Incidentally polycystic kidney disease identified by SPECT/CT with post-therapy radioiodine scintigraphy in a patient with differentiated thyroid carcinoma: A case report.

RATIONALE: Post-therapy or diagnostic whole-body radioiodine scintigraphy is widely employed to evaluate the residual, recurrence, or metastases of differentiated thyroid carcinoma because of the high sensitivity and accuracy. However, it has pitfalls. PATIENT CONCERNS: We described a 63-year-old male with a history of papillary thyroid carcinoma who was referred for iodine-131 ablation therapy. The post-therapy iodine-131 whole-body images demonstrated abnormal increased uptake of the tracer in the regions of bilateral upper abdomen. DIAGNOSES: The single photon emission computed tomography/computed tomography (SPECT/CT) showed the abnormal Iactivity was corresponded to multiple irregular cystic low densities in the both kidneys on the low-dose computed tomography images, so the diagnosis of polycystic kidney disease was confirmed. INTERVENTIONS AND OUTCOMES: The patient responded well to the lifestyle-based treatments. LESSONS: Polycystic kidney disease was one of the etiologies of the false-positive findings in the radioiodine scintigraphy.

Cloning and functional expression of a chitinase cDNA from the apple leaf miner moth Lithocolletis ringoniella.

Insect chitinase plays essential roles in chitin catabolism involved in digestion and molting during insect development. In the current work, we cloned a chitinase cDNA, LrCht5, from the apple leaf miner moth Lithocolletis ringoniella and characterized its amino acid sequence and protein properties. The L. ringoniella chitinase cDNA was 2136 bp in length with an open reading frame of 1737 bp that encodes a polypeptide of 579 amino acid residues with a predicted molecular mass of 64.4 kDa and pI of 5.49. The catalytic domain has several phosphorylation and glycosylation sites. The recombinant LrCht5 was expressed in Escherichia coli and the Spodoptera frugiperda cell line Sf9, and the LrCht5 expressed in insect cells exhibited chitinolytic activity. LrCht5 was most stable at pH 6.0 and 45°C. This work has potential application in the development of novel and more specific synthetic chitinase inhibitors for use as bioinsecticides.

Combined effects of all-trans-retinoic acid and trichostatin A on the induction of differentiation of thyroid carcinoma cells.

BACKGROUND AND OBJECTIVE: The effectiveness rate of all-trans-retinoic acid (RA) is only about 30% in the clinical application of inducing thyroid carcinoma differentiation. In addition, there are severe toxic side effects, which limit its clinical application. Phase I-III clinical studies have been conducted on the combined application of two or more kinds of inductors in tumors. Nevertheless, the combination of RA with histone deacetylase inhibitors is rarely reported. This article studied the effects of differentiation for papillary thyroid carcinoma and follicular thyroid carcinoma cell lines induced by RA combined with trichostatin A (TSA), enhancing the effect of induction, while reducing the toxic side effects of a single drug, to provide a theoretical basis for preclinical trials. METHODS: After incubation with RA combined with TSA, K1 and FTC-133 were grouped into Group 1 (RA 10(-4) mol/L plus TSA 1.65 x 10(-7) mol/L), Group 2 (RA 1 x 10(-4) mol/L plus TSA 3.31 x 10(-7) mol/L), Group 3 (RA 10(-5) mol/L plus TSA 1.65 x 10(-7) mol/L), Group 4 (RA 1 x10(-5) mol/L plus TSA 3.31 x 10(-7) mol/L) by four varied concentrations and three time points (12 h, 24 h, and 48 h). The cell proliferation, conformation, toxic effect, and induced differentiation on K1 and FTC-133 cell lines were studied microscopically with hematoxylin-eosin (HE) to observe cell quantity and morphology, methyl-thiazolyl-tetrazolium (MTT) to calculate cell survival rates, and electrochemiluminescence analysis measuring in vitro thyroglobulin (Tg) levels. RESULTS: The research showed that K1 and FTC-133 cells had cell spacing increases, with an outer edge of smooth, nuclear chromatin condensation after RA combined TSA. Survival rate were assessed by an analysis of variance (ANOVA) by concentration and time point, F values of K1 and FTC-133 were 23.52 and 170.14, and 57.09 and 224.35, respectively. There were significant differences for both cells (P < 0.01). The SNK analysis indicated that survival rates were in the order of Group 2 < Group 1 < Group 4 < Group 3. Tg was also assessed by ANOVA, F values of K1 were 69.63 and 101.07, and F values of FTC-133 were 79.77 and 81.72 (P < 0.01). Group 1 was compared with Group 3 of K1 and FTC-133 by the least significant difference (LSD) method, and there was no statistical difference between the two group (P = 0.06, 0.2, respectively; P > 0.05), yet a significant difference was seen between the other Groups. CONCLUSIONS: Lower concentrations of RA combined with lower concentrations of TSA have both inhibited cell proliferation, decreased toxicity of the drugs, and increased the effect of K1 and FTC-133 cell differentiation. The mechanism of action may be that TSA has pretranscription DNA regulation and that RA has posttranscriptional signal regulation to enhance the effects of inhibited proliferation and differentiation of cells by transcription systems.

