ABSTRACT
BACKGROUND: The successful performance of ostomies for the treatment of different diseases has been described since 1706. We report herein the first case of successful ostomy utilizing a synthetic stoma created in a patient with peritoneal carcinomatosis. CLINICAL CASE: A 40-year-old woman presented with abdominal carcinomatosis due to psammomatous papillotubular adenocarcinoma consistent with primary ovarian carcinoma. The patient had negative estrogen and progesterone receptors and Ki-67 proliferative activity was 83%. She was initially treated with cytoreduction therapy, chemotherapy, and hyperthermic intraperitoneal chemotherapy. Because the patient presented with enteric perforations and the extensive tumor invasion and adhesions in all the intestinal segments made it impossible to create autologous decompression stomas, a synthetic stoma was constructed. CONCLUSIONS: Synthetic stomas can be a good treatment option when autologous stomas can not be created.
INTRODUCCIÓN: Desde el año 1706 se han descrito ostomías realizadas con éxito para el tratamiento de diferentes enfermedades; los autores describen el primer caso de éxito en una ostomía sintética en la carcinomatosis peritoneal. CASO CLÍNICO: Mujer de 40 años de edad con carcinomatosis abdominal por adenocarcinoma papilar tubulopapilar psamomatoso más consistente con cáncer primario de ovario, negativo a receptores de estrógenos y progesterona, con marcador Ki-67 al 83% de actividad. De modo inicial se trató con cirugía de citorreducción, quimioterapia, quimioterapia intraperitoneal hipertérmica y por último realización de estomas sintéticos debido a perforaciones entéricas e imposibilidad de realizar estomas descompresivos autólogos por la invasión tumoral extensa y adherencias de todas las asas intestinales. CONCLUSIONES: Los estomas sintéticos pueden ser una buena opción terapéutica cuando es imposible realizar estomas autólogos.
Subject(s)
Adenocarcinoma, Papillary/secondary , Drainage/instrumentation , Intestinal Neoplasms/secondary , Intestinal Perforation/surgery , Ovarian Neoplasms/surgery , Surgical Stomas , Adenocarcinoma, Papillary/drug therapy , Adenocarcinoma, Papillary/etiology , Adenocarcinoma, Papillary/surgery , Adult , Antineoplastic Combined Chemotherapy Protocols/administration & dosage , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Argon Plasma Coagulation , Bevacizumab/administration & dosage , Carboplatin/administration & dosage , Combined Modality Therapy , Cytoreduction Surgical Procedures/methods , Docetaxel/administration & dosage , Doxorubicin/administration & dosage , Doxorubicin/analogs & derivatives , Fatal Outcome , Female , Humans , Hyperthermia, Induced , Intestinal Neoplasms/drug therapy , Intestinal Neoplasms/etiology , Intestinal Neoplasms/surgery , Intestinal Perforation/etiology , Mitomycin/administration & dosage , Polyethylene Glycols/administration & dosageABSTRACT
We report our experience with a synchronous case of gastrointestinal stromal tumor (GIST) and intraductal papillary neoplasm of the bile duct (IPNB) in an elderly woman with neurofibromatosis type 1 (NF-1). A 72-year-old woman presented with a 2-mo history of right upper abdominal pain unrelated to diet and indigestion. Fourteen years earlier, she had been diagnosed with NF-1, which manifested as café au lait spots and multiple nodules on the skin. Computed tomography (CT) revealed a multilocular low-density mass with septation, and mural nodules in the right hepatic lobe, as well as a 1.7-cm-sized well-demarcated enhancing mass in the third portion of the duodenum. The patient subsequently underwent right hepatectomy and duodenal wedge resection. We present here the first report of a case involving a synchronous IPNB and GIST in a patient with NF-1. Our findings demonstrate the possibility of various tumors in NF-1 patients and the importance of diagnosis at an early stage.
