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PubMed1989

Epithelial hyperplasia of the fallopian tube. Its association with serous borderline tumors of the ovary.

We examined sections of fallopian tube from 99 patients with serous borderline tumors of the ovary (SBT) to determine the prevalence of epithelial hyperplasia. Fifty-eight patients with carcinoma of the cervix (CC) and 30 with grade 2 or 3 ovarian carcinoma (OC) served as controls. Patient ages were similar in each group. Epithelial hyperplasia was identified in 68 of 99 patients with SBT (68.7%), compared with 15 of 58 with CC (25.9%) and 4 of 30 with OC (13.3%). Epithelial thickness and nuclear crowding were greater in hyperplastic than in normal fallopian tubes. There was no correlation between hyperplasia and menstrual cycle. In patients with SBT, the presence of epithelial hyperplasia correlated with tumor stage. Hyperplasia was present in 38 of 60 (63%) patients with Stage I tumors. In Stage II and III tumors, hyperplasia was present in 18 of 25 (72%) patients with noninvasive peritoneal implants and 12 of 14 (86%) with invasive implants. Fallopian tube epithelial hyperplasia may represent an example of a field effect in müllerian carcinogenesis.

Adult↗
PubMed1996

Prognostic importance of hyperplasia and atypia in endometriosis.

Endometriosis occasionally exhibits cytologic atypia in the lining of endometriotic cysts or hyperplasia resembling uterine endometrial hyperplasias, but the risk of development of adenocarcinoma in these patients is unknown. A total of 105 women with endometriosis were studied: 37 with cytologic atypia (usually in the lining of endometriotic cysts), 34 with hyperplasia resembling uterine endometrial hyperplasia, and 34 controls. For lesions resembling eutopic endometrial hyperplasia, the Kurman-Norris criteria for separating atypical hyperplasia from well-differentiated endometrial adenocarcinoma were used to subdivide this group into 23 complex atypical hyperplasias and 11 "early carcinomas." Some 62 women were successfully followed for a mean of 8.7 years. One patient with early carcinoma developed a poorly differentiated endometrioid adenocarcinoma at the vaginal apex 8.1 years later. A second patient with early carcinoma developed a mullerian mucinous tumor of low malignant potential in the contralateral ovary 7 years later. Both of the latter two patients had multifocal endometriosis. Except for persistent benign endometriotic lesions in four patients, and breast carcinoma in one, all remaining patients were alive and well at last contact. It is concluded that the Kurman-Norris criteria for eutopic endometrial adenocarcinoma may be useful in identifying rare patients with endometriosis in whom there may be an increased risk of neoplastic transformation of their endometriosis.

Adenocarcinoma↗
PubMed2006

The overlapping lower urinary tract symptoms of benign prostatic hyperplasia and prostatitis.

PURPOSE OF REVIEW: To investigate the relationship, diagnosis and treatment of the overlapping lower urinary tract symptoms experienced by men diagnosed with benign prostatic hyperplasia and prostatitis. RECENT FINDINGS: Recent studies have clearly shown that men can suffer from both benign prostatic hyperplasia and prostatitis. Approximately 5-20% of men diagnosed with benign prostatic hyperplasia suffer from prostatitis-like symptoms, while over one third of men diagnosed with benign prostatic hyperplasia have had a diagnosis of prostatitis in the past. Differentiation between these two symptom-based medical conditions can be difficult because of overlapping symptoms, but pain clearly identifies those patients with chronic prostatitis. Treatment for men with co-occurring benign prostatic hyperplasia and prostatitis may include alpha-blockers, 5alpha-reductase inhibitors and phytotherapies (saw palmetto and bee pollen extract), with evidence clearly showing the benefits of alpha-blocker therapy. SUMMARY: Benign prostatic hyperplasia and chronic prostatitis are a common cause of lower urinary tract symptoms and frequently co-occur in older men. The best treatment for men with lower urinary tract symptoms associated with both benign prostatic hyperplasia and prostatitis is alpha-blockers.

