tetracycline and Adenocarcinoma

Anatomic pathology has produced considerable knowledge about environmental teratogens and carcinogens. A special disease registry established by a pathologist provided details of the association between oral contraceptives and hepatic neoplams. Pathologists were also involved in establishing in the link between diethylstilbestrol use and clear-cell adenocarcinomas of the vagina. An area of particular interest has been gender and ethnic differences in the incidence of certain diseases. Pathologists further make use of animal studies to investigate the pathogenesis of human tumors. Finally, stored serum or tissue is often used by pathologists to help diagnose diseases retrospectively. Human skin fibroblasts grown in culture and stored have been especially valuable for laboratory research. This chapter briefly highlights some of the milestones in the detection of enviromental effects through anatomic pathology.

Topics: Adenocarcinoma; Animals; Ataxia Telangiectasia; Contraceptives, Oral; Diethylstilbestrol; Disease Models, Animal; Environment; Ethnicity; Female; Geography; Herpesvirus 4, Human; Humans; Liver Neoplasms; Lymphoproliferative Disorders; Osteosarcoma; Pathology, Clinical; Radiation, Ionizing; Sex Factors; Tetracycline; Thorium Dioxide; Tooth Discoloration; Vaginal Neoplasms; X Chromosome

Topics: Adenocarcinoma; Amoxicillin; Antacids; Anti-Bacterial Agents; Bismuth; Clarithromycin; Drug Resistance, Bacterial; Drug Therapy, Combination; Helicobacter Infections; Helicobacter pylori; Humans; Metronidazole; Microbial Sensitivity Tests; Omeprazole; Practice Guidelines as Topic; Proton Pump Inhibitors; Pyrroles; Rifabutin; Stomach Neoplasms; Sulfonamides; Tetracycline; Treatment Outcome

RNA interference (RNAi) is a powerful technique and is widely used to down-regulate expression of specific genes in cultured cells and in vivo. In this paper, we report our development of a new tetracycline-inducible RNAi expression using a modified TRE-mouse U6 promoter in which the distal sequence element (DSE) was replaced by the tetracycline-responsive element (TRE). The modified TRE-mouse U6 promoter can be activated by a Tet-on version tetracycline-regulated artificial activator rTetOct which was constructed by fusing the rtTA DNA binding domain with the Oct-1 POU activation domain. This rTetOct/TRE-U6 system was successfully applied to conditionally and reversibly down-regulate the expression of endogenous p53 gene in MCF7 cells, and the expression of beta-defensin gene (mBin1b) either transiently expressed in COS7 cells or stably expressed in CHO cells.

Topics: Adenocarcinoma; Animals; beta-Defensins; Breast Neoplasms; Chlorocebus aethiops; CHO Cells; COS Cells; Cricetinae; Cricetulus; Doxycycline; Humans; Mice; Octamer Transcription Factor-1; Promoter Regions, Genetic; RNA Interference; RNA, Small Interfering; RNA, Small Nuclear; Tetracycline; Tumor Suppressor Protein p53

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

p53, a major sensor of DNA damage, is a transcription factor that, depending on its phosphorylation status, regulates the cell cycle, DNA repair, or apoptosis. The protein kinase C (PKC) family of isozymes is also implicated in cell cycle and programmed cell death (PCD) control and has recently been shown to influence p53 function. Using three human colon adenocarcinoma cell lines SW480, EB-1, and HCT116 that either lack p53 function and were engineered to express inducible wild-type p53 (wt p53), or that constitutively express wt p53, we show that phorbol ester-mediated PKC activation potentiates p53-induced PCD. Despite the effectiveness of PKC/p53 synergy in inducing SW480 tumor cell death, however, a fraction of the cells invariably survive. To address the putative mechanisms that underlie resistance to PKC/p53-induced cell death, we generated a phorbol 12-myristate 13-acetate/p53-resistant SW480 subline and compared the gene expression profile of resistant and parental cells by DNA microarray analysis. The results of these experiments show that PKC/p53-resistant cells express a higher level of several matrix metalloproteinases (MMP), including MMP-9, MMP-10, and MMP-12, and corresponding real-time PCR assays indicate that p53 is a negative regulator of MMP-9 gene expression. Using MMP inhibitors and MMP-specific small interfering RNA, we show that MMP function confers protection from PKC/p53-induced apoptosis and identify the protective MMPs as MMP-9 and MMP-10. Taken together, these observations provide evidence that MMPs are implicated in tumor cell resistance to the synergistic proapoptotic effect of PKC and p53.

