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PubMed1999

Thymic hyperplasia after high-dose chemotherapy and autologous stem cell transplantation: incidence and significance in patients with breast cancer.

OBJECTIVE: The purpose of this study was to determine the incidence and clinical significance of thymic hyperplasia after high-dose chemotherapy and autologous stem cell transplantation for treatment of metastatic or high-risk primary (with at least four positive lymph nodes) breast cancer. MATERIALS AND METHODS: We retrospectively reviewed clinical records and CT scans of 102 breast cancer patients treated with high-dose chemotherapy and autologous stem cell transplantation. Patients were 26-63 years old (mean, 46 years). The length and width of the thymus gland were measured on serial CT scans obtained before and after treatment. Moderate thymic hyperplasia was recorded if a focal or diffuse increase was seen in the oblong, triangular soft-tissue opacity conforming to the configuration of the normal gland within the anterior mediastinum after therapy. Minimal hyperplasia was recorded when a minimal increase was seen in soft-tissue attenuation conforming to the configuration of the normal bilobed thymus gland within the anterior mediastinum, but no discrete mass was visible. RESULTS: CT showed no thymic hyperplasia in 91 (89%) of the 102 patients. CT showed thymic hyperplasia in the other 11 patients (11%). Three patients (3%) had moderate hyperplasia, and eight patients (8%) had minimal hyperplasia. When comparing patients with and without hyperplasia, we found no difference in mean age or survival. CONCLUSION: Thymic hyperplasia is rare after high-dose chemotherapy and autologous stem cell transplantation in adult patients with metastatic or high-risk primary breast cancer. In this population, thymic hyperplasia does not appear to correlate with survival.

Adult↗
PubMed2005

Atypical regenerative hyperplasia of the esophagus in endoscopic biopsy: a mimicker of squamous esophagic carcinoma.

CONTEXT: Atypical regeneration can mimic carcinoma in various epithelia. On endoscopic biopsies, atypical regenerative hyperplasia of the esophagus may show pleomorphism and atypia, simulating esophageal squamous cell carcinoma. OBJECTIVE: To establish the most useful histologic features to distinguish atypical regenerative hyperplasia from esophageal carcinoma in endoscopic biopsies. DESIGN: To study the frequency and histologic appearance of atypical regenerative hyperplasia, which simulate carcinoma, we reviewed 600 endoscopic biopsies (555 with chronic esophagitis and 45 with carcinomas of the esophagus). We selected those cases in which the differential diagnosis included regenerative atypical hyperplasia versus esophageal carcinoma and cases of atypical regenerative hyperplasia that were mistaken for carcinoma. For comparative purposes, we studied 10 cases of esophageal carcinoma from endoscopic biopsies that were confirmed by esophagectomy. RESULTS: Among the cases with chronic esophagitis, we found 10 biopsies (1.8%) in which atypical regenerative hyperplasia mimicked carcinoma. In 7 cases, there were 4 to 12 years of follow-up, and no patient developed esophageal neoplasm. The remaining 3 patients were submitted to esophagectomy. None of these patients had carcinoma or dysplasia in the esophageal resection (false-positive biopsies). The most useful architectural changes in squamous carcinoma included stromal infiltration by nests, cords, or thin prongs of neoplastic keratinocytes, palisading desmoplasia, and in situ carcinoma in the adjacent epithelium. Malignant keratinocytes showed variable degrees of differentiation with differently shaped and sized cells, squamous epithelial pearls, individual keratinization, and atypical mitosis. In contrast, biopsies with atypical hyperplasia showed detached nests or irregular fragments without stroma and were made up of immature and relatively monotonous medium or small keratinocytes that were intermixed with inflammatory cells. Individual keratinization was rare, and no squamous pearls were seen. Other features of atypical hyperplasia included granulated tissue with atypical endothelial cells, nonatypical mitosis, lymphoid hyperplasia, and the absence of dysplasia or carcinoma in situ. Two biopsies showed stromal pseudoinfiltration as a result of tangential sectioning and were characterized by thick, round prongs composed of keratinocytes that penetrated regions with granulation or the inflamed tissues of esophageal ulcers. CONCLUSIONS: Atypical esophageal regenerative hyperplasia may mimic carcinoma in a small percentage of esophageal biopsies. If the histologic changes are not sufficient to establish an accurate diagnosis, medical treatment and subsequent biopsies should be performed, particularly if there are no endoscopic or radiologic data to support the presence of a neoplasm.