Subject(s)
Adenocarcinoma, Papillary/diagnostic imaging , Bile Duct Neoplasms/diagnostic imaging , Gastrointestinal Stromal Tumors/diagnostic imaging , Neoplasms, Multiple Primary/diagnostic imaging , Neurofibromatosis 1/complications , Adenocarcinoma, Papillary/blood , Adenocarcinoma, Papillary/etiology , Adenocarcinoma, Papillary/surgery , Aged , Bile Duct Neoplasms/blood , Bile Duct Neoplasms/etiology , Bile Duct Neoplasms/surgery , Bile Ducts/diagnostic imaging , Bile Ducts/pathology , Bile Ducts/surgery , CA-19-9 Antigen/blood , Cholangiopancreatography, Magnetic Resonance , Duodenum/diagnostic imaging , Duodenum/pathology , Duodenum/surgery , Female , Gastrointestinal Stromal Tumors/blood , Gastrointestinal Stromal Tumors/etiology , Gastrointestinal Stromal Tumors/surgery , Hepatectomy , Humans , Neoplasms, Multiple Primary/etiology , Neoplasms, Multiple Primary/surgery , Neurofibromatosis 1/blood , Tomography, X-Ray ComputedABSTRACT
PURPOSE: Primary low-grade thyroid-like papillary adenocarcinomas are extremely rare neoplasms that generally originate in the nasopharynx. Here, we describe a novel case of a 15-year-old Chinese girl who was diagnosed with low-grade thyroid-like papillary adenocarcinoma, including a brief review of the literature to reveal the clinicopathological features of low-grade thyroid-like nasopharyngeal papillary adenocarcinoma. MATERIALS AND METHODS: Immunohistochemistry was used to evaluate the expression of pan-cytokeratin (CKpan), cytokeratin (CK) 7, thyroid transcription factor 1 (TTF-1), vimentin, epithelial membrane antigen (EMA), thyroglobulin, CD15, S100, P40, CK20, CDX-2, glial fibrillary acidic protein (GFAP), and Ki-67. Additionally, in situ hybridization investigation was utilized to identify the presence of small Epstein-Barr virus (EBV)-encoded RNA. RESULTS: Histopathological analysis revealed florid proliferation of papillary structures lined by columnar epithelial cells with fibrovascular cores. Immunohistochemically, the neoplastic cells were positive for CKpan, CK7, TTF-1, vimentin, and EMA, but negative for thyroglobulin, CD15, S100, P40, CK20, CDX-2, and GFAP. The Ki-67-labeling index reached 5% in the most concentrated spot. In situ hybridization for EBV was negative. CONCLUSION: Due to the distinct rarity of low-grade thyroid-like papillary adenocarcinomaswith a favorable clinical outcome, a nationwide effort to raise public awareness of this neoplasm is required.
Subject(s)
Adenocarcinoma, Papillary/diagnosis , Carcinoma/diagnosis , Nasopharyngeal Neoplasms/diagnosis , Adenocarcinoma, Papillary/etiology , Adolescent , Biomarkers , Biopsy , Carcinoma/etiology , Endoscopy , Female , Humans , Immunohistochemistry , Nasal Septum/pathology , Nasopharyngeal Carcinoma , Nasopharyngeal Neoplasms/etiologyABSTRACT
BACKGROUND: To investigate differentiated thyroid cancer risk factors in natives of French Polynesia is of interest because of the very high incidence of this cancer in the archipelago. MATERIALS AND METHODS: To assess the role of various potential risk factors of thyroid cancer in the natives of French Polynesia we performed a case-control study. The study included almost all the French Polynesians diagnosed with differentiated thyroid carcinoma between 1981 and 2003 (n=229) and 373 French Polynesian control individuals from the general population without cancer. RESULTS: Thyroid radiation dose received from nuclear fallout before the age of 15, a personal history of neck or/and head medical irradiation, obesity, tallness, large number of children, an artificial menopause, a familial history of thyroid cancer, a low dietary iodine intake, and having a spring as the main source of drinking water were found to be significant risk factors. No roles of smoking habits, alcohol consumption, iodine containing drugs, and exposure to pesticides were evidenced. CONCLUSIONS: Except for smoking, differentiated thyroid carcinoma risk factors in natives of French Polynesia are similar to those in other populations. Our finding on the role of having a spring as a drinking water origin is coherent with some other studies and could be due to geological factors.
Subject(s)
Adenocarcinoma, Follicular/epidemiology , Adenocarcinoma, Papillary/epidemiology , Thyroid Neoplasms/epidemiology , Adenocarcinoma, Follicular/etiology , Adenocarcinoma, Papillary/etiology , Adolescent , Adult , Case-Control Studies , Child , Female , Follow-Up Studies , Humans , Incidence , Male , Middle Aged , Neoplasm Staging , Polynesia/epidemiology , Prognosis , Risk Factors , Thyroid Neoplasms/etiology , Young AdultABSTRACT
Secondary cancers developing after allogeneic hematopoietic stem cell transplantation generally originate from recipient-derived cells. In this study, we analyzed the tumor cell origin of 5 epithelial malignant tumors (esophageal squamous cell carcinoma, lung adenocarcinoma, gastric adenocarcinoma, pharyngeal squamous cell carcinoma, and thyroid papillary carcinoma) that developed after allogeneic peripheral blood stem cell transplantation using anti-AE1/3 immunofluorescence with fluorescence in situ hybridization analysis for sex chromosomes and/or short-tandem repeat microsatellite analysis of laser-microdissected tumor cells. The results revealed that 1 of these 5 cancers was derived from donor cells. In this case, transfused pluripotent cells, which include both mesenchymal stem cells and hematopoietic stem cells, might have given rise to epithelial malignant cells. Our observations suggest that transfused peripheral blood cells may be involved in the development of cancers after allogeneic peripheral blood stem cell transplantation.