Topics: Adenocarcinoma; Apoptosis; Caspases; Cell Line, Tumor; Colonic Neoplasms; Down-Regulation; Humans; Intracellular Membranes; Matrix Metalloproteinase 10; Matrix Metalloproteinase 9; Membrane Potentials; Metalloendopeptidases; Mitochondria; Phosphatidylserines; Protein Kinase C; RNA, Small Interfering; Tetracycline; Tetradecanoylphorbol Acetate; Tumor Suppressor Protein p53

The impact of Helicobacter eradication therapy on the progression or regression of gastric lesions is poorly defined. This study examined the effects of eradication therapy on inflammation, atrophy, metaplasia, dysplasia, and cancer progression.. C57BL/6 mice were infected with Helicobacter felis and received bacterial eradication therapy after 2, 6, or 12 months of infection. The gastric mucosa was examined at early, mid, and late intervals after eradication and graded for histology, expression pattern of alpha-catenin and beta-catenin, and IQGAP1.. Eradication of Helicobacter infection after 2 or 6 months of infection led to a regression of inflammation, restoration of parietal cell mass, and reestablishment of normal architecture. Progression to adenocarcinoma was prevented. Bacterial eradication at 1 year was associated with the reappearance of parietal cells, partial regression of inflammation, and restoration of architecture. Hyperplasia scores significantly improved, and dysplasia did not progress. Infected mice developed antral adenocarcinoma and gastric outlet obstruction by 24 months. Only 30% of the mice receiving bacterial eradication therapy at 12 months developed antral carcinoma. Bacterial eradication at any time during the first year of infection prevented death due to gastric outlet obstruction. The expression pattern of alpha-catenin, beta-catenin, and IQGAP1 varied with cell type and paralleled histologic changes.. Inflammation, metaplasia, and dysplasia are reversible with early eradication therapy; progression of dysplasia was arrested with eradication therapy given as late as 1 year and prevented gastric cancer-related deaths.

Topics: Adenocarcinoma; Animals; Anti-Bacterial Agents; Atrophy; Disease Models, Animal; Gastric Mucosa; Helicobacter felis; Helicobacter Infections; Male; Mice; Mice, Inbred C57BL; Precancerous Conditions; Stomach Neoplasms; Tetracycline

Cas-family proteins have been implicated as signaling intermediaries in diverse processes including cellular attachment, motility, growth factor response, apoptosis and oncogenic transformation. The three defined Cas-family members (p130Cas, HEF1/Cas-L and Efs/Sin) are subject to multiple forms of regulation (including cell-cycle- and cell-attachment-mediated post-translational modification and cleavage) that complicate elucidation of the function of specific Cas proteins in defined biological processes. To explore the biological role of HEF1 further, we have developed a series of cell lines in which HEF1 production is regulated by an inducible promoter. In this system, HEF1 production rapidly induces changes in cellular morphology and motility, enhancing cell speed and haptotaxis towards fibronectin in a process partially dependent on intact ERK and p38 MAPK signaling pathways. Finally, cDNA expression array analysis and subsequent studies indicate that HEF1 production increases levels of mRNA transcripts encoding proteins that are associated with motility, cell transformation and invasiveness, including several metalloproteinases, MLCK, p160ROCK and ErbB2. Upregulation of such proteins suggests mechanisms through which misregulation of HEF1 may be involved in cancer progression.

Topics: Adaptor Proteins, Signal Transducing; Adenocarcinoma; Antibodies; Blotting, Western; Breast Neoplasms; Cell Movement; Cell Size; Clone Cells; Female; Gene Expression Regulation, Neoplastic; Humans; Kinetics; Microscopy, Confocal; Microscopy, Video; Mitogen-Activated Protein Kinases; Neoplasms; Oligonucleotide Array Sequence Analysis; p38 Mitogen-Activated Protein Kinases; Phosphoproteins; Promoter Regions, Genetic; Tetracycline; Transcription, Genetic; Transfection

