tetracycline and Prostatic-Neoplasms

The androgen receptor is a ligand-induced transcriptional factor, which plays an important role in normal development of the prostate as well as in the progression of prostate cancer to a hormone refractory state. We previously reported the identification of a novel AR coactivator protein, L-dopa decarboxylase (DDC), which can act at the cytoplasmic level to enhance AR activity. We have also shown that DDC is a neuroendocrine (NE) marker of prostate cancer and that its expression is increased after hormone-ablation therapy and progression to androgen independence. In the present study, we generated tetracycline-inducible LNCaP-DDC prostate cancer stable cells to identify DDC downstream target genes by oligonucleotide microarray analysis.. Comparison of induced DDC overexpressing cells versus non-induced control cell lines revealed a number of changes in the expression of androgen-regulated transcripts encoding proteins with a variety of molecular functions, including signal transduction, binding and catalytic activities. There were a total of 35 differentially expressed genes, 25 up-regulated and 10 down-regulated, in the DDC overexpressing cell line. In particular, we found a well-known androgen induced gene, TMEPAI, which wasup-regulated in DDC overexpressing cells, supporting its known co-activation function. In addition, DDC also further augmented the transcriptional repression function of AR for a subset of androgen-repressed genes. Changes in cellular gene transcription detected by microarray analysis were confirmed for selected genes by quantitative real-time RT-PCR.. Taken together, our results provide evidence for linking DDC action with AR signaling, which may be important for orchestrating molecular changes responsible for prostate cancer progression.

Topics: Adenocarcinoma; Androgens; Blotting, Western; Cell Line, Tumor; Dopa Decarboxylase; Enzyme Induction; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Genetic Vectors; Humans; Male; Neoplasm Proteins; Neoplasms, Hormone-Dependent; Oligonucleotide Array Sequence Analysis; Prostatic Neoplasms; Receptors, Androgen; Recombinant Fusion Proteins; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; RNA, Neoplasm; Tetracycline; Transfection

In a recent study, prostatectomy specimens from which Propionibacterium acnes was cultured were more likely to have inflammation than culture-negative specimens or specimens positive for other bacteria, leading the authors to hypothesize that P. acnes-mediated inflammation may contribute to prostate carcinogenesis. To indirectly explore associations between P. acnes and prostate cancer, we investigated severe acne, as measured by tetracycline use for 4 or more years, in relation to incident prostate cancer in the Health Professionals Follow-up Study. On the 1992 follow-up questionnaire, participants were asked whether they had ever used "tetracycline for at least 2 months at a time (e.g., for acne or other reason)" and their duration of use. Prostate cancer diagnoses were ascertained on each subsequent biennial questionnaire and confirmed by medical record review. Between 1992 and 2002, 2,147 cases of prostate cancer were reported among 34,629 eligible participants. Men who used tetracycline for 4 or more years had a significantly higher risk of prostate cancer (16 cases, 1,569 person-years) than men who did not use tetracycline (2,071 cases, 304,822 person-years, multivariable-adjusted RR = 1.70, 95% CI: 1.03-2.80). Although intriguing, this finding should be viewed cautiously because of the small number of exposed cases, indirect assessment of severe acne, and complex etiology of acne, which is not limited to P. acnes infection. Therefore, additional biologic and epidemiologic studies are necessary to determine and elucidate the possible role of P. acnes infection in prostate carcinogenesis.

Topics: Acne Vulgaris; Adult; Aged; Anti-Bacterial Agents; Gram-Positive Bacterial Infections; Health Personnel; Humans; Inflammation; Male; Middle Aged; Odds Ratio; Propionibacterium acnes; Prospective Studies; Prostatic Hyperplasia; Prostatic Neoplasms; Risk Assessment; Risk Factors; Surveys and Questionnaires; Tetracycline; Time Factors; United States

The aim of this study was to investigate means of increasing the efficiency with which cancer cell death following local radiation therapy (RT) is translated into the generation of tumor immunity since, if this were to be achieved, it would be expected to enhance the rates of disease-free recurrence and survival. Our investigations centered around the use of interleukin-3 (IL-3), expressed intratumorally using an inducible adenoviral vector, to alter the immunogenicity of established murine TRAMP-C1 prostate cancer receiving a course of fractionated local RT (7 Gy per fraction per day for 5 days). Because high systemic levels of IL-3 can be associated with toxicity, a tetracycline-regulated gene delivery system was employed. The results show that while intratumoral IL-3 expression or RT alone caused a modest delay in TRAMP-C1 tumor growth, the combination was synergistic with 50% of mice being cured and developing a long-term, tumor-specific state of immunity. Immunological analyses performed on splenic lymphocytes demonstrated that, compared to RT or IL-3 alone, combined treatment significantly increased the number of tumor-specific IFN-gamma-secreting and cytotoxic T cells. The study demonstrates that tetracycline-regulated IL-3 gene expression within tumors can enhance the immune response to prostate cancer and this can augment the efficacy of a course of RT without additional side effects.