Aged↗
PubMed1997

[Evaluation on ISGP classification of endometrial hyperplasia in clinical application].

To evaluate clinical application of International Society of Gynecologic Pathologists Classification of endometrial hyperplasia 424 patients with endome trial hyperplasia were treated in our hospital from Sept. 1989 to Feb. 1995. Our of these cases, 339 were simple hyperplasia, 28 were complex hyperplasia and 57 atypical hyperplasia. We made an analysis of the cases of complex and atypical hyperplasia in terms of the ISGP classification. The total rate of curettage was 63.5%. The agreement rate for pathologic diagnoses before and after operation was 78%. Under the age of 40, 18 patients had atypical hyperplasia and 15 of them underwent hysterectomy. Eight patients had complex hyperplasia and 3 of them underwent hysterectomy. Above the age of 40, 39 patients had atypical hyperplasia and 30 of them had uterus removed. Twenty patients had complex hyperplasia and 12 of them had uterus removed. These suggest that the ISGP pathologic diagnostic method is good to avoid overdiagnosis and overtreatment. Yet, diagnostic curettage is still the best means in diagnosis before operation.

Adult↗
PubMed2000

Descriptive epidemiology of endometrial hyperplasia in patients with abnormal uterine bleeding.

PURPOSE OF INVESTIGATION: To evaluate the prevalence and epidemiologic characteristics of endometrial hyperplasias in women with abnormal uterine bleeding. METHODS: We performed a retrospective analysis on data gained from 294 patients with histologically documented endometrial hyperplasia (with or without atypia), detected among 1,469 women who underwent fractional dilatation and curettage in our department due to abnormal uterine bleeding from 1986 to 1998. Epidemiologic characteristics were abstracted from the patients' medical charts. RESULTS: 294/1469 women were found with endometrial hyperplasia (258 without atypia and 36 atypical hyperplasias). Thirty-six of them were under 40 years of age. Four of the detected endometrial hyperplasias progressed to endometrial carcinoma (one with simple hyperplasia, two with complex and one with atypical hyperplasia). Obesity and hypertension were justified as risk factors in our study population. CONCLUSIONS: The prevalence of endometrial hyperplasia according to our data was 20%. There were statistically significant differences in most epidemiologic parameters between the two types of hyperplasia. The progression of four endometrial hyperplasias to endometrial adenocarcinoma indicates the need for intense follow-up even in cases where patients undergo conservative therapy.

Adult↗
PubMed2002

Dual-phase 99mTc-sestamibi imaging: its utility in parathyroid hyperplasia and use of immediate/delayed image ratios to improve diagnosis of hyperparathyroidism.

OBJECTIVE: Dual-phase (99m)Tc-sestamibi (methoxyisobutylisonitrile [MIBI]) imaging is the technique of choice for hyperparathyroidism (HPT), especially for localizing parathyroid adenomas. Prior studies have shown its utility for detecting hyperplasia is equivocal, but we believe this is not true. We attempted to quantitate the region-of-interest counts per pixel between immediate images and delayed images (I/D ratio) and use this ratio to distinguish normal parathyroid versus hyperplasia versus adenoma. METHOD: Anterior pinhole and upper thorax images with a low-energy, high-resolution collimator at 20 min and 2 h after (99m)Tc-MIBI injection were obtained on 54 subjects. The results were analyzed retrospectively as hyperplasia, adenoma, or normal parathyroid by the persistence of activity in 2 or more foci, a solitary focus, or no activity on the delayed images. These interpretations were compared with pathology when available. I/D ratios were computed for all scans, and mean ratios were calculated for each type of pathology (normal parathyroid, hyperplasia, and adenoma). The resulting ratios were analyzed with a t test to determine significant differences between the ratios. RESULTS: Sensitivity and specificity were 96% and 88%, respectively, for parathyroid hyperplasia. Mean I/D ratios were 2.26 +/- 0.68, 2.80 +/- 0.95, and 3.10 +/- 0.77 for subjects with hyperplasia, adenoma, and normal parathyroid, respectively (hyperplasia vs. normal, P = 0.020; adenoma vs. normal, P = 0.381; hyperplasia vs. adenoma, P = 0.033). CONCLUSION: Dual-phase (99m)Tc-MIBI imaging is more sensitive and specific for parathyroid hyperplasia than reported previously, supporting its use to localize hyperplastic glands preoperatively and to help guide resection. A thyroid ratio between immediate and delayed images will aid in distinguishing hyperplasia from normal parathyroid in uncertain cases.