Imaging of radioiodine-labeled KH901, a tumor-specific oncolytic recombinant adenovirus, in nude mice with human hepatocellular carcinoma.

OBJECTIVE: To study the biodistribution and imaging of I/I-labeled KH901, a tumor-specific oncolytic recombinant adenovirus, in nude mice bearing human hepatocarcinoma. METHODS: KH901 was labeled with I/I according to the N-bromosuccinimide labeling method. The activity of granulocyte-macrophage colony-stimulating factor was determined by enzyme-linked immunosorbent assay. After I-KH901 was injected into the tumor, the label was followed in different organs and tumor tissues in nude mice with hepatocellular carcinoma. I-KH901 was injected directly into the tumor of nude mice bearing hepatocellular carcinoma, and their concentrations were detected at different times on radionuclide images. RESULTS: The radiochemical purity of I/I-KH901 was over 95%. I-KH901 stimulated massive expression of granulocyte-macrophage colony-stimulating factor in tumor cells. Twenty-four hours after the addition of I-KH901, the concentrations of granulocyte-macrophage colony-stimulating factor were 183.27+/-6.90 and 20.44+/-0.77 pg/ml in tumor and normal cells, respectively. I-KH901 was mainly distributed in the tumor and had a longer retention time, which was 14.93%ID/g at 24 h. Radionuclide imaging showed that the radioactive retention of I-KH901 in the tumor was significant. The tumor was shown clearly in the whole-body scan at 2 h after injection. CONCLUSION: I or I-KH901 concentrates specifically at the tumor site, which makes it a novel drug (combination of oncolytic adenovirus and radionuclide therapies) for the treatment of cancer.

[Effect of 131I-labeled recombinant human tumor necrosis factor-alpha on the nude mice bearing human hepatoma].

OBJECTIVE: To test the effect of recombinant human tumor necrosis factor-alpha (rhTNF-alpha) labeled with 131I on tumor growth in the nude mice bearing human hepatoma. METHODS: The biological activity of 131I-rhTNF-alpha was tested through in vitro combination of the radioactive drug and SMMC-7721 cells. The BALB/c-nu/ nu mice model bearing human hepatoma were established by injecting single cell suspension of SMMC-7721 cells. When the tumor was 1 cm in diameter, the therapeutic experiment was carried out. Twenty-four nude mice bearing human hepatoma were divided into six groups according the area of tumor, weight and sex of the nude mice. After i. v administration of 131I-rhTNF-alpha, the body biodistribution of 131I-rhTNF-alpha was assessed during a short-term (30 min, 1 h, 6 h) and a long-term (12 h, 24 h, 48 h) period. The biological activity and tumor accumulation of 131I-rhTNF-alpha were investigated. In the end of the experiment, histopathologic examinations of tumor samples were undertaken. RESULTS: The combination of 131I-rhTNF-alpha with the human hepatoma SMMC-7721 cells existed dose dependence and saturability. The 131I-rhTNF-alpha had satisfactory immunoreactivity. The 131I-rhTNF-alpha accumulated in tumor tissues well and kept stable for several days. The tumor tissues accumulated the highest radioactivity at 6 h, and still maintained 67.5% of that radioactivity at 48 h. The 131I-rhTNF-alpha administrated either intravenously or intratumorally could inhibit tumor growth. The 131I-rhTNF-alpha had similar radioactivity as the positive control (P>0.05), but greater radioactivity than the control groups including 131I, rhTNF-alpha and the negative groups (P<0.05). CONCLUSION: The radioactive compound of 131I-rhTNF-alpha can inhibit and kill tumor cells, which demonstrates its potential for treating hepatocarcinoma.

Feasibility of herpes simplex virus type 1 mutants labeled with radionuclides for tumor treatment.

For over one hundred years, viruses have been recognized as capable of killing tumor cells. At present, people are still researching and constructing more suitable oncolytic viruses for treating different malignant tumors. Although extensive studies have demonstrated that herpes simplex virus type 1 (HSV-1) is the most potential oncolytic virus, therapies based on herpes simplex virus type 1 vectors still arouse bio-safety and risk management issues. Researchers have therefore introduced the new idea of treating cancer with HSV-1 mutants labeled with radionuclides, combining radionuclide and oncolytic virus therapies. This overview briefly summarizes the status and mechanisms by which oncolytic viruses kill tumor cells, discusses the application of HSV-1 and HSV-1 derived vectors for tumor therapy, and demonstrates the feasibility and prospect of HSV-1 mutants labeled with radionuclides for treating tumors.