Topics: Adenoviridae; Animals; Combined Modality Therapy; Genetic Therapy; Genetic Vectors; Interleukin-3; Male; Mice; Mice, Inbred C57BL; Prostatic Neoplasms; Tetracycline

Prostate cancer is one of the most common cancers in men. Several lines of evidence have suggested that bone morphogenetic protein (BMP) signals play important roles in the generation and progression of prostate cancers. In the present study, we show that BMP-7 inhibits the proliferation of androgen-insensitive PC-3 and DU-145 prostate cancer cells in a medium containing 1% fetal bovine serum, observed as decreased incorporation of [(3)H]thymidine and decreased cell number. Cell cycle analysis by flow cytometry showed an increased fraction of cells in the G1 phase and subsequent decrease in both S and G2/M phase after BMP-7 stimulation. BMP-7 caused an upregulation of the cyclin-dependent kinase inhibitor (CDKI) p21(CIP1/WAF1), and decreased the activity of Cdk2, leading to hypophosphorylation of Rb proteins. Furthermore, in order to evaluate the impact of BMP signals on prostate tumor growth, we generated the PC-3 cell lines expressing a constitutively active BMP type I receptor (constitutively active (c.a.) activin receptor-like kinase (ALK)-6) in a tetracycline (Tet)-regulated manner. Tet/doxycycline-regulated expression of c.a.ALK-6 resulted in the inhibition of in vitro cell proliferation and reduction of the size of tumors derived from the PC-3 cells subcutaneously injected into immune-deficient mice. Collectively, these findings suggest that BMP signals inhibit growth and proliferation of prostate tumor cells through induction of CDKI. Furthermore, this is the first report of a role for BMP signaling in reducing growth kinetics of androgen-insensitive prostate tumors.

Topics: Androgens; Animals; Bone Morphogenetic Protein 7; Bone Morphogenetic Protein Receptors, Type I; Bone Morphogenetic Proteins; CDC2-CDC28 Kinases; Cell Cycle Proteins; Cell Line, Tumor; Cell Proliferation; Cyclin-Dependent Kinase 2; Cyclin-Dependent Kinase Inhibitor p21; Immunoprecipitation; Male; Mice; Mice, Inbred BALB C; Phosphorylation; Prostatic Neoplasms; Protein Serine-Threonine Kinases; Receptors, Growth Factor; Retinoblastoma Protein; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction; Tetracycline; Transforming Growth Factor beta; Up-Regulation

Overexpression of the proinflammatory enzyme cyclooxygenase (COX)-2 is associated with the progression of various malignancies; the role of COX-2 in prostate cancer is less clear. The significance of COX-2 in prostate cancer growth and response to chemotherapy was investigated in an androgen-refractory prostate cancer cell line using a Tet-inducible antisense COX-2 expression system.. An antisense COX-2 cDNA construct under the control of a doxycycline-inducible promoter was transfected into a prostate cancer cell line, PC-3ML. Modulations of cell growth, apoptosis, and chemosensitivity in the presence or absence of doxycycline were analyzed. Tumor incidence, growth rate, and response to two cytotoxic drugs, COL-3 [chemically modified tetracycline-3-(6-demethyl-6-deoxy-4-dedimethylamino-tetracycline)] and Taxotere (docetaxel), were investigated in tumor xenografts. Apoptotic incidences and tumor microvessel density in tumors were determined by immunohistochemistry.. Conditional suppression of COX-2 in PC-3ML caused reduced cell proliferation, decreased levels of phosphorylated AKT, G(0)-G(1) arrest, and increased apoptosis and caspase-3 activity. Suppression of COX-2 increased Bax protein and decreased Bcl-x(L) protein in vitro. COX-2 antisense-expressing PC-3ML tumors showed a 57% growth delay compared with nontransfected or vector controls. Oral administration of COL-3 (40 mg/kg, oral gavage) or Taxotere (2.3 mg/kg, intraperitoneally; 3x per week) in tumor-bearing mice further slowed tumor growth (65% and approximately 94%, respectively). Compared with the control group, the occurrence of apoptosis in antisense COX-2 tumors was eight times higher, and the tumor microvessel density was three times lower.. These results provide direct evidence that constitutive expression of COX-2 in prostate cancer has both angiogenic and cytoprotective functions. Suppression of tumor cell COX-2 is sufficient to enhance chemotherapy response in prostate cancer.