Adrenergic alpha-Antagonists↗
PubMed2006

Severity of basal cell hyperplasia differs in reflux versus eosinophilic esophagitis.

OBJECTIVES: Basal cell hyperplasia of the esophageal epithelium is a frequent finding in children with histological evidence of esophagitis. The aim of this study was to compare the severity of basal cell hyperplasia in gastroesophageal reflux vs eosinophilic esophagitis. METHODS: A cohort of pediatric patients who underwent same-day endoscopy with esophageal biopsy and 24-hour esophageal pH monitoring was divided into groups based on endoscopic and pH monitoring findings. Basal cell hyperplasia was defined as normal (< or = 25% of esophageal epithelial height), mild (26%-50%), moderate (51%-75%) or severe (> 75%). The severity of basal cell hyperplasia in patients with abnormal pH monitoring studies, both with and without endoscopic abnormalities of the esophagus, was compared with the severity in patients with eosinophilic esophagitis. RESULTS: Twenty-seven children with abnormal pH monitoring were identified. Of these 27 children, 11 had endoscopic findings consistent with reflux esophagitis. Thirty patients with eosinophilic esophagitis were identified. Patients with eosinophilic esophagitis had significantly increased severity (P < 0.001) of basal cell hyperplasia (87% severe, 3% moderate, 3% mild, 7%, normal) than patients with abnormal esophageal pH monitoring alone (11% severe, 4% moderate, 15% mild, 70% normal) or in combination with endoscopic abnormalities (18% severe, 9% moderate, 18% mild, 55% normal). CONCLUSIONS: Basal cell hyperplasia is more severe in children with eosinophilic esophagitis than in those with reflux esophagitis. The finding of basal cell hyperplasia is a powerful clue into the underlying etiology of pediatric esophagitis and, along with epithelial eosinophil count, can be used as information to guide therapy.

Child↗
PubMed2004

Mohs micrographic surgery for angiolymphoid hyperplasia with eosinophilia.

BACKGROUND: Angiolymphoid hyperplasia with eosinophilia is a benign vascular proliferation that typically presents on the head and neck. Multiple treatment modalities have been proposed for angiolymphoid hyperplasia with eosinophilia, each with limited success or undesirable side effects. At this time, standard surgical excision is considered the treatment of choice but carries recurrence rates of 33% to 50%. OBJECTIVE: The objective was to present a case of angiolymphoid hyperplasia with eosinophilia successfully extirpated using Mohs micrographic surgery. METHODS: A 52-year-old woman presented with an ill-defined solitary plaque of angiolymphoid hyperplasia with eosinophilia within her left conchal bowl that enlarged despite conservative therapy with intralesional and topical corticosteroids. Mohs micrographic surgery using the fresh tissue technique and standard hematoxylin and eosin staining was performed. The characteristic histologic features of angiolymphoid hyperplasia with eosinophilia were readily identifiable on frozen sections and complete extirpation required two stages of micrographically controlled resection. RESULTS: Resection of angiolymphoid hyperplasia with eosinophilia of the conchal bowl with complete resolution of symptoms and no evidence of clinical recurrence 8 months after surgery. CONCLUSION: Given the high recurrence rates reported for standard excision, Mohs micrographic surgery with complete margin examination should be considered as a treatment option for angiolymphoid hyperplasia with eosinophilia, particularly for lesions with ill-defined margins or in locations where tissue sparing is desirable.

Angiolymphoid Hyperplasia with Eosinophilia↗
PubMed1985

What is the significance of pancreatic ductal mucinous hyperplasia?

