Rostate Cancer Research Articles

Situación epidemiológica del cáncer de próstata en España

AbstractProstate cancer is the third most frequent neoplasms in Spanish men and the third cause of cancer death. Incidence grows up with the increase of age. 90% of cases are diagnostic in people over 65 years old. Etiology is quite unknown and has been associated with environmental exposure, life style, family sign and genetic factors. In 2002 mortality rate was 21.5/ 100.000 (situated among the lowest in Europe), with more than 5.000 deaths. Trend of mortality has grown up until 1998, from this year it has decreased due to improve on diagnostic and treatment. In order to study prostate cancer incidence we find a difficulty due to shortage of population cancer register. Estimations have found incidence rates of 45.33/100.000 which are among the lowest in Europe. Annual incidence of prostatic cancer has grown up in all Spanish registers, not only improve in register systems explains it, but also the development of diagnosis tests with a higher survival from the beginning of 90s (86% the first year after diagnosis and 65,5% five years after diagnosis), similar to other European countries. Blow up the cancer register system is necessary to know the incidence and prevalence, to assess survival and effectiveness of screening programs and to improve the knowledge of risk factors.

A Blocking Antibody to Nerve Growth Factor Attenuates Skeletal Pain Induced by Prostate Tumor Cells Growing in Bone

Prostate cancer is unique in that bone is often the only clinically detectable site of metastasis. Prostate tumors that have metastasized to bone frequently induce bone pain which can be difficult to fully control as it seems to be driven simultaneously by inflammatory, neuropathic, and tumorigenic mechanisms. As nerve growth factor (NGF) has been shown to modulate inflammatory and some neuropathic pain states in animal models, an NGF-sequestering antibody was administered in a prostate model of bone cancer where significant bone formation and bone destruction occur simultaneously in the mouse femur. Administration of a blocking antibody to NGF produced a significant reduction in both early and late stage bone cancer pain-related behaviors that was greater than or equivalent to that achieved with acute administration of 10 or 30 mg/kg of morphine sulfate. In contrast, this therapy did not influence tumor-induced bone remodeling, osteoblast proliferation, osteoclastogenesis, tumor growth, or markers of sensory or sympathetic innervation in the skin or bone. One rather unique aspect of the sensory innervation of bone, that may partially explain the analgesic efficacy of anti-NGF therapy in relieving prostate cancer-induced bone pain, is that nearly all nerve fibers that innervate the bone express trkA and p75, and these are the receptors through which NGF sensitizes and/or activates nociceptors. The present results suggest that anti-NGF therapy may be effective in reducing pain and enhancing the quality of life in patients with prostate tumor-induced bone cancer pain.

Small-interfering RNA–induced androgen receptor silencing leads to apoptotic cell death in prostate cancer

Prostate cancer is the second leading cause of cancer death in the United States and, thus far, there has been no effective therapy for the treatment of hormone-refractory disease. Recently, the androgen receptor (AR) has been shown to play a critical role in the development and progression of the disease. In this report, we showed that knocking down the AR protein level by a small interfering RNA (siRNA) approach resulted in a significant apoptotic cell death as evidenced by an increased annexin V binding, reduced mitochondrial potential, caspase-3/6 activation, and DFF45 and poly(ADP-ribose) polymerase cleavage. The apoptotic response was specifically observed in those siRNA-transfected cells that harbor a native AR gene. No cell death was found in the AR-null prostate cancer cell PC-3 or its subline that has been reconstituted with an exogenous AR gene, as well as two breast cancer cell lines that are AR positive. Moreover, in parallel with the siRNA-induced AR silencing, the antiapoptotic protein Bcl-xL was significantly reduced, which might account for the apoptotic cell death because ectopic enforced expression of Bcl-xL protein partially inhibited apoptosis after AR silencing. Taken together, our data showed that knocking down the AR protein level in prostate cancer cells leads to apoptosis by disrupting the Bcl-xL-mediated survival signal downstream of AR-dependent survival pathway.

Animal models of prostate cancer.

