Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A loop cutaneous ureterostomy was performed as an emergency treatment in 6 patients with bladder or prostatic cancer. Out of 9 operated ureters, only one stenosis was observed. Infection is a possible complication which can sometimes alter the renal function.
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PMID:Loop cutaneous ureterostomy as a method of urinary diversion in the adult. 43 72

In a study of the disease pattern of the elderly in Rwanda, all patients aged 60 or more, hospitalized in a one-year period at the Medical Department, University Hospital, Butare, were examined prospectively. One hundred and ninety-two patients were included; most were subsistence farmers having a mainly vegetarian diet and living in large families. Infections (37.5% of the patients) and liver cirrhosis (31.8%) were the problems most frequently encountered. Primary hepatocellular cancer was diagnosed in 5.7% of the patients and was the most frequent malignancy. The hospitalized elderly occupied 17.5% of the available beds in the Medical Department. Their disease pattern was different from that of younger patients, making heavier demands on the medical resources. Malaria and upper intestinal inflammation were less frequent in the elderly; liver cirrhosis, primary hepatocellular cancer, pneumonia, prostatic cancer, cardiovascular pathology, chronic renal pathology and chronic lung disease were more prevalent. Several age-related conditions frequently observed in industrialized countries (e.g. coronary heart disease, stroke, gallstones, renal cysts, dementia) were rare. The study thus illustrates the concept of 'secondary aging': to the primary changes induced by the aging process, additional alterations are added which depend upon the environment and the lifestyle, resulting in a varying disease pattern. Health policies thus must take into account that the demographic transition in developing countries may result in a pattern of diseases different from that seen in industrialized countries; care must be taken when transposing data obtained from elderly populations in industrialized countries.
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PMID:The disease pattern of elderly medical patients in Rwanda, central Africa. 841 4

We report three cases of iatrogenically induced vertebral osteomyelitis due to Pseudomonas aeruginosa. One case was a post-nucleotomy and post-operative complication of herniated disk treatment, one was related to infection of an epidural catheter in a patient suffering from rheumatoid arthritis and the third followed urinary investigation in a patient with prostate cancer. Infection was cured in all patients with antibiotic treatment. These case reports shed light on the possibility of infections with pseudomonas aeruginosa, in addition to the more common infections such as by staphylococci, especially following iatrogenic maneuvers.
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PMID:Iatrogenically induced vertebral osteomyelitis due to Pseudomonas aeruginosa. 873 27

Urologic refertilization microsurgery such as vaso-vasostomy or vaso-epididymostomy benefits from perioperative antibiotic prophylaxis. The ability of ampicillin and sulbactam to penetrate sufficiently into mixed epididymis or testis tissue was investigated in nine patients (bodyweights ranged from 58 kg to 92 kg, mean 77.3 kg) undergoing orchiectomy for testicular cancer or advanced prostatic cancer. Each patient received a single infusion of 3 g ampicillin/sulbactam (ratio 2:1) preoperatively for antibiotic prophylaxis. The concentrations of both components were determined in serum and in epididymis/testis tissue samples taken 30 min to 65 min after infusion. Ampicillin was determined by bioassay and sulbactam was determined by gas chromatography/ mass spectrometry. Mean tissue concentrations of ampicillin were 38.5 +/- 15.9 mg/kg. Mean tissue concentrations of sulbactam at the same time were 19.8 +/- 5.2 mg/kg. Comparison of the tissue/serum ratios for both agents showed no significant difference. These values indicate that both compounds achieve high concentrations in the scrotal organs. The concentrations exceed the MIC (minimal inhibitory concentration) values of important bacterial pathogens such as Staphylococcus aureus involved in postoperative wound infections. The combination of ampicillin and sulbactam may be effective for perioperative prophylaxis in reconstructive scrotal urologic surgery.
Infection
PMID:Penetration of ampicillin and sulbactam into human epididymis and testis. 892 48

We have previously described potent growth-inhibitory effect of a recombinant adenovirus expressing wild type p53 (AdWTp53) in metastatic prostate cancer cells via activation of cellular p53 pathways. We have extended these observations to analyze the effects of AdWTp53 on primary cultures of radical prostatectomy specimens (RPS) and have also evaluated the gene therapeutic potential of the AdWTp53 in a nude mice model. Infection of primary cultures of prostate cancer specimens resulted in about 80% cell growth inhibition in comparison with cultures treated with control adenovirus dl312. Single injection of AdWTp53 into pre-established tumor nodules of DU145 prostate cancer cells suppressed tumor growth significantly (p = 0.0407) as determined by comparison of tumor volumes of the AdWTp53-treated vs. control vector (dl312) or PBS-treated groups. Moreover, there was no significant difference in tumor growth inhibition between single vs. multiple injections of AdWTp53. Our observations support the potential of AdWTp53 for gene therapy of prostate cancer.
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PMID:Inhibition of the growth of pre-established subcutaneous tumor nodules of human prostate cancer cells by single injection of the recombinant adenovirus p53 expression vector. 913 72