The prevalence, distribution, and clinical associations of pancreatic ductal mucinous hyperplasia were studied in 102 non-malignant pancreases. Ductal mucinous hyperplasia was found in over 60% of specimens and was frequently associated with increased fibrosis--occasionally resembling pancreatitis. Significantly more ductal mucinous hyperplasia was found in pancreas from patients who were receiving corticosteroid treatment. Neither a history of hypercalcaemia in the three months before death, diabetes mellitus, alcoholism, tobacco smoking, nor the presence of gall stones was associated with an increase in ductal mucinous hyperplasia. The age of maximum prevalence, and the distribution of ductal mucinous hyperplasia in the pancreas were similar to those of pancreatic carcinoma. These similarities may be because both ductal mucinous hyperplasia and pancreatic carcinoma are proliferative responses, rather than because ductal mucinous hyperplasia is a precursor of pancreatic carcinoma.

Adrenal Cortex Hormones↗
PubMed1996

Hematopoietic bone marrow hyperplasia: correlation of spinal MR findings, hematologic parameters, and bone mineral density in endurance athletes.

PURPOSE: To determine the frequency of hematopoietic hyperplasia on spinal magnetic resonance (MR) images in endurance athletes and to correlate MR alterations with clinical parameters. MATERIALS AND METHODS: In 15 endurance athletes, MR images of the lumbar spine were analyzed for hematopoietic hyperplasia; vertebral T1 and T2 were determined. Bone mineral density (BMD) was determined, blood tests were performed, and maximum oxygen consumption (VO2max) was measured. RESULTS: Nine subjects showed evidence of hematopoietic hyperplasia: Eight showed T1 prolongation, and six had patchy or diffuse T1 hypointensity. No definite correlation existed between hematopoietic hyperplasia and duration of training, hematologic results, or VO2max levels. Borderline significance existed between hematopoietic hyperplasia and anemia (P = .103) and intensity of training (P = .09). BMD had no statistically significant effect on T1. CONCLUSION: Changes in BMD do not appear to contribute to MR marrow changes that are consistent with hematopoietic hyperplasia. Depleted iron reserves or increased hematopoiesis probably contribute to hematopoietic hyperplasia in endurance athletes.

Adult↗
PubMed2000

Dihydrotestosterone and the concept of 5alpha-reductase inhibition in human benign prostatic hyperplasia.

OBJECTIVE: The development of the human benign prostatic hyperplasia clearly requires a combination of testicular androgens and aging. Although the role of androgens as the causative factor for human benign prostatic hyperplasia is debated, they undoubtedly have at least a permissive role. The principal prostatic androgen is dihydrotestosterone (DHT). Although not elevated in human benign prostatic hyperplasia, DHT levels in the prostate remain at a normal level with aging, despite a decrease in the plasma testosterone. RESULTS: DHT is generated by reduction of testosterone. Two isoenzymes of 5alpha-reductase have been discovered. Type 1 is present in most tissues of the body where 5alpha-reductase is expressed and is the dominant form in sebaceous glands. Type2 5alpha-reductase is the dominant isoenzyme in genital tissues, including the prostate. Finasteride is a 5alpha-reductase inhibitor that has been used for the treatment of benign prostatic hyperplasia and male-pattern baldness. At doses used clinically, its major effect is through suppression of type 2 5alpha-reductase, because it has a much lower affinity for the type 1 isoenzyme. Finasteride suppresses DHT by about 70% in serum and by as much as 85-90% in the prostate. The remaining DHT in the prostate is likely to be the result of type 1 5alpha-reductase. Suppression of both 5alpha-reductase isoenzymes with GI198745 result in greater and more consistent suppression of serum dihydrotestosterone than that observed with a selective inhibitor of type 2 5alpha-reductase. Physiological and clinical studies comparing dual 5alpha-reductase inhibitors, such as GI198745, with selective type 2, such as finasteride, will be needed to determine the clinical relevance of type 1 5alpha-reductase within the prostate. Two large international multicenter, phase III trials have been published documenting the safety and efficacy of finasteride in the treatment of human benign prostatic hyperplasia. Combining these two studies, randomized, controlled data are available for 12 months. Noncontrolled extension of these data from a subset of patients, who elected to continue drug treatment for 3, 4 or 5 years, are also available. Long-term medical therapy with finasteride can reduce clinically significant endpoints such as acute urinary retention or surgery. According to the meta-analysis of six randomised clinical trial with finasteride, finasteride is most effective in men with large prostates. A more effective dual inhibitor of type 1 and 2 human 5alpha-reductase may lower circulating DHT to a greater extent than finasteride and show advantages in the treatment of human benign prostatic hyperplasia and other disease states that depend on DHT. CONCLUSION: Clinical evaluation of potent dual 5alpha-reductase inhibitors may help define the relative roles of human type 1 and 2 5alpha-reductase in the pathophysiology of benign prostatic hyperplasia and other androgen-dependent diseases.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMedDate not supplied