Subject(s)
Adenocarcinoma, Papillary/etiology , Adenocarcinoma/etiology , Carcinoma, Squamous Cell/etiology , Neoplasms, Multiple Primary/etiology , Peripheral Blood Stem Cell Transplantation/adverse effects , Tissue Donors , Adenocarcinoma/genetics , Adenocarcinoma/pathology , Adenocarcinoma, Papillary/genetics , Adenocarcinoma, Papillary/pathology , Adult , Anion Exchange Protein 1, Erythrocyte/genetics , Antiporters/genetics , Bone Marrow Cells/chemistry , Bone Marrow Cells/pathology , Carcinoma, Squamous Cell/genetics , Carcinoma, Squamous Cell/pathology , Cell Lineage , DNA, Neoplasm/analysis , Esophageal Neoplasms/etiology , Esophageal Neoplasms/genetics , Esophageal Neoplasms/pathology , Female , Fluorescent Antibody Technique, Indirect , Humans , In Situ Hybridization, Fluorescence , Laser Capture Microdissection , Lung Neoplasms/etiology , Lung Neoplasms/genetics , Lung Neoplasms/pathology , Male , Microsatellite Repeats/genetics , Middle Aged , Neoplasms, Multiple Primary/genetics , Neoplasms, Multiple Primary/pathology , Pharyngeal Neoplasms/etiology , Pharyngeal Neoplasms/genetics , Pharyngeal Neoplasms/pathology , Sex Chromosomes/genetics , Stomach Neoplasms/etiology , Stomach Neoplasms/genetics , Stomach Neoplasms/pathology , Thyroid Neoplasms/etiology , Thyroid Neoplasms/genetics , Thyroid Neoplasms/pathology , Transplantation ChimeraABSTRACT
BACKGROUND: Only three cases of serous adenocarcinoma arising from Mullerian epithelial inclusions of the lymph node have been reported. Herein reported is a case of serous papillary adenocarcinoma arising probably from epithelial (Mullerian) inclusions of the hepatic hilar lymph node. CASE REPORT: A 73-year-old woman presented with peripheral neuropathy, which was thought to be a paraneoplastic syndrome associated with visceral malignancy. Total body examination, including X-P, US, CT, MRI, PET, and upper and lower gastrointestinal endoscopy was done. As the results, only lymph node swelling was detected in the hepatic hilus. Tumor was not identified in other sites. The physicians considered malignant lymphoma, and laparotomic excision of the hepatic hilar mass was performed. Cytological examination of abdominal cavity washing revealed no malignant cells. Grossly, the mass was firm and white and measured 4 × 5 × 5 cm. Microscopically, the mass showed carcinoma cells arranged in papillary and tubular patterns. The appearances strongly resembled serous papillary adenocarcinoma of the ovary. Lymph node structures were noted in some peripheral areas. No benign epithelial inclusions were recognized. Immunohistochemically, the carcinoma cells were positive for ER, PgR, CA125, WT1, p53. They were negative for TTF-1 and CDX-2. Because the positive ER, PgR, CA125, WT1, p53 and p16 are indicative of gynecologic malignancy, simple hysterectomy and bilateral salpingo-oophorectomy were performed, which showed no abnormalities. Cytological examination of abdominal cavity washing fluid revealed no malignant cells. The patient was treated by paclitaxel and carboplatin, and is now alive without metastasis 2 years after the first manifestation. CONCLUSION: The author reported a case of serous papillary adenocarcinoma arising probably from epithelial (Mullerian) inclusions of the hepatic hilar lymph node.
Subject(s)
Adenocarcinoma, Papillary/pathology , Epithelial Cells/pathology , Lymph Node Excision , Lymph Nodes/pathology , Lymphoproliferative Disorders/pathology , Adenocarcinoma, Papillary/etiology , Adenocarcinoma, Papillary/surgery , Aged , Female , Humans , Liver , Lymph Nodes/surgery , Lymphoproliferative Disorders/etiology , Lymphoproliferative Disorders/surgeryABSTRACT
BACKGROUND: : Radiation exposure is an established cause of clinical thyroid cancer, but little is known about radiation effects on papillary microcarcinoma (PMC) of the thyroid, a relatively common subclinical thyroid malignancy. Because the incidence of these small thyroid cancers has been increasing, it is important to better understand them and their relation to radiation. METHODS: : PMCs were identified in a subset of 7659 members of the Life Span Study of atomic bomb survivors who had archived autopsy or surgical materials. We conducted a pathology review of these specimens and evaluated the histological features of the tumors and the association between PMCs and thyroid radiation dose. RESULTS: : From 1958 to 1995, 458 PMCs were detected among 313 study subjects. The majority of cancers exhibited pathologic features of papillary thyroid cancers. Overall, 81% of the PMCs were of the sclerosing variant and 91% were nonencapsulated, psammoma bodies that occurred in 13% and calcification was observed in 23%. Over 95% had papillary or papillary-follicular architecture and most displayed nuclear overlap, clear nuclei, and nuclear grooves. Several of these features increased with increasing tumor size, but no association was found with radiation dose. A significant radiation-dose response was found for the prevalence of PMCs (estimated excess odds ratio/Gy = 0.57; 95% confidence interval, 0.01-1.55), with the excess risk observed primarily among women. CONCLUSIONS: : Exposure to low-to-moderate doses of ionizing radiation appears to increase the risk of thyroid PMCs, even when exposure occurs during adulthood. Cancer 2010. (c) 2010 American Cancer Society.
