Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reviewed our experience with ultrasound-guided biopsies of masses of the thyroid gland that were either nonpalpable or difficult to localize by palpation to evaluate the technique and correlate the results. Thirty-two biopsies were performed upon 25 patients whose clinical presentations were palpable nodule (six patients), throat discomfort (two patients), postpartial thyroidectomy follow-up evaluation (two patients), incidental discovery of a mass--by ultrasound of the neck (two patients), roentgenogram of the chest (two patients), computed tomography of the chest (one patient) and during tracheostomy placement (one patient). Other presentations were eliminate infection (one patient), odynophagia (one patient), hoarseness (one patient), cold nodule on a nuclear medicine study (one patient), hyperparathyroidism (one patient), rule out metastasis from carcinoma of the colon (one patient), persistent cough (one patient), enlarged thyroid gland (one patient) or family history of carcinoma of the thyroid gland (one patient). Fifteen patients had nuclear medicine studies showing either a cold nodule (ten patients), multinodular goiter (one patient), normal examination (two patients), hot nodule (one patient) or no thyroid gland activity (one patient). The ultrasound examinations showed either a hypoechoic nodule (25 patients), inhomogeneous or mixed echogenic nodule (six patients) or a hyperechoic nodule with hypoechoic rim (one patient). The nodules ranged in size from 3 milliliters to 7 centimeters. Twenty-six lesions were less than 3 centimeters in diameter; of the other six, four were substernal goiters. Six patients had a previous nondiagnostic biopsy directed by palpation only. Biopsy was performed using real-time ultrasound guidance with various needles. One patient had a small hematoma, which was the only complication in the study. The results of the biopsies were diagnostic in 26 of 32 patients. The final diagnosis was benign follicular cells (ten patients), adenomatous nodule (seven patients), follicular neoplasm (three patients), colloid cyst (two patients), aspergillus (two patients), fibrosis (one patient) and papillary carcinoma (one patient). Six of the biopsies yielded unsatisfactory specimens. One of the patients with a diagnosis of benign follicular cells on biopsy had a follicular carcinoma after surgical pathologic factors were obtained; that was the only false-negative result. We conclude that ultrasound-guided biopsy of the thyroid is a safe and useful method of evaluating nonpalpable and difficult to palpate thyroid masses.
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PMID:Ultrasound guided biopsy of nonpalpable and difficult to palpate thyroid masses. 815 14

It is well known that non-toxic goiter is not uncommon in acromegaly, but hyperthyroidism only occasionally occurs. In addition, the risk for the development of a malignant process is increased, the most often seen is carcinoma of the colon. Thyroid carcinoma is not frequent, nevertheless the rate in these patients is higher than general population. In this article, a case of hyperthyroidism, papillar carcinoma and acromegaly is presented. We reviewed the literature an discussed the possible pathogenesis.
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PMID:[Acromegaly, multinodular toxic goiter and papillary carcinoma of the thyroid, potential role of G proteins]. 1198 3

The aim of the study was to screen the malignancy in an acromegalic patient group and to determine whether there was any increased risk and the incidence of malignancy and its association with disease characteristics such as duration of disease, latency in diagnosis, and GH and IGF-1 levels. One hundred-five (65 female, 40 male) patients with acromegaly followed and treated at Cerrahpasa Medical School, Endocrinology and Metabolism outpatient clinic between 1983 and 2007 were included in this study. The patients were screened with colonoscopy, mammography, and thyroid and prostate ultrasonography (US). Malignancy was detected in 16 (15%) patients. Thyroid cancer was found in 5 patients (4.7%), breast cancer in 3 (2.8%), colon cancer in 2 (1.9%), lung cancer in 2 (1.9%), cervix cancer in 1 (0.9%), myelodysplastic syndrome (MDS) in 1 (0.9%), cholangiocarcinoma in 1 (0.9%), and multiple endocrine neoplasm (MEN) type 1 in 1 patient (0.9%). Cancer was more common in the male patients (P = 0.046) and high levels of GH increased the risk of cancer development (P = 0.046). In this series, the most commonly detected cancer types were thyroid followed by breast and colon cancers. Although high levels of initial GH seemed to increase the risk of cancer development in acromegalic patients, age, gender, age at the time of diagnosis, duration of disease, and initial IGF-I levels were not associated with cancer development.
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PMID:Thyroid cancer is the most common cancer associated with acromegaly. 2021 83