Topics: Animals; Apoptosis; bcl-2-Associated X Protein; bcl-X Protein; Cell Proliferation; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; DNA, Complementary; Docetaxel; Drug Therapy, Combination; Gene Expression Regulation, Enzymologic; Male; Mice; Microcirculation; Neoplasms, Hormone-Dependent; Oligonucleotides, Antisense; Prostaglandin-Endoperoxide Synthases; Prostatic Neoplasms; Proto-Oncogene Proteins c-bcl-2; Taxoids; Tetracycline; Tumor Cells, Cultured

RNA interference (RNAi) is a powerful tool to induce loss-of-function phenotypes by inhibiting gene expression post-transcriptionally. Synthetic short interfering RNAs (siRNAs) as well as vector-based siRNA expression systems have been used successfully to silence gene expression in a variety of biological systems. We describe the development of an inducible siRNA expression system that is based on the tetracycline repressor and eukaryotic RNA polymerase III promoters (U6 and 7SK). For proof of concept we selectively inhibited expression of two catalytic subunits of the phosphatidylinositol 3-kinase (PI 3-kinase), p110alpha and p110beta, by using vector-derived short hairpin RNAs (shRNAs). Stable pools of human prostate cancer cells (PC-3) exhibiting reduced levels of both PI 3-kinase catalytic subunits due to the expression of corresponding shRNAs in an inducible fashion were established and analyzed for their invasive potential in vitro as well as in an orthotopic metastatic mouse model. This inducible system for RNAi allows an unbiased and comparable analysis of loss-of-function phenotypes by comparing selected isogenic cell populations on the induced and non-induced level. In addition, conditional RNAi allows the study of essential and multifunctional genes involved in complex biological processes by preventing inhibitory and compensatory effects caused by constitutive knockdown.

Topics: Animals; Catalytic Domain; Cell Line, Tumor; Disease Models, Animal; Gene Expression Regulation, Neoplastic; Humans; Male; Mice; Molecular Sequence Data; Nucleic Acid Conformation; Phosphatidylinositol 3-Kinases; Promoter Regions, Genetic; Prostatic Neoplasms; Protein Subunits; RNA Interference; RNA Polymerase III; RNA, Small Interfering; Tetracycline

The molecular mechanisms leading to prostate cancer remain poorly understood, especially concerning the progression to the metastatic form. SSeCKS, a major protein kinase C substrate with tumor suppressor activity, is likely the rodent orthologue of human Gravin/AKAP12, a scaffolding protein for protein kinases A and C. Gravin was mapped as a single-copy gene to 6q24-25.2, a hotspot for deletion in advanced prostate cancer, and therefore, we investigated the role of SSeCKS/Gravin in prostate oncogenesis. SSeCKS/Gravin protein was detected in untransformed rat and human prostate epithelial cell lines EP12 and PZ-HPV-7, respectively, and in human prostatic epithelium, especially basal epithelial cells. In contrast, SSeCKS/Gravin protein and RNA levels were severely reduced in human (PC-3, PPC-1, LNCaP, DU145, and TSU) and rat Dunning (AT3.1 and MatLyLu) prostate cancer cell lines. The regulated reexpression of SSeCKS in MatLyLu cells induced filopodia-like projections and a decrease in anchorage-independent growth. In nude mice, SSeCKS reexpression slightly decreased primary-site tumor growth but severely decreased the formation of lung metastases. Primary-site tumors that progressed lost regulated SSeCKS reexpression. SSeCKS/Gravin expression was detected in benign human prostatic lesions and well-differentiated carcinomas but not in undifferentiated lesions with Gleason sums > or =6. Our data suggest a role for the loss of SSeCKS/Gravin in the metastatic progression of human prostate cancer.