Subject(s)
Adenocarcinoma, Papillary/epidemiology , Neoplasms, Radiation-Induced/epidemiology , Nuclear Weapons , Thyroid Neoplasms/epidemiology , Adenocarcinoma, Papillary/drug therapy , Adenocarcinoma, Papillary/etiology , Adenocarcinoma, Papillary/pathology , Aged , Aged, 80 and over , Autopsy , Dose-Response Relationship, Radiation , Female , Humans , Incidence , Japan/epidemiology , Male , Middle Aged , Nuclear Warfare , Radiation, Ionizing , Risk Factors , Survivors , Thyroid Neoplasms/etiology , Thyroid Neoplasms/pathologySubject(s)
Adenocarcinoma, Mucinous/epidemiology , Carcinoma, Pancreatic Ductal/epidemiology , Pancreatic Neoplasms/epidemiology , Adenocarcinoma, Mucinous/etiology , Adenocarcinoma, Mucinous/pathology , Adenocarcinoma, Papillary/epidemiology , Adenocarcinoma, Papillary/etiology , Adenocarcinoma, Papillary/pathology , Blood Glucose/metabolism , CA-19-9 Antigen/blood , Carcinoma, Pancreatic Ductal/etiology , Carcinoma, Pancreatic Ductal/pathology , Diabetes Mellitus/physiopathology , Humans , Incidence , Multivariate Analysis , Pancreatic Neoplasms/etiology , Pancreatic Neoplasms/pathology , Risk FactorsABSTRACT
The authors observed 149 patients with nodal goiter and 39 patients with thyroid cancer for thyroid cancer risk factors. Frequency of thyroid cancer, malignancies and thyroid gland diseases was studied in the families of the observed patients. BRAF T1796A gene mutation was identified in 50 tissue samples of thyroid cancer of the patients. It has been shown, presence in relatives thyroid cancer and malignant new growths is thyroid cancer risk factor. BRAF T1796A mutation was identified in 27% of papillary thyroid cancer samples and its identification may be used to determine this risk factor of the development of papillary thyroid cancer clinical form.
Subject(s)
Adenocarcinoma, Papillary/etiology , Genetic Predisposition to Disease , Goiter/genetics , Proto-Oncogene Proteins B-raf/genetics , Thyroid Neoplasms/genetics , Adenocarcinoma, Papillary/epidemiology , Adenocarcinoma, Papillary/genetics , Female , Goiter/epidemiology , Humans , Male , Mutation , Pedigree , Risk Factors , Thyroid Neoplasms/epidemiology , Thyroid Neoplasms/etiologyABSTRACT
Radiation in childhood is a known risk factor for thyroid carcinoma, but may also be related to benign nodular hyperplasias. Recent evidence from comparative genomic hybridization indicates that radiation can induce clonal DNA damage in cultured rat thyrocytes. We used a loss of heterozygosity analysis for the loci identified by comparative genomic hybridization to study human thyroids. Thyroids from patients with a history of radiation, patients who had recent therapeutic external beam radiation for laryngeal carcinoma, and patients who had no radiation and underwent incidental thyroidectomy with laryngectomy for laryngeal carcinoma were included. PCR was performed for 18 different genetic loci defined by prior reported comparative genomic hybridization study. A semiquantitative capillary electrophoresis analysis was used and frequency of allelic loss was calculated from the number of losses/the number of informative loci. A total of 40 cases of thyroids from patients with childhood radiation, 12 cases of recently radiated thyroids, and 15 cases of nonradiated thyroids were included. In the nonradiated and recently radiated thyroids, the mean frequency of allelic loss was 2.3%. In the thyroids from patients radiated as children, the mean frequency of allelic loss was 39%. Losses were seen at every locus with a range of 7-100% of the cases analyzed (mean 49.6%). Radiation in childhood was associated with both benign nodular disease and carcinomas of the thyroid. The frequency of allelic loss was very high in all lesions in these patients, as compared to control thyroid glands. These data from human thyroids support prior cell culture experiments and show that radiation induces genetic mutational damage even in benign proliferative processes in these thyroids.