Fibroblast growth factor-2 (FGF2) is a pleiotropic heparin-binding growth factor endowed with a potent angiogenic activity in vitro and in vivo. To investigate the impact of the modulation of FGF2 expression on the neovascularization at different stages of tumor growth, we generated stable transfectants (Tet-FGF2) from the human endometrial adenocarcinoma HEC-1-B cell line in which FGF2 expression is under the control of the tetracycline-responsive promoter (Tet-off system). After transfection, independent clones were obtained in which FGF2 mRNA and protein were up-regulated compared with parental cells. Also, the conditioned medium of Tet-FGF2 transfectants caused proliferation, urokinase-type plasminogen activator up-regulation, migration, and sprouting of cultured endothelial cells. A 3-day treatment of Tet-FGF2 cell cultures with tetracycline abolished FGF2 overexpression and the biological activity of the conditioned medium without affecting their proliferative capacity. Tet-FGF2 cells formed tumors when nude mice received s.c. injections. The administration of 2.0 mg/ml tetracycline in the drinking water before cell transplantation, continued throughout the whole experiment, inhibited FGF2 expression in Tet-FGF2 tumor lesions. This was paralleled by a significant decrease in the rate of tumor growth and vascularization to values similar to those observed in lesions generated by parental HEC-1-B cells. Tetracycline administration 20 days after tumor cell implant, although equally effective in reducing FGF2 expression and inhibiting tumor vascularity, only minimally impaired the growth of established Tet-FGF2 tumors. The results indicate that FGF2 expression deeply affects the initial tumor growth and neovascularization of HEC-1-B human endometrial adenocarcinoma in nude mice. On the contrary, the growth of established tumors appears to be independent of the inhibition of FGF2 expression and decreased vascular density. The possibility that a significant reduction of angiogenesis may not affect the progression of large tumors points to the use of antiangiogenic therapy in early tumor stage.

Topics: Adenocarcinoma; Animals; Cell Division; DNA, Complementary; Endometrial Neoplasms; Female; Fibroblast Growth Factor 2; Gene Expression; Genetic Vectors; Humans; Mice; Mice, Nude; Neovascularization, Pathologic; Promoter Regions, Genetic; Tetracycline; Time Factors; Transfection; Tumor Cells, Cultured; Xenograft Model Antitumor Assays

p73, a member of the p53 family, can induce apoptosis in cancer cells. Since p53-mediated apoptosis can be augmented by various cancer chemotherapeutic agents, it has been hypothesized that the status of the endogenous p53 gene in cancer cells is a key determinant in the outcome of cancer therapy. To determine whether p73 can sensitize cancer cells to apoptosis by DNA damage agents, several MCF7 adenocarcinoma cell lines that inducibly express p73 or p53 under a tetracycline-regulated promoter were generated. We found that at relevant physiological levels, p73, but not p53, is capable of sensitizing MCF7 cells to apoptosis induced by chemotherapeutic agents. In addition, we found that p73 can cooperate with the DNA damaging agent camptothecin to activate the initiator caspase 2. Furthermore, we found that p73 can cooperate with DNA damaging agents or p53 to induce some p53 target genes and activate their promoters. In contrast, in MCF7E6 cells that ectopically express the human papillomavirus E6 oncogene and are functionally p53-null, the ability of p73 to sensitize cells to apoptosis is abrogated. Taken together, these results suggest that a functional interaction between p53 and p73 in MCF7 cells leads to enhanced induction of apoptosis.

Topics: Adenocarcinoma; Apoptosis; Breast Neoplasms; Camptothecin; Caspases; DNA Damage; DNA-Binding Proteins; Doxorubicin; Female; Gene Expression Regulation, Neoplastic; Genes, p53; Genes, Reporter; Genes, Tumor Suppressor; Humans; Luciferases; Neoplasm Proteins; Nuclear Proteins; Promoter Regions, Genetic; Recombinant Fusion Proteins; Tetracycline; Transcription, Genetic; Tumor Cells, Cultured; Tumor Protein p73; Tumor Suppressor Protein p53; Tumor Suppressor Proteins

To investigate the role of an activated K-Ras gene in the initiation and maintenance of lung adenocarcinomas, we developed transgenic mice that express murine K-Ras4b(G12D) under the control of doxycycline in type II pneumocytes. Focal proliferative lesions of alveolar type II pneumocytes were observed as early as seven days after induction with doxycycline; after two months of induction, the lungs contained adenomas and adenocarcinomas, with focal invasion of the pleura at later stages. Removal of doxycycline caused a rapid fall in levels of mutant K-Ras RNA and concomitant apoptotic regression of both the early proliferative lesions and the tumors. Tumor burden was dramatically decreased by three days after withdrawal, and tumors were undetectable after one month. When similar experiments were performed with animals deficient in either the p53 gene or the Ink4A/Arf locus, tumors arose more quickly (within one month of exposure to doxycycline) and displayed more obvious histological features of malignancy; nevertheless, these tumors also regressed rapidly when the inducer was removed, implying that continued production of mutant K-Ras is necessary to maintain the viability of tumor cells in the absence as well as the presence of tumor suppressor genes. We also show that the appearance and regression of these pulmonary tumors can be readily monitored in anesthetized transgenic animals by magnetic resonance imaging.