Adenoma↗
PubMed1990

The role of mast cell degranulation products in mast cell hyperplasia. I. Mechanism of action of nerve growth factor.

A variety of mast cell degranulating agents have previously been shown to induce mast cell hyperplasia in adult rats. In neonates 2.5 S nerve growth factor (NGF) induces a hyperplasia of both mucosal and connective tissue mast cells (MMC and CTMC). We have examined the role of the potent mast cell degranulating properties of NGF on its ability to induce mast cell hyperplasia. Administration of NGF in combination with the mast cell stabilizing agent disodium cromoglycate was found to abrogate the CTMC hyperplasia induced by NGF alone. Treatment of neonatal rats with the alternate degranulating agent compound 48/80 was found to induce a limited CTMC but not a MMC hyperplasia. A supernatant obtained by degranulating purified adult rat peritoneal mast cells with anti-IgE was found to induce hyperplasia of the CTMC population similar to that observed with NGF administration. However, this degranulation product supernatant only induced a limited MMC hyperplasia as judged by RMCP II content of the tissues. These results suggest that NGF has dual action inducing mast cell hyperplasia; CTMC hyperplasia being dependent on the ability of NGF to degranulate mast cells. MMC hyperplasia induced by NGF is independent of CTMC degranulation. Degranulation products from peritoneal mast cells act to increase both MMC and CTMC populations in the neonate. These data suggest that the CTMC population may be regulated by an autocrine positive feedback mechanism in vivo.

Animals↗
PubMed1987

[Relations between atypical hyperplasia, dysplasia and prostatic cancer and the significance of its appearance for the clinician].

In 89 preparations of patients with a carcinoma of the prostate and 100 preparations of patients with a hyperplasia of the prostate (adenoma of the neck of the bladder) the appearance of primarily atypical hyperplasias was investigated. In these cases in the carcinoma group in the uniform as well as in the pluriform carcinomas a coincidence of carcinoma and atypical hyperplasia of 55% was found. The coincidence is particularly high in adenocarcinomas and in carcinomas with dominating adenoid part, respectively, i. e. in more mature glandular structures. Among the various histological types of the atypical hyperplasia the microglandular/papillary clear-cellular form is dominating with 82%. In the group of the benign hyperplasia of the prostate gland a coincidence of the atypical hyperplasia of 33% was found. Though this rate, in comparison to other investigators, seems to be relatively high, it is still significantly lower than in the carcinoma. From this follows that the atypical hyperplasia, particularly its severest forms and dysplastic deformations from other hyperplasias (postatrophic hyperplasia, basal cell hyperplasia, atrophy and metaplasia of the prostate) now as ever are suspected that these cases in question are precancerous lesions. For the clinically working urologist the task is derived in such histopathological diagnoses by clinical and bioptical follow-up controls to find an already existing, but still unrecognized, or developing carcinoma of the prostate gland. In no case the diagnosis may cause surplus therapeutic consequences.