External collar inhibits balloon-induced intimal hyperplasia in rabbits.

Intimal hyperplasia is a common complication following vascular interventions. To understand the underlying pathophysiology, the focus has mainly been on the intima and media. The adventitia has been less investigated, although adventitial hyperplasia is seen together with intimal hyperplasia. If the adventitial response is an important part of the process, the adventitia might be a target to inhibit intimal hyperplasia. In the present study we investigated whether an external collar attenuating the adventitial thickness could inhibit a balloon-induced intimal hyperplasia. The common carotid artery was injured in rabbits (n = 6) with a 3-french balloon catheter. The mid portion of the injured artery was encircled with a silicone collar (diameter = 2.0 mm). After 14 days the balloon-induced neointima was reduced by 54 +/- 6.3% underneath the collar. The adventitial and medial thickenings were also attenuated (36 +/- 8.7 and 44 +/- 4.3%, respectively). This study demonstrates that intimal hyperplasia following balloon injury can be inhibited with an external collar. This supports the idea of the adventitia as a potential target to inhibit intimal hyperplasia.

Actins↗
PubMed2004

Diagnostic hysteroscopy in endometrial hyperplasia.

OBJECTIVES: To assess the reproducibility of hysteroscopic diagnosis in the various types of endometrial hyperplasias and to compare different classifications of endometrial hyperplasia from this point of view. STUDY DESIGN: 109 endometrial hyperplasias, diagnosed in the last 5 years with hysteroscopy, were all biopsied and had a pathological examination. We tried to estimate the accuracy of hysteroscopy comparing the various classifications of endometrial hyperplasia to the final pathologic diagnosis. RESULTS: Using older endometrial hyperplasia classification, the overall diagnostic accuracy of hysteroscopy was 76% as for the correct type of hyperplasia. Classifying them at hysteroscopy into two categories only, i.e. hyperplasias and neoplasias, gave a more accurate result (90.26%). CONCLUSIONS: The newer classification is better from the hysteroscopist's point of view.

Diagnosis, Differential↗
PubMed2002

Distinction in genetic determinants for injury-induced neointimal hyperplasia and diet-induced atherosclerosis in inbred mice.

Five inbred strains of mice differing in susceptibility to diet-induced atherosclerosis were compared for neointimal hyperplasia after endothelial denudation with an epoxy resin-modified catheter probe. Results showed that all animals responded similarly to the arterial injury, with increased medial area and thickness after 14 days. In contrast, a significant strain-specific difference in neointimal formation after injury was observed. The atherosclerosis-susceptible C57L/J mice were also susceptible to injury-induced neointimal hyperplasia, and the C3H mice were resistant to both forms of vascular diseases. The 129/Sv mice, which displayed an intermediate level of diet-induced atherosclerosis, also displayed an intermediate level of injury-induced neointimal hyperplasia. Interestingly, the atherosclerosis-susceptible C57BL/6 mice were resistant to neointimal hyperplasia after endothelial denudation, whereas the atherosclerosis-resistant FVB/N mice were susceptible, displaying massive neointimal hyperplasia after arterial injury. All (C57L/JxC57BL/6)F1 hybrid mice were resistant to injury-induced neointimal hyperplasia. Moreover, N2 mice generated from backcrossing the F1 hybrid mice to the susceptible C57L/J mice displayed a range of arterial response to injury, spanning the most severe to the most resistant phenotype. These results indicate that injury-induced neointimal hyperplasia and diet-induced atherosclerosis are controlled by distinct sets of genes; the former appeared to be determined by recessive genes at > or =2 loci.