Topics: A Kinase Anchor Proteins; Animals; Biomarkers, Tumor; Cell Cycle Proteins; Cell Differentiation; Cell Division; Chromosome Banding; Chromosome Mapping; Chromosomes, Human, Pair 6; Female; Gene Expression Regulation, Neoplastic; HeLa Cells; Humans; In Situ Hybridization, Fluorescence; Male; Mice; Mice, Nude; Mitogens; Molecular Weight; Neoplasm Metastasis; Neoplasm Transplantation; Neoplasms, Experimental; Prostatic Neoplasms; Protein Isoforms; Proteins; Rats; RNA, Neoplasm; Tetracycline; Transplantation, Heterologous; Tumor Cells, Cultured

Cell-type-restricted transgene expression delivered by adenovirus vectors is highly desirable for gene therapy of cancer, as it can limit cytotoxic gene expression to tumor cells. However, many tumor- and tissue-specific promoters are weaker than the constitutively active promoters and are thus less effective. To combine cell-type specificity with high-level regulated transgene expression, we have developed a complex adenoviral vector. We have placed the tetracycline transactivator gene under the control of a prostate-specific ARR2PB promoter, and a mouse Tnfsf6 (encoding FASL)-GFP fusion gene under the control of the tetracycline responsive promoter. We have incorporated both expression cassettes into a single construct. We show that FASL-GFP expression from this vector is essentially restricted to prostate cancer cells, in which it can be regulated by doxycycline. Higher levels of prostate-specific FASL-GFP expression were generated by this approach than by driving the FASL-GFP expression directly with ARR2PB. More FASL-GFP expression correlated with greater induction of apoptosis in prostate cancer LNCaP cells. Mouse studies confirmed that systemic delivery of both the prostate-specific and the prostate-specific/tet-regulated vectors was well tolerated at doses that were lethal for FASL-GFP vector with CMV promoter. This strategy should be able to improve the safety and efficacy of cancer gene therapy using other cytotoxic genes as well.

Topics: Adenoviridae; Animals; Apoptosis; Cell Survival; Doxycycline; Fas Ligand Protein; Gene Expression Regulation; Genetic Vectors; Green Fluorescent Proteins; Humans; Liver; Luminescent Proteins; Male; Membrane Glycoproteins; Mice; Organ Specificity; Promoter Regions, Genetic; Prostate; Prostatic Neoplasms; Tetracycline; Time Factors; Tumor Cells, Cultured

In the prostate gland of adult mammals, most epithelial cells are in a state of proliferative quiescence. Androgens regulate this effect by inducing cell cycle arrest in the G(0)/G(1) phase. Potential mediators of this androgen-induced proliferative shutoff were identified by means of subtracted cDNA libraries. The expression pattern of one of these sequences, AS3, strongly correlated with the expression of the androgen-induced proliferative shutoff both temporally and dosewise. The AS3 gene is located on chromosome 13 q12.3, in close proximity to the BRCA2 gene. The loss of chromosomal regions where AS3 alleles are located correlates with various human cancers, including prostate. The biological effect of AS3 was tested in two stable cell lines, one expressing sense and another expressing antisense AS3 constructs, both under tetracycline regulation. S9 cells were obtained by retroviral infection with virions containing a tetracycline-regulated sense AS3 construct. In these cells, sense AS3 was negatively regulated by tetracycline. Tetracycline withdrawal increased the expression of AS3 mRNA and protein. The expression of tetracycline-regulated AS3 resulted in inhibition of cell proliferation. A4 cells were obtained by retroviral infection with virions containing a tetracycline-regulated antisense AS3 construct. Vector-driven expression of antisense-AS3 blocked the induction of androgen-induced endogenous AS3 mRNA and blocked the inhibitory effect of androgens on cell proliferation. Tetracycline-regulated expression of the empty vector control had no effect on cell proliferation. These experiments strongly suggest that AS3 is a mediator of the androgen-induced proliferative shutoff.