Adenocarcinoma↗
PubMed1988

Worldwide experience in newborn screening for classical congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

The need for a reliable screening test for classical congenital adrenal hyperplasia prompted development of newborn screening programs. Worldwide incidence of classical congenital adrenal hyperplasia in this report was taken from newborn screening programs in France, Italy, Japan, New Zealand, Scotland, and the United States. Two populations in which the occurrence of congenital adrenal hyperplasia among live births has been reported with greater than usual frequency are the Yupik Eskimos of southwestern Alaska (1:282) and the people of La Reunion, France (1:2,141). Aside from these populations, 1,093,310 newborns were screened between 1980 and 1988, of whom 77 had congenital adrenal hyperplasia. Thus, worldwide incidence of this disorder was estimated at 1:14,199 live births for homozygous patients, 1:60 for heterozygous subjects, with a gene frequency of 0.0083. Incidence of congenital adrenal hyperplasia among whites was estimated to be 1:11,909 (41:488,279) for homozygous patients, 1:55 for heterozygous subjects with a gene frequency of 0.0091. Incidence for the salt-wasting form of congenital adrenal hyperplasia was 1:18,850 (58:1,093,310) compared with 1:57,543 (19:1,093,310) for congenital adrenal hyperplasia in the simple virilizing form. Thus, salt-wasting congenital adrenal hyperplasia was three times more common than simple virilizing congenital adrenal hyperplasia. Estimated incidence of congenital adrenal hyperplasia in white populations in Italy and France (1:10,866) was higher than in Scotland (1:17,098), New Zealand (1:14,500). The incidence in an Asian population (Japan) (1:15,800) did not differ significantly from that of the white population. In four of five populations, overall incidence was higher than previously reported, as was the frequency of the salt-wasting form (75% v 50% to 66%), suggesting improved case detection by newborn screening.(ABSTRACT TRUNCATED AT 250 WORDS)

17-alpha-Hydroxyprogesterone↗
PubMed1979

Relation of pancreatic duct hyperplasia to carcinoma.

In order to find a relationship between ductal hyperplasia and carcinoma of the pancreas, histological and histochemical examinations were made on pancreatic specimens of 1,174 autopsy patients with special attention to the age incidence of the former. Ductal hyperplasia was divided into 3 types; nonpapillary, papillary, and atypical hyperplasia. All three types of hyperplasia and ductal carcinoma showed a similar tinctorial property in mucous histochemistry. In general, atypical hyperplasia was seen in the pancreas having papillary hyperplasia which was found in the pancreas associated with nonpapillary hyperplasia. All three types of hyperplasia were apparently more frequent in cancerous pancreases than in non-cancerous ones. They were also more common in the head of the pancreas than in the body and tail. Age incidence also suggests a sequential change from nonpapillary hyperplasia through papillary and atypical ones to carcinoma.

Adolescent↗
PubMed2000

Hormone replacement therapy in postmenopausal women: endometrial hyperplasia and irregular bleeding.