Subject(s)
DNA Mutational Analysis , Laryngeal Neoplasms/radiotherapy , Neoplasms, Radiation-Induced/genetics , Thyroid Neoplasms/genetics , Thyroidectomy , Adenocarcinoma, Papillary/etiology , Adenocarcinoma, Papillary/genetics , Adenocarcinoma, Papillary/surgery , Adenoma/etiology , Adenoma/genetics , Adenoma/surgery , Adolescent , Adult , Aged , Aged, 80 and over , Child , DNA, Neoplasm/analysis , Electrophoresis, Capillary , Female , Humans , Loss of Heterozygosity , Male , Middle Aged , Mutation , Neoplasms, Radiation-Induced/etiology , Neoplasms, Radiation-Induced/surgery , Nucleic Acid Hybridization , Polymerase Chain Reaction , Proto-Oncogene Proteins B-raf/genetics , Proto-Oncogene Proteins B-raf/metabolism , Thyroid Neoplasms/etiology , Thyroid Neoplasms/surgeryABSTRACT
The aim of this study is to present a retrospective clinical pathological study of 17 cases of tubal malignancies. The 17 cases were diagnosed and treated in our department between July 1985 and July 2005. Clinical information and pathological data were obtained by review of hospital records. Carcinomas were staged according to the FIGO criteria; assignment of stage was made on the operative data and the pathological findings. Four patients had Stage I tumour (23.5%), six had Stage II (35.4%), five patients had Stage III (29.4%) and two had Stage IV (11.7%). The histological type of all our specimens was primary papillary adenocarcinoma of the fallopian tube. Initially, all patients were subjected to surgery. Primary fallopian tube cancer (PFTC) is a rare gynaecological malignancy, similar to ovarian cancer, but with poorer prognosis. The PFTC should be considered in the differential diagnosis of any pelvic mass. The treatment was surgical followed by adjuvant chemotherapy.
Subject(s)
Adenocarcinoma, Papillary/epidemiology , Fallopian Tube Neoplasms/epidemiology , Adenocarcinoma, Papillary/drug therapy , Adenocarcinoma, Papillary/etiology , Adenocarcinoma, Papillary/pathology , Adenocarcinoma, Papillary/surgery , Aged , Combined Modality Therapy , Databases, Factual , Fallopian Tube Neoplasms/drug therapy , Fallopian Tube Neoplasms/etiology , Fallopian Tube Neoplasms/pathology , Fallopian Tube Neoplasms/surgery , Female , Greece/epidemiology , Humans , Medical Records , Middle Aged , Neoplasm Staging , Pathology Department, Hospital , Pregnancy , Retrospective StudiesABSTRACT
Data of the literature on the epidemiology, patogenesis, diagnosis, peculiarities of the symptoms and the treatment of the intraduct papillar pancreatic tumor, are analyzed in this review. These tumors are rare, there are up to 1% of the exocrine pancreatic tumors. Intraduct proliferation of the mucin producing cells, that are disposed as papillars is typical of these tumors. There are the symptoms of the acute or chronic pancreatitis, sometimes the diagnosis of this tumor is accidental. The main diagnostic methods are ultrasound (US) and computed tomography (CT). Endoluminal ultrasound (EUS) and magnetic resonance cholangiopancreatography (MRCP) are the main methods to reveal the intraduct growth. The surgical treatment is necessary for these patients.
Subject(s)
Adenocarcinoma, Mucinous/diagnosis , Adenocarcinoma, Papillary/diagnosis , Carcinoma, Pancreatic Ductal/diagnosis , Pancreatic Neoplasms/diagnosis , Adenocarcinoma, Mucinous/epidemiology , Adenocarcinoma, Mucinous/etiology , Adenocarcinoma, Papillary/epidemiology , Adenocarcinoma, Papillary/etiology , Carcinoma, Pancreatic Ductal/epidemiology , Carcinoma, Pancreatic Ductal/etiology , Diagnosis, Differential , Humans , Pancreatic Neoplasms/epidemiology , Pancreatic Neoplasms/etiologyABSTRACT
The incidence of thyroid cancer has been reported to be 0.5-1.3%, when assessed by sonographic examination and 3.7-28.4% by histologic examination at autopsies. These incidences are much higher than those of clinically evident thyroid cancer, which are 2.0/100,000 for males and 7.2/100,000 for females, reported in Japan. In iodine deficient areas, chronic stimulation by TSH causes multinodular autonomous growth and function, leading to hyperthyroidism in middle-aged and elderly subjects. Incidence of Plummer's disease among Japanese with sufficient iodine intake is very low, accounting for 0.5-0.8% of all thyroid nodules and 0.3% of all thyrotoxic patients. The Plummer/Graves ratio was higher than 1 in endemic goiter area before iodine supplementation. Iodine intake affects the type of thyroid carcinoma. Decreased intake of iodine is associated with higher frequency of follicular and anaplastic cancers and lower frequency of papillary cancer. The high prevalence of papillary cancer(>85%) with good prognosis may explain the preferred selection of partial rather than total thyroidectomy in Japan.