Topics: Amino Acid Sequence; Androgens; Cell Nucleus; Chromosome Mapping; Chromosomes, Human, Pair 13; DNA-Binding Proteins; DNA, Antisense; DNA, Complementary; Gene Expression Regulation, Neoplastic; Gene Library; Humans; Male; Molecular Sequence Data; Neoplasm Proteins; Prostatic Neoplasms; Repressor Proteins; Tetracycline; Trans-Activators; Transcription Factors; Transcription, Genetic; Transfection; Tumor Cells, Cultured

Features that distinguish tumor vasculatures from normal blood vessels are sought to enable the destruction of preformed tumor vessels. We show that blood vessels in both a xenografted tumor and primary human tumors contain a sizable fraction of immature blood vessels that have not yet recruited periendothelial cells. These immature vessels are selectively obliterated as a consequence of vascular endothelial growth factor (VEGF) withdrawal. In a xenografted glioma, the selective vulnerability of immature vessels to VEGF loss was demonstrated by downregulating VEGF transgene expression using a tetracycline-regulated expression system. In human prostate cancer, the constitutive production of VEGF by the glandular epithelium was suppressed as a consequence of androgen-ablation therapy. VEGF loss led, in turn, to selective apoptosis of endothelial cells in vessels devoid of periendothelial cells. These results suggest that the unique dependence on VEGF of blood vessels lacking periendothelial cells can be exploited to reduce an existing tumor vasculature.

Topics: Androgens; Animals; Apoptosis; Blood Vessels; Down-Regulation; Endothelial Growth Factors; Gene Expression Regulation, Neoplastic; Glioma; Humans; In Situ Nick-End Labeling; Lymphokines; Male; Mice; Mice, Nude; Neoplasms, Experimental; Prostatic Neoplasms; RNA, Messenger; Tetracycline; Transplantation, Heterologous; Tumor Cells, Cultured; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors

Neutral endopeptidase 24.11 (NEP) is a cell-surface enzyme expressed by prostatic epithelial cells that cleaves and inactivates neuropeptides implicated in the growth of androgen-independent prostate cancer (PC). We report that NEP expression and catalytic activity are lost in vitro in androgen-independent but not androgen-dependent PC cell lines. In vivo, NEP protein expression is commonly decreased in cancer cells of metastatic PC specimens from patients with androgen-independent but not androgen-dependent PC. Overexpression of NEP in androgen-independent PC cells or incubation with recombinant NEP inhibits PC cell growth. Furthermore, in androgen-dependent PC cells, expression of NEP is transcriptionally regulated by androgen and decreases with androgen withdrawal. These data suggest that decreased NEP expression, common in androgen-independent PCs, is facilitated by the elimination of androgens, and that NEP loss plays an important role in the development of androgen-independent PC by allowing PC cells to use mitogenic neuropeptides as an alternate source to androgen in order to stimulate cell proliferation.

Topics: Biomarkers, Tumor; Biopsy; Cell Division; Cell Nucleus; Dihydrotestosterone; Disease Progression; Gene Transfer Techniques; Humans; Kinetics; Male; Neoplasm Metastasis; Neprilysin; Polymerase Chain Reaction; Prostatic Neoplasms; Recombinant Proteins; Tetracycline; Time Factors; Transfection; Tumor Cells, Cultured

Studies of genes that may inhibit growth or induce death of cells are facilitated greatly by tightly controlled expression of those genes. A promising system for control of transgene expression over a wide range is the tetracycline-repressible transactivator (tTA) system developed by Gossen and Bujard [Proc Natl Acad Sci USA 1992;89:5547-5551]. We investigated the effectiveness of this system in three well-established human prostate cancer cell lines.. LNCaP, PC-3, and Tsu-Pr1 cells were transfected with a vector coding for the tTA protein and/or a luciferase reporter vector, and luciferase activity was measured in the presence and absence of tetracycline or the tTA protein.. In the absence of tetracycline, the tTA system yielded high levels of luciferase activity in all three cell lines. Background luciferase activity in the presence of tetracycline was nearly undetectable in LNCaP cells, moderate in Tsu-Pr1 cells, and more than 20-fold higher in PC-3 than in Tsu-Pr1 cells. Similar background activity was observed in Tsu-Pr1 and PC-3 cells, even in the absence of the transactivator protein.. The tTA system should be useful for stable transfection of cytotoxic transgenes in LNCaP cells and for control of transgene expression over a wide range in Tsu-Pr1 and PC-3 cells.