BACKGROUND: The decline in circulating oestrogen around the time of the menopause often induces unacceptable symptoms that affect the health and well being of women. Hormone replacement therapy (both unopposed oestrogen and oestrogen and progestogen combinations) is an effective treatment for these symptoms. In women with an intact uterus, unopposed oestrogen may induce endometrial stimulation and increase the risk of endometrial hyperplasia and carcinoma. The addition of progestogen reduces this risk but may cause unacceptable symptoms, bleeding and spotting which can affect adherence to therapy. OBJECTIVES: The objective of this review is to assess which hormone replacement therapy regimens provide effective protection against the development of endometrial hyperplasia and/or carcinoma with a low rate of abnormal vaginal bleeding. SEARCH STRATEGY: Electronic searches for relevant randomised controlled trials of the Cochrane Menstrual Disorders and Subfertility Group Register of Trials, MEDLINE, EMBASE, PsychLIT, Current Contents, Biological Abstracts, Social Sciences Index and CINAHL were performed. Attempts were also made to identify trials from citation lists of review articles and drug companies were contacted for unpublished data. In most cases, the corresponding author of each included trial was contacted for additional information. SELECTION CRITERIA: The inclusion criteria were randomised comparisons of unopposed oestrogen therapy, combined continuous oestrogen-progestogen therapy and sequential oestrogen-progestogen therapy with each other and placebo administered over a minimum treatment period of six months. Trials had to assess which regimen was the most protective against the development of endometrial hyperplasia/carcinoma and/or caused the lowest rate of irregular bleeding. DATA COLLECTION AND ANALYSIS: Twenty three RCTs were identified and five were excluded. The reviewers assessed the eighteen included studies for quality, extracted the data independently and odds ratios for dichotomous outcomes were estimated. Outcomes analysed included frequency of endometrial hyperplasia or carcinoma, frequency of irregular bleeding and unscheduled biopsies or dilation and curettage, and adherence to therapy. MAIN RESULTS: Unopposed moderate or high dose oestrogen therapy was associated with a significant increase in rates of endometrial hyperplasia with increasing rates at longer duration of treatment and follow up. Odds ratios ranged from 5.4 (1. 4-20.9) for 6 months of treatment to 16.0 (9.3-27.5) for 36 months of treatment with moderate dose oestrogen (in the PEPI trial, 62% of those who took moderate dose oestrogen had some form of hyperplasia at 36 months compared to 2% of those who took placebo). Irregular bleeding and non adherence to treatment were also significantly more likely under these unopposed oestrogen regimens with greater effects with higher dose therapy. There was no evidence of increased hyperplasia rates, however, with low dose oestrogen. The addition of progestogens, either in continuous combined or sequential regimens, helped to prevent the development of endometrial hyperplasia and improved adherence to therapy (odds ratios of 3.7 for sequential therapy and 6.0 for continuous therapy). Irregular bleeding, however, was more likely under a continuous than a sequential oestrogen-progestogen regimen (OR = 2.3, 95% CI 2.1-2.5) but at longer duration of treatment, continuous therapy was more protective than sequential therapy in preventing endometrial hyperplasia (OR = 0.3, 95% CI 0.1-0.97). There was evidence of a higher incidence of hyperplasia under long cycle sequential therapy (progestogen given every 3 months) compared to monthly sequential therapy (progestogen given every month). No increase in endometrial cancer was seen in any of the treatment groups during the limited duration (maximum of 3 years) of these trials. (ABSTRACT TRUNCATED)

Endometrial Hyperplasia↗
PubMed1996

Endometrial carcinoma associated with hyperplasia.

The aim of this study was to clarify the relationship of endometrial hyperplasia to endometrial carcinoma. From 1979 through 1990, 115 cases of stage I-IV endometrial carcinomas treated initially by hysterectomy were reviewed histologically. Forty-two of 115 (36.3%) patients had hyperplasia in the endometrium adjacent to the carcinoma. Women with both endometrial carcinoma and hyperplasia were significantly younger than those with carcinoma without hyperplasia (P < 0.05). In a comparison of patients with carcinoma without hyperplasia, those with hyperplasia were better differentiated (P = 0.0072), and lacked deep myometrial invasion (P < 0.0001), cervical involvement (P = 0.0192), lymph-vascular space invasion (P = 0.0102), and para-aortic lymph node metastases (P = 0.0434). The presence of endometrial metaplasia (P = 0.0001). The estimated 5-year survival rates for patients with carcinoma with hyperplasia and those with carcinoma without hyperplasia were 96.55 and 73.33%, respectively (P = 0.0016). In endometrial carcinomas, the presence of endometrial hyperplasia may demonstrate a more favorable prognosis.

Adult↗
PubMed1998

Concomitant endometrial hyperplasia in patients with endometrial carcinoma.

OBJECTIVES: The aim of this study was to compare the histopathologic features and prognosis of patients with endometrial carcinoma with and without concomitant hyperplasia. METHODS: Histologic slides of the surgical specimens of 214 consecutive patients who underwent surgery as primary treatment for endometrial carcinoma from 1985 through 1991 were reviewed. RESULTS: Ninety-two of the 214 patients (43%) with endometrial carcinoma had concomitant endometrial hyperplasia. Patients with endometrial carcinoma with hyperplasia were significantly younger than those without hyperplasia (mean age 62 +/- 10 vs 65 +/- 9 years, P < 0.05). Carcinomas associated with hyperplasia were better differentiated and of lower surgical stage. By univariate analysis the frequency of recurrence was significantly lower (4% vs 17%, P < 0.004) and the estimated 5-year survival rate significantly higher (96% vs 85%, P < 0.01) in patients with endometrial carcinoma with concomitant hyperplasia. However, in multivariate analysis the presence of endometrial hyperplasia was not an independent prognostic factor and the 5-year survival rates of patients with or without hyperplasia did not differ significantly in any surgical stage. CONCLUSION: The presence or absence of concomitant endometrial hyperplasia is strongly correlated with the surgical stage of endometrial carcinoma.