Subject(s)
Adenocarcinoma, Follicular/epidemiology , Adenocarcinoma, Papillary/epidemiology , Iodine/administration & dosage , Thyroid Neoplasms/epidemiology , Adenocarcinoma, Follicular/etiology , Adenocarcinoma, Papillary/etiology , Age Factors , Female , Graves Disease/epidemiology , Graves Disease/etiology , Humans , Hyperthyroidism/epidemiology , Hyperthyroidism/etiology , Incidence , Iodine/adverse effects , Iodine/deficiency , Japan/epidemiology , Male , Sex Factors , Thyroid Neoplasms/etiology , Thyroid Nodule/epidemiology , Thyroid Nodule/etiologyABSTRACT
UNLABELLED: Iodine is a trace element that is essential for the synthesis of thyroid hormone. Both chronic iodine deficiency and iodine excess have been associated with hypertrophy and hyperplasia of follicular cells, attributed to excessive secretion of TSH. This may be associated to thyroid cancer risk, particularly in women. Experimental studies have documented thyroid cancer induction by elevation of endogenous TSH, although in a small number of animals. Iodine deficiency associated with carcinogenic agents and chemical mutagens will result in a higher incidence of thyroid malignancy. Inadequate low iodine intake will result in increased TSH stimulation, increased thyroid cell responsiveness to TSH, increased thyroid cell EGF-induced proliferation, decreased TGFbeta 1 production and increased angiogenesis, all phenomena related to promotion of tumor growth. Epidemiological studies associating iodine intake and thyroid cancer led to controversial and conflicting results. There is no doubt that introduction of universal iodine prophylaxis in population previously in chronic iodine-deficiency leads to a changing pattern of more prevalent papillary thyroid cancer and declining of follicular thyroid cancer. Also anaplastic thyroid cancer is practically not seen after years of iodine supplementation. Iodine excess has also been indicated as a possible nutritional factor in the prevalence of differentiated thyroid cancer in Iceland, Hawaii and, more recently, in China. IN CONCLUSION: available evidence from animal experiments, epidemiological studies and iodine prophylaxis has demonstrated a shift towards a rise in papillary carcinoma, but no clear relationship between overall thyroid cancer incidence and iodine intake.
Subject(s)
Adenocarcinoma, Follicular/etiology , Adenocarcinoma, Papillary/etiology , Iodine , Thyroid Neoplasms/etiology , Adenocarcinoma, Follicular/epidemiology , Adenocarcinoma, Follicular/pathology , Adenocarcinoma, Papillary/epidemiology , Adenocarcinoma, Papillary/pathology , Animals , Argentina/epidemiology , Diet , Disease Models, Animal , Epidemiologic Studies , Epidermal Growth Factor/metabolism , Female , Hawaii/epidemiology , Humans , Iceland/epidemiology , Iodine/administration & dosage , Iodine/deficiency , Italy/epidemiology , Male , Thyroid Gland/drug effects , Thyroid Gland/metabolism , Thyroid Neoplasms/epidemiology , Thyroid Neoplasms/pathology , Thyrotropin/drug effects , Thyrotropin/metabolismABSTRACT
Iodine is a trace element that is essential for the synthesis of thyroid hormone. Both chronic iodine deficiency and iodine excess have been associated with hypertrophy and hyperplasia of follicular cells, attributed to excessive secretion of TSH. This may be associated to thyroid cancer risk, particularly in women. Experimental studies have documented thyroid cancer induction by elevation of endogenous TSH, although in a small number of animals. Iodine deficiency associated with carcinogenic agents and chemical mutagens will result in a higher incidence of thyroid malignancy. Inadequate low iodine intake will result in increased TSH stimulation, increased thyroid cell responsiveness to TSH, increased thyroid cell EGF-induced proliferation, decreased TGFbeta 1 production and increased angiogenesis, all phenomena related to promotion of tumor growth. Epidemiological studies associating iodine intake and thyroid cancer led to controversial and conflicting results. There is no doubt that introduction of universal iodine prophylaxis in population previously in chronic iodine-deficiency leads to a changing pattern of more prevalent papillary thyroid cancer and declining of follicular thyroid cancer. Also anaplastic thyroid cancer is practically not seen after years of iodine supplementation. Iodine excess has also been indicated as a possible nutritional factor in the prevalence of differentiated thyroid cancer in Iceland, Hawaii and, more recently, in China. In conclusion: available evidence from animal experiments, epidemiological studies and iodine prophylaxis has demonstrated a shift towards a rise in papillary carcinoma, but no clear relationship between overall thyroid cancer incidence and iodine intake.