Animals↗
PubMed2001

Effects of balloon injury on neointimal hyperplasia in streptozotocin-induced diabetes and in hyperinsulinemic nondiabetic pancreatic islet-transplanted rats.

BACKGROUND: The mechanisms of increased neointimal hyperplasia after coronary interventions in diabetic patients are still unknown. METHODS AND RESULTS: Glucose and insulin effects on in vitro vascular smooth muscle cell (VSMC) proliferation and migration were assessed. The effect of balloon injury on neointimal hyperplasia was studied in streptozotocin-induced diabetic rats with or without adjunct insulin therapy. To study the effect of balloon injury in nondiabetic rats with hyperinsulinemia, pancreatic islets were transplanted under the kidney capsule in normal rats. Glucose did not increase VSMC proliferation and migration in vitro. In contrast, insulin induced a significant increase in VSMC proliferation and migration in cell cultures. Furthermore, in VSMC culture, insulin increased MAPK activation. A reduction in neointimal hyperplasia was consistently documented after vascular injury in hyperglycemic streptozotocin-induced diabetic rats. Insulin therapy significantly increased neointimal hyperplasia in these rats. This effect of hyperinsulinemia was totally abolished by transfection on the arterial wall of the N17H-ras-negative mutant gene. Finally, after experimental balloon angioplasty in hyperinsulinemic nondiabetic islet-transplanted rats, a significant increase in neointimal hyperplasia was observed. CONCLUSIONS: In rats with streptozotocin-induced diabetes, balloon injury was not associated with an increase in neointimal formation. Exogenous insulin administration in diabetic rats and islet transplantation in nondiabetic rats increased both blood insulin levels and neointimal hyperplasia after balloon injury. Hyperinsulinemia through activation of the ras/MAPK pathway, rather than hyperglycemia per se, seems to be of crucial importance in determining the exaggerated neointimal hyperplasia after balloon angioplasty in diabetic animals.

Angioplasty, Balloon↗
PubMed1995

Cigarette smoking accelerates carotid artery intimal hyperplasia in a dose-dependent manner.

BACKGROUND AND PURPOSE: Intimal hyperplasia is the single most important cause of early restenosis after carotid endarterectomy. Cigarette smoking is an independent risk factor associated with peripheral vascular disease and cerebrovascular accidents. We undertook a dose-response experiment to determine the effect of cigarette smoke on development of intimal hyperplasia in a rat carotid artery intimal injury model. METHODS: Seventy-two rats were divided into six equal groups and underwent standardized balloon injury to the carotid artery. Each group received 0 (controls), 1, 2, 3, 6, or 8 cigarettes per day for 4 weeks. Resultant intimal hyperplasia was expressed as a percentage of original lumen replaced by intimal hyperplasia. RESULTS: Percent intimal hyperplasia development (+/- SD) was as follows: controls (0 cigarettes per day), 17.7 +/- 13.2; 1 cigarette per day, 22.8 +/- 15.0; 2 cigarettes per day, 20.0 +/- 14.7; 3 cigarettes per day, 19.2 +/- 12.1; 6 cigarettes per day, 43.5 +/- 15.5; and 8 cigarettes per day, 36.7 +/- 9.8. Six and 8 cigarettes per day significantly increased the development of intimal hyperplasia after intimal injury (P < .01). CONCLUSIONS: High-dose cigarette smoke accelerates development of intimal hyperplasia and may pose a significant risk factor in developing carotid restenosis.

Animals↗
PubMed1991

Sustainability of forestomach hyperplasia in rats treated with ethyl acrylate for 13 weeks and regression after cessation of dosing.