Topics: Cell Line; Gene Expression Regulation, Neoplastic; Humans; Luciferases; Male; Plasmids; Prostate; Prostatic Neoplasms; Protein Synthesis Inhibitors; RNA, Messenger; Tetracycline; Trans-Activators; Transfection; Tumor Cells, Cultured

Bone metastases are a common complication in prostate and breast cancer patients. It leads to extensive morbidity and eventually mortality. Matrix metalloproteinases are implicated in various steps of development of metastasis, through their ability to degrade the extracellular matrix. Increased matrix metalloproteinase activity of tumor cells has been associated with a higher metastatic potential. Inhibitors of metalloproteinases have been shown to effectively reduce or prevent the formation of metastases. The family of tetracyclines is able to inhibit matrix metalloproteinase activity through chelation of the zinc ion at the active site of the enzyme. Using tumor cell lines relevant to bone metastases, i.e. PC-3, MDA-MB-231, Hs696, B16/F1, we showed that tetracycline and derivatives of tetracycline, namely doxycycline and minocycline, also induced cytotoxicity. The effective concentrations are relatively high for plasma, but are clinically achievable in the bone, since tetracyclines are osteotropic. All four bone-metastasizing tumor cells produced and secreted various matrix metalloproteinases. Doxycycline was able to inhibit the activity of 72- and 92-kDa type IV collagenase secreted by bone-metastasizing cells by 79-87%. These characteristics could make tetracycline a unique candidate as a therapeutic agent to prevent bone metastases in cancer patients with a high likelihood for development of bone metastasis. Studies using animal models of experimental bone metastasis will be necessary to confirm this.

Topics: Adenocarcinoma; Animals; Anti-Bacterial Agents; Blotting, Western; Bone Neoplasms; Breast Neoplasms; Cell Survival; Collagenases; Culture Media, Conditioned; Doxycycline; Extracellular Matrix; Gelatinases; Humans; Male; Matrix Metalloproteinase 1; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; Matrix Metalloproteinase Inhibitors; Melanoma; Metalloendopeptidases; Mice; Minocycline; Prostatic Neoplasms; Protease Inhibitors; Tetracycline; Tetracyclines; Tumor Cells, Cultured

Topics: Aged; Diagnosis, Differential; Diagnostic Errors; Haemophilus Infections; Haemophilus influenzae; Humans; Intestinal Mucosa; Intestine, Small; Lymphatic Diseases; Male; Prostatic Neoplasms; Tetracycline; Whipple Disease

Topics: Adult; Aged; Cystitis; Drug Resistance, Microbial; Escherichia coli; Female; Humans; Infusions, Parenteral; Klebsiella; Male; Middle Aged; Minocycline; Postoperative Complications; Prostatic Hyperplasia; Prostatic Neoplasms; Proteus; Pseudomonas; Pyelonephritis; Staphylococcus; Tetracycline; Urologic Diseases

Topics: Adult; Aged; Ascitic Fluid; Bone Neoplasms; Breast Neoplasms; Cardiovascular Diseases; False Negative Reactions; False Positive Reactions; Female; Filtration; Gastrointestinal Neoplasms; Humans; Male; Membranes, Artificial; Methods; Middle Aged; Neoplasms; Ovarian Neoplasms; Pleural Effusion; Prostatic Neoplasms; Respiratory Tract Diseases; Respiratory Tract Neoplasms; Testicular Neoplasms; Tetracycline; Tuberculosis

Topics: Acute Kidney Injury; Adenocarcinoma; Anesthesia, Inhalation; Candida; Candidiasis; Drug Synergism; Humans; Kidney; Male; Methoxyflurane; Middle Aged; Nephrectomy; Postoperative Complications; Prostatectomy; Prostatic Neoplasms; Seminal Vesicles; Tetracycline; Urography

Topics: Fluorescence; Humans; Male; Prostatic Neoplasms; Tetracycline; Urinary Bladder Neoplasms

Topics: Adult; Aged; Biological Assay; Blood Urea Nitrogen; Bronchopneumonia; Cachexia; Cerebrovascular Disorders; Creatine; Female; Heart Failure; Humans; Laryngeal Neoplasms; Male; Mastectomy; Methacycline; Middle Aged; Neoplasms; Prostatic Neoplasms; Tetracycline; Urinary Tract Infections

Topics: Biomedical Research; Cystitis; Fluorescence; Humans; Kidney Neoplasms; Male; Neoplasms; Prostatic Neoplasms; Tetracycline; Urinary Bladder Neoplasms; Urinary Diversion; Urine

Topics: Blood Proteins; Chemistry Techniques, Analytical; Chromatography, Gel; Dialysis; Diethylstilbestrol; Humans; Hydrocortisone; Male; Prostatic Neoplasms; Protein Binding; Renal Dialysis; Research; Serum Albumin; Tetracycline