Topics: Adenocarcinoma; Adenoma; Animals; Apoptosis; Bromodeoxyuridine; Cyclin-Dependent Kinase Inhibitor p16; DNA Primers; Gene Expression Regulation, Neoplastic; Genes, ras; Genes, Tumor Suppressor; Genotype; In Situ Nick-End Labeling; Lung Neoplasms; Mice; Mice, Knockout; Mice, Transgenic; Models, Genetic; Neoplasm Recurrence, Local; Reverse Transcriptase Polymerase Chain Reaction; Tetracycline; Transgenes; Tumor Suppressor Protein p53

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

Pelvic lymphocysts developed in 3 of 124 patients undergoing radical surgery for cervical cancer. All were managed by percutaneous aspiration under local anesthesia in an outpatient setting. Sclerosis was required in one patient. This management plan is superior to laparotomy in being less morbid and equally effective.

Topics: Adenocarcinoma; Adult; Anesthesia, Local; Drainage; Female; Humans; Hysterectomy; In Vitro Techniques; Lymphatic Diseases; Lymphocele; Middle Aged; Postoperative Complications; Tetracycline; Uterine Cervical Neoplasms

Topics: Adenocarcinoma; Biliary Fistula; Female; Humans; Liver Neoplasms; Middle Aged; Postoperative Complications; Sclerosing Solutions; Sigmoid Neoplasms; Tetracycline

In chylous fistulas following radical neck dissections, we have found reexploration to be unrewarding, with infrequent identification of a specific leakage site intraoperatively and persistent fluid accumulation postoperatively. As an alternative, we injected tetracycline hydrochloride into the supraclavicular wound bed. This procedure resulted in a rapid, sustained decline in fistula output in two of three cases, avoiding surgical intervention. Tetracycline sclerotherapy has been described for treatment of intrathoracic and other intracavitary fluid collections. We believe that tetracycline sclerotherapy is an effective adjunct in the management of chylous fistulas following radical neck dissections and that this therapy should be attempted before surgical reexploration.

Topics: Adenocarcinoma; Aged; Carcinoma, Squamous Cell; Chyle; Drainage; Female; Fistula; Head and Neck Neoplasms; Humans; Male; Methods; Neck Dissection; Parotid Neoplasms; Postoperative Complications; Sclerosing Solutions; Tetracycline; Time Factors

Five patients who developed seromas following mastectomy with lymph node dissection were treated with aspiration of the seromas and instillation of a sclerosant solution containing tetracycline. All seromas resolved promptly without infection, flap necrosis, or recurrence. The technique is recommended for treatment of this postoperative complication.

Topics: Adenocarcinoma; Aged; Breast Neoplasms; Edema; Female; Humans; Mastectomy; Middle Aged; Postoperative Complications; Sclerosing Solutions; Surgical Wound Infection; Tetracycline

Salmonella empyema in an immunologically compromised patient with malignant pleural effusion is described. Antimicrobial treatment was ineffective when given parenterally. Intrapleural administration of antibiotics resulted in a rapid rise of the antibacterial activity of the pleural fluid, leading to rapid clinical improvement and eradication of the infections.

Topics: Adenocarcinoma; Empyema; Humans; Lung Neoplasms; Male; Microbial Sensitivity Tests; Middle Aged; Neoplasm Metastasis; Pleural Effusion; Salmonella; Salmonella Infections; Tetracycline; Thyroid Neoplasms

Topics: Adenocarcinoma; Animals; Cell Division; Female; Kidney; Kinetics; Liver; Mammary Neoplasms, Experimental; Muscles; Neoplasms, Experimental; Rats; Tetracycline; Tissue Distribution; Tritium

Topics: Adenocarcinoma; Animals; Carcinoma, Bronchogenic; Carcinoma, Hepatocellular; Gallium; Glioblastoma; Hodgkin Disease; Humans; L-Lactate Dehydrogenase; Liver Neoplasms; Lung Neoplasms; Mediastinal Neoplasms; Methane; Mice; Muscular Diseases; Neoplasm Metastasis; Neoplasm Transplantation; Neoplasms, Experimental; Nitrosourea Compounds; Osteosarcoma; Rabbits; Radioisotopes; Radionuclide Imaging; Rats; Sarcoma; Sarcoma, Experimental; Technetium; Tetracycline; Transplantation, Homologous