Semliki Forest Virus (SFV) is a broad host range RNA virus capable of high-level recombinant protein expression and apoptosis induction in many cell types. We have successfully used a recombinant, replication deficient SFV vector to express the LacZ marker gene product in seven human prostate cell lines, as well as in human prostate tissue explants. Flow cytometry revealed that 40-60% of PPC-1 prostate cancer cells died 24-72 h after infection with SFV-LacZ virus. Most human prostate cancer cell lines expressed high levels of recombinant protein. Infection of human prostate tissue ex vivo led to similarly high expression levels but the recombinant beta-galactosidase was confined to duct epithelial cells. Infection of cell and tissue cultures resulted in detachment of adherent cells from the culture surface and detachment of epithelial cells from the basement membrane of tissue. Our results indicate that SFV may be useful in targeting recombinant protein expression and apoptosis to prostatic duct epithelial cells.
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PMID:Recombinant Semliki forest virus infects and kills human prostate cancer cell lines and prostatic duct epithelial cells ex vivo. 1067 63

The underlying causes for different apoptotic responses in neoplastic cells are still not fully understood. We demonstrate here that a human breast cancer cell line, MDA-MB-468, which lacks the retinoblastoma protein (RB), is particularly sensitive to low doses of ultraviolet (UV) radiation. These cells are 15-20-fold more sensitive to UV radiation than RB-positive cell lines, as measured by both apoptosis and clonogenic assays. In addition, a prostate cancer cell line that lacks functional RB, DU-145, was found to have a similar apoptotic response to low doses of UV radiation. Based on these data, we hypothesized that the lack of RB is responsible for the extreme sensitivity of these cells to UV-radiation-induced apoptosis. To further examine the role of RB in apoptosis, cells of RB-positive human breast cancer and normal cell lines were infected with the human papilloma virus type 16 (HPV-16) E7 and assessed for UV-radiation sensitivity. The HPV-16 E7 protein is known to decrease levels of free RB in cells. Infection of RB-positive human breast cancer or normal cells with E7 resulted in a 4-5-fold increase in sensitivity to UV radiation compared to controls. The above data suggest a role for the RB protein in protecting cells from undergoing apoptosis in response to UV radiation.
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PMID:Lack of RB protein correlates with increased sensitivity to UV-radiation-induced apoptosis in human breast cancer cells. 1102 55

We find that the prostate cancer cell lines ALVA-31, PC-3, and DU 145 are highly sensitive to apoptosis induced by TRAIL (tumor-necrosis factor-related apoptosis-inducing ligand), while the cell lines TSU-Pr1 and JCA-1 are moderately sensitive, and the LNCaP cell line is resistant. LNCaP cells lack active lipid phosphatase PTEN, a negative regulator of the phosphatidylinositol (PI) 3-kinase/Akt pathway, and demonstrate a high constitutive Akt activity. Inhibition of PI 3-kinase using wortmannin and LY-294002 suppressed constitutive Akt activity and sensitized LNCaP cells to TRAIL. Treatment of LNCaP cells with TRAIL alone induced cleavage of the caspase 8 and XIAP proteins. However, processing of BID, mitochondrial release of cytochrome c, activation of caspases 7 and 9, and apoptosis did not occur unless TRAIL was combined with either wortmannin, LY-294002, or cycloheximide. Blocking cytochrome c release by Bcl-2 overexpression rendered LNCaP cells resistant to TRAIL plus wortmannin treatment but did not affect caspase 8 or BID processing. This indicates that in these cells mitochondria are required for the propagation rather than the initiation of the apoptotic cascade. Infection of LNCaP cells with an adenovirus expressing a constitutively active Akt reversed the ability of wortmannin to potentiate TRAIL-induced BID cleavage. Thus, the PI 3-kinase-dependent blockage of TRAIL-induced apoptosis in LNCaP cells appears to be mediated by Akt through the inhibition of BID cleavage.
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PMID:Elevated AKT activity protects the prostate cancer cell line LNCaP from TRAIL-induced apoptosis. 1127 84