In a chronic study conducted by the National Toxicology Program (NTP), gavage administration of 100 or 200 mg ethyl acrylate (EA)/kg/day, 5 days/week, to F344 rats and B6C3F1 mice resulted in a significant dose-dependent increase in the incidence of squamous cell papillomas and carcinomas of the forestomach of both sexes of rats and mice. No increase in the incidence of tumors was observed at any other site in these rats. Chemically-induced cell proliferation is currently thought to play a role in the development and progression of chemically-induced neoplasia. Therefore, a stop-study was initiated where 100 or 200 mg EA/kg (in corn oil) was administered daily, 5 days/week, for 13 weeks. Rats sacrificed at the end of the treatment regimen had severe epithelial hyperplasia of the forestomach. No lesions were observed in the glandular stomach or liver of EA-treated rats. Forestomach hyperplasia induced by EA included upward and downward cell proliferation. However, forestomachs of rats treated for 13 weeks and sacrificed 8 weeks after the last EA dose exhibited a significant decline in the incidence and severity of forestomach mucosal hyperplasia. Histopathologic evaluation of forestomachs of EA-treated rats (13 weeks) which were allowed a 19-month-recovery (with no exposure to EA) showed further decline in the incidence and severity of mucosal cell hyperplasia. These results indicate that gavage administration of EA to rats results in extensive and sustained forestomach mucosal hyperplasia. The sustainability of forestomach hyperplasia is apparently dependent on the continued exposure of rats to ethyl acrylate, and regressed after cessation of dosing. Furthermore, although enough post-treatment time was allowed for tumors to develop after cessation of EA administration, forestomachs exhibited a nearly complete recovery with no increased incidence of papillomas or carcinomas. It, therefore, remains to be determined what duration of exposure or other factors are critical for reversibility or progression of EA-induced forestomach mucosal hyperplasia to neoplasia.

Acrylates↗
PubMed2001

Thyroid hormone-responsive pituitary hyperplasia independent of somatostatin receptor 2.

Mice homozygous for the targeted disruption of the glycoprotein hormone alpha-subunit (alphaGsu) display hypertrophy and hyperplasia of the anterior pituitary thyrotropes. Thyrotrope hyperplasia results in tumors in aged alphaGsu(-/-) mice. These adenomatous pituitaries can grow independently as intrascapular transplants in hypothyroid mice, suggesting that they have progressed beyond simple hyperplasia. We used magnetic resonance imaging to follow the growth and regression of thyrotrope adenomatous hyperplasia in response to thyroid hormone treatment and discovered that the tumors retain thyroid hormone responsiveness. Somatostatin (SMST) and its diverse receptors have been implicated in cell proliferation and tumorigenesis. To test the involvement of SMST receptor 2 (SMSTR2) in pituitary tumor progression and thyroid hormone responsiveness in alphaGsu(-/-) mutants, we generated Smstr2(-/-), alphaGsu(-/-) mice. Smstr2(-/-), alphaGsu(-/-) mice develop hyperplasia of thyrotropes, similar to alphaGsu(-/-) mutants, demonstrating that SMSTR2 is dispensable for the development of pituitary adenomatous hyperplasia. Thyrotrope hyperplasia in Smstr2(-/-), alphaGsu(-/-) mice regresses in response to T4 treatment, suggesting that SMSTR2 is not required in the T4 feedback loop regulating TSH secretion.

Animals↗
PubMed1993

Relationship between the time of sustained ethyl acrylate forestomach hyperplasia and carcinogenicity.