A new generation of anticancer therapeutics called target drugs has quickly developed in the 21st century. These drugs are tailored to inhibit cancer cell growth, proliferation, and viability by specific interactions with one or a few target proteins. However, despite formally known molecular targets for every "target" drug, patient response to treatment remains largely individual and unpredictable. Choosing the most effective personalized treatment remains a major challenge in oncology and is still largely trial and error. Here we present a novel approach for predicting target drug efficacy based on the gene expression signature of the individual tumor sample(s). The enclosed bioinformatic algorithm detects activation of intracellular regulatory pathways in the tumor in comparison to the corresponding normal tissues. According to the nature of the molecular targets of a drug, it predicts whether the drug can prevent cancer growth and survival in each individual case by blocking the abnormally activated tumor-promoting pathways or by reinforcing internal tumor suppressor cascades. To validate the method, we compared the distribution of predicted drug efficacy scores for five drugs (Sorafenib, Bevacizumab, Cetuximab, Sorafenib, Imatinib, Sunitinib) and seven cancer types (Clear Cell Renal Cell Carcinoma, Colon cancer, Lung adenocarcinoma, non-Hodgkin Lymphoma, Thyroid cancer and Sarcoma) with the available clinical trials data for the respective cancer types and drugs. The percent of responders to a drug treatment correlated significantly (Pearson's correlation 0.77 p = 0.023) with the percent of tumors showing high drug scores calculated with the current algorithm.
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PMID:A method for predicting target drug efficiency in cancer based on the analysis of signaling pathway activation. 2632 Jan 81

Thyroid cancer is a common malignant tumor. Long non-coding RNA colon cancer-associated transcript 1 (lncRNA CCAT1) is highly expressed in many cancers; however, the molecular mechanism of CCAT1 in thyroid cancer remains unclear. Hence, this study aimed to investigate the effect of CCAT1 on human thyroid cancer cell line FTC-133. FTC-133 cells were transfected with CCAT1 expressing vector, CCAT1 shRNA, miR-143 mimic, and miR-143 inhibitor, respectively. After different treatments, cell viability, proliferation, migration, invasion, and apoptosis were measured. Moreover, the regulatory relationship of CCAT1 and miR-143, as well as miR-143 and VEGF were tested using dual-luciferase reporter assay. The relative expressions of CCAT1, miR-143, and VEGF were tested by qRT-PCR. The expressions of apoptosis-related factors and corresponding proteins in PI3K/AKT and MAPK pathways were analyzed using western blot analysis. The results suggested that CCAT1 was up-regulated in the FTC-133 cells. CCAT1 suppression decreased FTC-133 cell viability, proliferation, migration, invasion, and miR-143 expression, while it increased apoptosis and VEGF expression. CCAT1 might act as a competing endogenous RNA (ceRNA) for miR-143. Moreover, CCAT1 activated PI3K/AKT and MAPK signaling pathways through inhibition of miR-143. This study demonstrated that CCAT1 exhibited pro-proliferative and pro-metastasis functions on FTC-133 cells and activated PI3K/AKT and MAPK signaling pathways via down-regulation of miR-143. These findings will provide a possible target for clinical treatment of thyroid cancer.
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PMID:lncRNA CCAT1 promotes cell proliferation, migration, and invasion by down-regulation of miR-143 in FTC-133 thyroid carcinoma cell line. 2979 90

Backgrounds: Thyroid cancer (TC) is a prevalent type of cancer in endocrine system. Past decades have seen the rising mortality and morbidity of TC. Long noncoding RNAs are renowned modulators of cancer onset and progression as validated by mounting studies. Long intergenic non-protein coding RNA 1410 (LINC01410) has been suggested as tumor-promoting gene in colon cancer and gastric cancer, but its role in TC is elusive. This study investigated the impact and mechanism of LINC01410 in TC. Materials and Methods: RT-qPCR and western blot were used to detect gene expression levels. Cell counting kit-8 (CCK-8) and ethynyl-2'-deoxyuridine (EdU) assays were used to determine proliferation. Caspase-3 activity assay was used to examine apoptosis. Intermolecular interaction was investigated by luciferase reporter assay and chromatin immunoprecipitation (ChIP) assay. Results: We confirmed the elevation of LINC01410 expression in TC cells. Loss-of-function experiments indicated that LINC01410 knockdown suppressed proliferation and facilitated apoptosis in TC. Mechanism research illustrated that LINC01410 positively regulated forkhead box M1 (FOXM1) expression through targeting miR-3619-5p, and that FOXM1 in turn transcriptionally activated LINC01410. Rescue experiments validated that LINC01410 regulated TC proliferation and apoptosis through miR-3619-5p/FOXM1. Conclusions: This study demonstrated that LINC01410/miR-3619-5p/FOXM1 positive feedback loop regulated cell proliferation and apoptosis in TC, shedding a light on the molecular target identification and promising treatment improvement in TC.
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PMID:LINC01410/miR-3619-5p/FOXM1 Feedback Loop Regulates Papillary Thyroid Carcinoma Cell Proliferation and Apoptosis. 3164 16