K(+) channel-associated protein/protein inhibitor of activated STAT (KChAP/PIAS3beta) is a potassium (K(+)) channel modulatory protein that boosts protein expression of a subset of K(+) channels and increases currents without affecting gating. Since increased K(+) efflux is an early event in apoptosis, we speculated that KChAP might induce apoptosis through its up-regulation of K(+) channel expression. KChAP belongs to the protein inhibitor of activated STAT family, members of which also interact with a variety of transcription factors including the proapoptotic protein, p53. Here we report that KChAP induces apoptosis in the prostate cancer cell line, LNCaP, which expresses both K(+) currents and wild-type p53. Infection with a recombinant adenovirus encoding KChAP (Ad/KChAP) increases K(+) efflux and reduces cell size as expected for an apoptotic volume decrease. The apoptosis inducer, staurosporine, increases endogenous KChAP levels, and LNCaP cells, 2 days after Ad/KChAP infection, show increased sensitivity to staurosporine. KChAP increases p53 levels and stimulates phosphorylation of p53 residue serine 15. Consistent with activation of p53 as a transcription factor, p21 levels are increased in infected cells. Wild-type p53 is not essential for induction of apoptosis by KChAP, however, since KChAP also induces apoptosis in DU145 cells, a prostate cancer cell line with mutant p53. Consistent with its proapoptotic properties, KChAP prevents growth of DU145 and LNCaP tumor xenografts in nude mice, indicating that infection with Ad/KChAP might represent a novel method of cancer treatment.
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PMID:Increased K+ efflux and apoptosis induced by the potassium channel modulatory protein KChAP/PIAS3beta in prostate cancer cells. 1187 52

Infection with the human immunodeficiency virus (HIV) invariably leads to the development of acquired immunodeficiency syndrome (AIDS) in most infected humans, yet does so rarely, if at all, in HIV-infected chimpanzees. The differences between the two species are not due to differences in cellular receptors or an inability of the chimpanzee to be infected, but rather to the lack of pan-immune activation in the infected primate. This results in reduced apoptotic death in CD4+ T-helper lymphocytes and a lower viral load. In humans the degree of chronic immune activation correlates with virus load and clinical outcome with high immune activation leading to high viral loads and the more rapid progression to AIDS and death. The type of immune perturbation seen in HIV-associated AIDS is similar to that of chronic graft-versus-host disease (GVHD) where reduced cell-mediated immune (CMI) responses occur early in the course of the disease and where humoral responses (HI) predominate. A reduced CMI response occurs in a number of chronic infectious diseases, including tuberculosis and leishmaniasis. More recently, it has become increasingly apparent that the CMI response is suppressed in virtually all malignant diseases, including melanoma and colorectal and prostate cancer. This raises the possibility that, as the malignant process develops, the cancer cells evolve to subvert the CMI response. Moreover, the reduced CMI response seen in colorectal cancer (CRC) patients is completely reversed following curative surgery strongly supporting the hypothesis that CRC can suppress the systemic immune response. Wound healing, ovulation, embryo implantation, and fetal growth are all associated with suppressed CMI and neovascularization (the formation of new blood vessels) or angiogenesis (the formation of new blood vessels from an existing vasculature). If unresolved, wound healing results in chronic inflammation, which can give rise to the phenomenon of "scar cancers." Indeed all the chronic inflammatory conditions known to be associated with the subsequent development of malignant disease, including chronic obstructive airway disease (COPD), ulcerative colitis (UC), and asbestosis, give rise to similar proangiogenic, suppressed CMI, and HI-predominant environments. In keeping with this CMI-associated cytokines such as interleukin (IL)-2 and interferon (IFN)-gamma tend to be antiangiogenic, whereas HI cytokines such as IL-6 tend to be proangiogenic. Furthermore, chronic immune activation leads to the synthesis and release of factors such as macrophage inflammatory protein (MIP)-1 that inhibit apoptosis through suppression of p53 activity. The "Golden Triangle" of suppressed CMI, angiogenesis, and reduced apoptosis would provide the ideal environment for the serial mutations to occur that are required for the development of malignant disease. If the observed association is relevant to carcinogenesis, then treatments aimed at reducing the components of these inflammatory conditions may be useful both in the setting of chemoprevention and the therapeutic management of established disease.
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PMID:Chronic immune activation and inflammation in the pathogenesis of AIDS and cancer. 1188 29


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