Chronic administration of ethyl acrylate (EA) by gavage at 100 or 200 mg/kg/day resulted in a significant dose-dependent increase in the incidence of forestomach (FS) squamous cell papillomas and carcinomas in both sexes of F344 rats and B6C3F1 mice. Subsequent work in this laboratory was designed to investigate the relationship between EA-induced FS hyperplasia and carcinogenicity. Current studies have focused on determining the time required for sustained FS hyperplasia to produce neoplastic transformation. Results of these studies demonstrated that gavage administration of EA to male F344 rats at 200 mg/kg/day for 6 or 12 months caused a sustained increase in FS epithelial hyperplasia for as long as exposure to EA continued. However, FS hyperplasia regressed, and no neoplasms developed when animals receiving EA for 6 months were allowed to recover until they were sacrificed at 24 months of age. In contrast, rats treated for 12 months and allowed 9 months recovery developed FS squamous cell carcinomas (3/13) and papillomas (1/13) for a combined incidence of 4/13. No gross lesions were detected in the liver of any of the rats treated with EA or corn oil vehicle, confirming the tissue specificity in the relationship between EA-induced FS hyperplasia and carcinogenesis. In conclusion, the present work has demonstrated that FS hyperplasia is selectively sustained at the site of EA-induced carcinogenicity for as long as EA is administered and has also demonstrated a temporal relationship between FS mucosal hyperplasia and the development of FS neoplasia by EA.(ABSTRACT TRUNCATED AT 250 WORDS)

Acrylates↗
PubMed2001

Mutational analysis of the PTEN gene in endometrial carcinoma and hyperplasia.

To determine the potential role of PTEN in the process of endometrial carcinogenesis, we examined a series of endometrial carcinoma and hyperplasia of the uterine corpus for the presence of a PTEN mutation. The entire coding region of the gene was screened for the presence of mutations by single-strand conformation polymorphism analysis, and mutations were confirmed by sequencing. We detected mutations in 14 of 57 endometrial carcinomas (13 of 50 endometrioid adenocarcinomas and 1 of 7 nonendometrioid adenocarcinomas) and 7 of 73 endometrial hyperplasias (1 of 24 simple hyperplasias without atypia, none of 16 complex hyperplasias without atypia, and 6 of 33 complex hyperplasias with atypia). Most (88%) mutations were clustered in exons 5, 7, and 8. Of the 24 mutations detected in 21 cases, 12 were frameshifts, 9 were nonsense, 2 were missense, and 1 was a silent mutation. Patients with a PTEN mutation had a better prognosis than those with no PTEN mutation. The presence of PTEN mutations in hyperplasia suggests that PTEN inactivation may occur as an initiating event in endometrial carcinogenesis and is involved in the development of cytologic atypia in hyperplasia.

Carcinoma↗
PubMed2001

C-cell hyperplasia and medullary thyroid microcarcinoma.

Since the discovery of the thyroid C-cell, considerable progress has been made regarding its origin, function, and pathology. In this article an attempt is made to summarize and update our knowledge about physiologic or reactive C-cell hyperplasia, neoplastic C-cell hyperplasia (medullary carcinoma in situ), and medullary microcarcinoma. Seldom recognized preoperatively, physiologic C-cell hyperplasia is associated with inflammatory, metabolic, and neoplastic thyroid disorders as well as with hypercalcemia. However, the pathogenesis is still unclear. Although physiologic C-cell hyperplasia may progress to medullary carcinoma, the full malignant potential is unknown. Problems related to the definition of physiologic C-cell hyperplasia are discussed. Immunohistochemistry and quantitative analysis are required for the diagnosis. By contrast, C-cell hyperplasia associated with MEN II syndromes or familial medullary carcinoma can be diagnosed preoperatively in asymptomatic children or adolescents by the detection of germline mutations of the RET protooncogene. Morphologic and genetic abnormalities support the idea that C-cells in the familial form of C-cell hyperplasia are neoplastic and can be recognized with conventional stains. Therefore, the number of C-cells is irrelevant for the diagnosis. Medullary microcarcinoma is a neoplasm that measures < 1 cm. The sporadic variant is usually an incidental microscopic finding, whereas the familial form can be diagnosed by genetic testing. Its morphologic features and biologic behavior differ from those of larger medullary carcinomas. The frequency of medullary microcarcinoma will probably increase with the use of genetic testing.

Adolescent↗