O iodo é essencial para a síntese de hormônios tireóideos e tanto a deficiência crônica deste halogeno como o excesso nutricional de iodo levam a hiperplasia e hipertrofia dos elementos foliculares (por excesso de TSH). Esse fenômeno pode se associar a maior risco de câncer de tireóide, especialmente no sexo feminino. Estudos experimentais documentam indução de câncer de tireóide após prolongado excesso circulante de TSH, o qual induz aumento da proliferação celular medida por fator de crescimento epidermal (EGF), decréscimo de síntese de fator de transformação do crescimento (TGFbeta 1) e aumento da angiogenese. Estudos epidemiológicos entre nutrição de iodo e câncer de tireóide são conflitantes. É, todavia, aceito que a correção de prévia deficiência de iodo com aporte nutricional adequado deste halogeno leva à maior prevalência de carcinoma papilífero (e decréscimo de carcinoma folicular). Em alguns países, o excesso de iodo foi apontado como causa aparente de maior prevalência de câncer de tireóide. Em conclusão: não existe uma relação causa-efeito entre iodo nutricional e prevalência de câncer de tireóide, e outros fatores intervenientes ambientais devem ser considerados.
Subject(s)
Animals , Female , Humans , Male , Adenocarcinoma, Follicular/etiology , Adenocarcinoma, Papillary/etiology , Iodine , Thyroid Neoplasms/etiology , Adenocarcinoma, Follicular/epidemiology , Adenocarcinoma, Follicular/pathology , Adenocarcinoma, Papillary/epidemiology , Adenocarcinoma, Papillary/pathology , Argentina/epidemiology , Diet , Disease Models, Animal , Epidemiologic Studies , Epidermal Growth Factor/metabolism , Hawaii/epidemiology , Iceland/epidemiology , Iodine/administration & dosage , Iodine/deficiency , Italy/epidemiology , Thyroid Gland/drug effects , Thyroid Gland/metabolism , Thyroid Neoplasms/epidemiology , Thyroid Neoplasms/pathology , Thyrotropin/drug effects , Thyrotropin/metabolismABSTRACT
Solid pseudopapillary tumors (SPT) of the pancreas are rare neoplasms that occur mostly in young women. Despite of a low malignant potential, 10% to 15% of the cases have aggressive behavior with metastatic dissemination possibly leading to death. To date, no pathological factor can reliably predict the outcome of these tumours. Galectin-3, a major actor in the carcinogenesis of pancreatic ductal adenocarcinoma, has not been investigated in SPT. The presence of progesterone receptors is frequently reported in SPT, whereas that of estrogen receptor (ER) is unclear. We studied 5 cases of SPT consisting of 4 pancreatic tumors and 1 metastatic case. The morphological distinctive feature of metastatic nodules was the presence of polygonal or spindle cells with pleiomorphic nuclei and high mitotic count exhibiting a diffuse, infiltrative growth pattern. We found a strong expression of galectin-3 in all SPTs, whereas, interestingly, it was lower in metastatic nodules. Conversely, no galectin-3 expression was found in normal pancreatic endocrine cells or in neuroendocrine tumors. We suggest therefore that galectin-3 is a useful marker to distinguish SPT from neuroendocrine tumor, and also indicator of behavior because its low expression is associated with metastatic spreading. Moreover, the presence of galectin-3 in both SPT and pancreatic ducts rises the hypothesis of a posible ductal origin of these tumors. Specific antibodies for anti-ERalpha and anti-ERbeta demonstrated a strong expression of ERbeta whereas ERalpha was not detected. In conclusion, the present study brings the first evidence of the involvement of galectin-3 in SPT but also brought up clues which allowed to reconcile previously conflicting results on the presence of ER.
Subject(s)
Adenocarcinoma, Papillary/etiology , Pancreatic Neoplasms/etiology , Adenocarcinoma, Papillary/chemistry , Adenocarcinoma, Papillary/secondary , Biomarkers, Tumor/analysis , Cell Nucleus/pathology , Estrogen Receptor beta/analysis , Galectin 3/analysis , Humans , Neoplasm Metastasis/pathology , Pancreas/anatomy & histology , Pancreas/chemistry , Pancreatic Ducts/chemistry , Pancreatic Ducts/pathology , Pancreatic Neoplasms/chemistry , Pancreatic Neoplasms/pathologyABSTRACT
Papillary thyroid carcinoma (PTC) is the most common thyroid malignancy, with an incidence of approximately 22,000 cases in 2004 in the USA. Incidence is increasing, with a global estimate of half a million new cases this year. PTC is found in a variety of morphologic variants, usually grows slowly and is clinically indolent, although rare, aggressive forms with local invasion or distant metastases can occur. In recent years, thyroid cancer has been at the forefront of molecular pathology as a result of the consequences of the Chernobyl disaster and the recognition of the role of Ret/PTC rearrangements in PTC. Nonetheless, the molecular pathogenesis of this disease remains poorly characterized. In the clinical setting, benign thyroid nodules are far more frequent, and distinguishing between them and malignant nodules is a common diagnostic problem. It is estimated that 5-10% of people will develop a clinically significant thyroid nodule during their lifetime. Although the introduction of fine-needle aspiration has made PTC identification more reliable, clinicians often have to make decisions regarding patient care on the basis of equivocal information. Thus, the existing diagnostic tools available to distinguish benign from malignant neoplasms are not always reliable. This article will critically evaluate recently described putative biomarkers and their potential future role for diagnostic purposes in fine-needle aspiration cytology samples. It will highlight the evolution of our understanding of the molecular biology of PTC, from a narrow focus on specific molecular lesions such as Ret/PTC rearrangements to a pan-genomic approach.
