗
PubMed2007

Broad tumor spectrum in a mouse model of multiple endocrine neoplasia type 1.

Multiple endocrine neoplasia type 1 (MEN1) is an inherited cancer predisposition syndrome typified by development of tumors in parathyroid, pituitary and endocrine pancreas, as well as less common sites including both endocrine and nonendocrine organs. Deletion or mutation of the tumor suppressor gene MEN1 on chromosome 11 has been identified in many cases of MEN1 as well as in sporadic tumors. The molecular biology of menin, the protein encoded by MEN1, remains poorly understood. Here we describe a mouse model of MEN1 in which tumors were seen in pancreatic islets, pituitary, thyroid and parathyroid, adrenal glands, testes and ovaries. The observed tumor spectrum therefore includes types commonly seen in MEN1 patients and additional types. Pancreatic pathology was most common, evident in over 80% of animals, while other tumor types developed with lower frequency and generally later onset. Tumors of multiple endocrine organs were observed frequently, but progression to carcinoma and metastasis were not evident. Tumors in all sites showed loss of heterozygosity at the Men1 locus, though the frequency in testicular tumors was only 36%, indicating that a different molecular mechanism of tumorigenesis occurs in those Leydig tumors that do not show loss of the normal Men1 allele. Menin expression was below the level of detection in ovary, thyroid and testis, but loss of nuclear menin immunoreactivity was observed uniformly in all pancreatic islet adenomas and in some hyperplastic islet cells, suggesting that complete loss of Men1 is a critical point in islet tumor progression in this model.

Adenoma↗