Topics: Adenocarcinoma; Adult; Aged; Ampicillin; Breast Neoplasms; Carcinoma; Cross Infection; Cysts; Disease Outbreaks; Erythromycin; Female; Foot; Gentamicins; Hallux Valgus; Herniorrhaphy; Humans; Kidney Diseases, Cystic; Leg; Male; Middle Aged; Ovarian Diseases; Penicillins; Peptic Ulcer; Quebec; Streptococcal Infections; Surgical Wound Infection; Tetracycline

Topics: Adenocarcinoma; Animals; Boron Compounds; Methods; Mice; Mice, Inbred DBA; Microsomes; Mitochondria; Neoplasm Proteins; Neoplasm Transplantation; Neoplasms, Experimental; Neoplastic Cells, Circulating; Neutrons; Ribosomes; Tetracycline

Topics: Adenocarcinoma; Carcinoma; Female; Fluorescence; Gastric Lavage; Gastritis; Humans; Male; Polyps; Stomach Neoplasms; Stomach Ulcer; Tetracycline

Topics: Adenocarcinoma; Aged; Bacterial Infections; Catheterization; Colostomy; Female; Humans; Kanamycin; Ligation; Male; Methods; Middle Aged; Neoplasm Seeding; Penicillins; Postoperative Complications; Rectal Neoplasms; Tetracycline

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: Adenocarcinoma; Carcinoma, Squamous Cell; Cytodiagnosis; Female; Genital Neoplasms, Female; Humans; Microscopy, Fluorescence; Ovarian Neoplasms; Tetracycline; Uterine Cervical Neoplasms; Uterine Neoplasms; Vulvar Neoplasms

Topics: Adenocarcinoma; Carcinoma; Colonic Neoplasms; Diagnosis, Differential; Diverticulitis, Colonic; Fluorescence; Humans; Microscopy, Fluorescence; Prognosis; Rectal Neoplasms; Sigmoid Neoplasms; Stomach Neoplasms; Tetracycline

Topics: Adenocarcinoma; Fluorescence; Fluorometry; Gastrointestinal Neoplasms; Hodgkin Disease; Humans; In Vitro Techniques; Tetracycline

Topics: Adenocarcinoma; Animals; Calcinosis; Calcium; Cricetinae; Cytoplasm; Fluorescence; Humans; Neoplasm Transplantation; Neoplasms, Experimental; Tetracycline

Topics: Adenocarcinoma; Animals; Formaldehyde; Injections, Intraperitoneal; Leukemia; Leukemia, Experimental; Mice; Mustard Plant; Neoplasms; Neoplasms, Experimental; Nitrogen Mustard Compounds; Pharmacology; Research; Sarcoma 180; Tetracycline

Topics: Adenocarcinoma; Aged; Bile Duct Neoplasms; Chloramphenicol; Cholangitis; Drug Therapy; Gallstones; Geriatrics; Humans; Surgical Procedures, Operative; Tetracycline

Topics: Adenocarcinoma; Cytodiagnosis; Fluorescence; Gastric Lavage; Humans; Leiomyosarcoma; Neoplasms; Protein Synthesis Inhibitors; Stomach Neoplasms; Tetracycline

Topics: Adenocarcinoma; Carcinoma; Carcinoma, Squamous Cell; Cystoscopy; Fluorescence; Humans; Tetracycline; Ultraviolet Rays; Urinary Bladder Neoplasms

Topics: Adenocarcinoma; Diagnosis, Differential; Fluorescence; Gastritis; Humans; Neoplasms; Sarcoma; Stomach Neoplasms; Stomach Ulcer; Tetracycline

Topics: Adenocarcinoma; Animals; Calcium; Calcium, Dietary; Cortisone; Cricetinae; Fluorescence; Humans; Lung Neoplasms; Neoplasm Transplantation; Research; Tetracycline

Topics: Adenocarcinoma; Adenocarcinoma, Mucinous; Carcinoma; Colloids; Diagnosis, Differential; Duodenal Ulcer; Fluorescence; Humans; Stomach Neoplasms; Stomach Ulcer; Tetracycline; Ultraviolet Rays