Subject(s)
Adenocarcinoma, Papillary/classification , Adenocarcinoma, Papillary/metabolism , Biomarkers, Tumor/classification , Biomarkers, Tumor/metabolism , Molecular Diagnostic Techniques , Thyroid Neoplasms/classification , Thyroid Neoplasms/metabolism , Adenocarcinoma, Papillary/etiology , Adenocarcinoma, Papillary/pathology , Animals , Cell Cycle , Diabetes Mellitus, Type 1/immunology , Humans , Thyroid Neoplasms/etiology , Thyroid Neoplasms/pathologyABSTRACT
PURPOSE OF INVESTIGATION: To review risk factors, clinical presentation, diagnostic methods, and histopathologic findings in 27 cases of endometrial cancer in polyps. METHODS: A descriptive, retrospective study of 204 consecutive patients with endometrial carcinoma who were diagnosed at our institution between June 1998 to June 2001. Endometrial cancer arising in polyps occurred in 27 patients (13.2%) and accounted for 1.8% of 1492 endometrial polyps diagnosed during this period. RESULTS: Patients had a mean age of 62 years. All except one woman were postmenopausal. Three breast cancer patients were currently given tamoxifen. Metrorrhagia was the presenting symptom in 74% of cases, although 22% of patients were asymptomatic at the time of diagnosis. Ultrasonography performed in 22 patients showed images compatible with an endometrial polyp in 50% of cases, myoma in 5%, and inconclusive findings in 45%. The median endometrial thickness was 11 mm (range 4-33 mm). Diagnosis was made by aspiration-biopsy in 13 patients and by hysteroscopic endometrial sampling in 13 (in one patient endometrial carcinoma was incidentally found in the surgical specimen). All patients were in FIGO Stage IA. Endometrioid carcinoma was found in 81.5% of cases. Retroperitoneal metastases were not found in 25 patients undergoing pelvic lymphadenectomy, nor neoplastic growth in the specimens of six polypeptomies performed during hysteroscopy. All patients are free of relapse after a mean follow-up of 30 months. CONCLUSIONS: Postmenopausal women with endometrial polyps diagnosed by ultrasonography should undergo directed biopsies under hysteroscopic vision. The present series confirms the good prognosis of endometrial cancer in polyps.
Subject(s)
Endometrial Neoplasms/epidemiology , Polyps/epidemiology , Adenocarcinoma, Papillary/diagnostic imaging , Adenocarcinoma, Papillary/epidemiology , Adenocarcinoma, Papillary/etiology , Adenocarcinoma, Papillary/pathology , Aged , Aged, 80 and over , Carcinoma, Adenosquamous/diagnostic imaging , Carcinoma, Adenosquamous/epidemiology , Carcinoma, Adenosquamous/etiology , Carcinoma, Adenosquamous/pathology , Carcinoma, Endometrioid/diagnostic imaging , Carcinoma, Endometrioid/epidemiology , Carcinoma, Endometrioid/etiology , Carcinoma, Endometrioid/pathology , Endometrial Neoplasms/diagnostic imaging , Endometrial Neoplasms/etiology , Endometrial Neoplasms/pathology , Female , Humans , Medical Records , Middle Aged , Polyps/diagnostic imaging , Polyps/etiology , Polyps/pathology , Prevalence , Retrospective Studies , Risk Factors , Spain/epidemiology , UltrasonographyABSTRACT
Se presenta el caso de una paciente de 65 años, operada hace 40 de una esofagocoloplastia por esofagitis cáustica, atendida en el hospital Hermanos Ameijeiras, Cuba, por disfagia de 5 meses de evolución. Se le diagnosticó un adenocarcinoma en el segmento de colon transpuesto. Se realizó resección del tumor, con márgenes oncológicos, y el restablecimiento adecuado del tránsito(AU)
We report the case of a 65-year-old woman who presented to the Hermanos Ameijeiras Hospital in Cuba due to dysphagia for the previous 5 months. Forty years previously, she had undergone esophagocoloplasty for caustic esophagitis. Adenocarcinoma was diagnosed in the colonic interposition. The tumor was resected with oncologic margins and food transit was successfully restored(AU)