AbstractProstate cancer is now the most common malignancy and the second highest cause of cancer death of men in Western society. It has a reasonably slow doubling time, is initially androgen dependent (AD) or androgen sensitive (AS), produces prostate-specific antigen (PSA), and prostate specific membrane antigen (PSMA) and, with time, metastasizes to lymph nodes, bone, and other organs; it progresses to an androgen-independent (AI) state. Prostate cancer rarely arises spontaneously in animals, and human and animal prostates differ in their anatomy, cellular content, and in the development of spontaneous benign hyper-plasia that commonly occurs in men as they age but rarely in other species. Existing prostate cancer models include rodent models, human cell lines (in the main derived from metastatic deposits), and gene transfer and transgenic models. Only the transgenic models provide the spectrum of disease as it occurs in men, with progression from prostate intraepithelial neoplasia (PIN) through AD to AI disease with metastases. Special systems have been devised to study the growth of prostate cancer cells in bone; these are described elsewhere in this book. The in vivo systems provide the appropriate cellular milieu allowing for epithelial cell-stromal cell interactions that are crucial to the behavior of prostate cancer cells. This chapter provides a critical appraisal of the models and some of their uses in studies of disease progression and for testing new therapeutic options.KeywordsProstate CancerAndrogen ReceptorBenign Prostatic HyperplasiaProstate Intraepithelial NeoplasiaProstate Specific Membrane AntigenThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Epidemiological investigation of prostate cancer.

AbstractProstate cancer is the most common male cancer diagnosed in Western populations. Autopsy studies have shown that with increasing age, the majority of men will develop microscopic foci of cancer (often termed “latent” prostate cancer) and that this is true in populations that are at both high and low risk for the invasive form of the disease (1). However, only a small percentage of men will develop invasive prostate cancer. The prevalence of prostate cancer is, thus, very common; but to most men, prostate cancer will be only incidental to their health and death.KeywordsProstate CancerAndrogen ReceptorProstate Cancer RiskAndrogen Receptor GeneInvasive Prostate CancerThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Targeted alpha therapy of prostate cancer.

AbstractProstate cancer (PC) is now the second most common cause of death from cancer in men after lung cancer (1). Brachytherapy, prostatectomy, or external beam radiation can effect a cure, with a life expectancy of at least 10 yr at diagnosis (2). Survival depends on the disease being organ confined, specimen confined, or margin positive, with failure rates of 12, 30, and 60%, respectively. Despite aggressive therapy, a significant percentage of men will die of disseminated disease (3). Moreover, radical therapy can have distressing side effects. ranging from surgical mortality, incontinence, impotence, bowel damage, and stricture (4).KeywordsProstate CancerProstate Cancer CellLinear Energy TransferRelative Biological EffectivenessPlasminogen Activator Inhibitor TypeThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Progression model of prostate cancer.

AbstractProstate cancer is the most common form of cancer diagnosed in men (other than skin cancer). In 1999, in the United States alone there were approximately 179,300 new cases and 37,000 deaths due to prostate cancer (1). In 1999, the prostate cancers diagnosed accounted for 29% of cancers in men and 14.7% of all cancers (other than skin) in both sexes, making it the most diagnosed cancer in the total population. In the prostate, the formation of histologically identifiable neoplastic lesions is a very frequent event, occurring in nearly one-third of the male population over 45 years of age (2). Fortunately, it has been estimated that only a small percentage of these men will actually die from prostate cancer (3–6). There is evidence to support environmental (including cell-cell interactions), epigenetic, and other factors playing a role in prostate tumorigenesis (7–17). However, that cancer in general is a genetic disease is currently the most widely accepted model of tumor etiology (18,19). A number of genetic changes have been documented in prostate cancer. Consistently, allelic losses of specific chromosomes are observed in prostate tumors, but this is not true for mutations on specific genes (20–22). Prostate cancers require many years to develop. It is believed that during these years they accumulate a number of genetic alterations. However, the molecular events that underlie the development of prostate neoplasia are not well defined (22). Thus, it has been difficult to establish a genetic model for the progression of prostate cancer.KeywordsProstate CancerAndrogen ReceptorGenetic AlterationProstate TumorProstatic Intraepithelial NeoplasiaThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Radiofrequency Transurethral Hyperthermia and Complete Androgen Blockade: A Nonsurgical Approach to Treating Prostate Cancer

rostate cancer (PC) is a major health problem in the Western world being the second most common male malignancy in the European Union. The age-standardized incidence of PC var ies more than one hundredfold between areas with the highest incidence (e.g., the United States) and the lowest incidence (e.g., Japan) in the world. In certain parts of the world, in particular the Western countries, the incidence of this disease has increased rapidly over the past 20 years. There are several environmental and genetic factors that partially explain these variations, although the incidence probably depends most of all on the extent to which small latent tumors are detected. Being that the clinical significance of small tumors is uncertain, the value of early diagnosis and early aggressive treatment is controversial. More than half of patients with diagnosed PC do not have metastatic disease. This may be the result of better and earlier screening processes.' Common treatment of PC with local manifestations