Adenocarcinoma↗
PubMed1998

Bile duct obstruction is not a prerequisite for type I biliary epithelial cell hyperplasia.

Biliary obstruction, produced by common bile duct ligation or alpha-naphthylisothiocyanate (ANIT) treatment in rats, has been associated with the development of type I biliary epithelial cell (BEC) hyperplasia. However, the exact mechanism(s) by which bile duct obstruction lead(s) to this proliferative lesion are not clear. The present studies were designed to determine if cholestasis, in the absence of biliary obstruction, would result in type I BEC hyperplasia. Male Sprague-Dawley rats were given a single oral dose of 150 mg/kg ANIT or i.v. doses of estradiol glucuronide (E2-17G; 21 mumol/kg/h for 48 h) to produce obstructive and non-obstructive cholestasis, respectively. E2-17G treatment resulted in cholestasis that was comparable in extent and duration to that observed following ANIT treatment. E2-17G and ANIT treatments produced comparable increases in serum bile acids (55- to 60-fold) and activities of ALT (36- to 38-fold), ALP (4- to 5-fold), and 5'-nucleotidase (7- to 11-fold), respectively, compared to controls. Both ANIT and E2-17G also increased serum bilirubin concentrations. ANIT treatment resulted in significant increases in biliary glucose concentrations that were associated with BEC damage/necrosis and obstruction of the bile duct lumen. Conversely, no evidence of BEC damage was observed in E2-17G-treated rats. Nonetheless, BEC hyperplasia was observed in the majority of rats following treatment with either ANIT or E2-17G, assessed by light microscopy and by BrdU immunohistochemistry. These data indicate that E2-17G treatment produces nonobstructive cholestasis and type I BEC hyperplasia, suggesting that biliary obstruction is not a prerequisite for type I BEC hyperplasia in rats. Differences in the time of onset of hyperplasia were observed: hyperplasia was noted immediately following 48 h of E2-17G-induced cholestasis but occurred several days after ANIT-induced cholestasis had subsided. Since the magnitude/duration of cholestasis was similar in the two models but the temporal association between cholestasis and type I BEC hyperplasia were different, these data suggest that the proliferative stimulus may be different in the two models and that E2-17G-induced type I BEC hyperplasia may not be attributed solely to cholestasis.

1-Naphthylisothiocyanate↗
PubMed1993

Oncocytic hyperplasia in the human minor salivary glands: a post-mortem study.

Oncocytic hyperplasia in the human labial salivary glands was sought in a series of 217 post-mortem subjects. Oncocytic change occurred in 183 subjects and hyperplasia was found in 19 of those (the overall incidence being 8.8%), ranging in age from the third decade to the ninth. The sex distribution showed a significantly greater rate in males (16 of 139 males, 11.5%; 3 of 78 females, 3.8%). Oncocytic hyperplasia occurred in the duct system, and not in the acinar regions; it was frequently seen in the interlobular and intralobular ducts. Oncocytic hyperplasia was classified into four types; focal hyperplasia of the duct wall resulting in partial thickening of the duct wall; marked hyperplasia resulting in thickening of the duct wall, extending over half of the circumference; marked hyperplasia extending to the whole duct wall and intralobular adeno-tubular hyperplasia with or without cystic dilatation. About half of the subjects with oncocytic hyperplasia showed a few hyperplastic foci in one gland. The changes increased in severity in older subjects.

Adolescent↗
PubMed1999

[Algorithm of endometrial meta- and hyperplasia].

As to to their frequency and variety, endometrial meta- and hyperplasias are the most impressive examples of the growth and differentiation potential of the Muellerian system and the inductive power of steroid hormones and related inter- and intracellular factors. Characteristic steroid reactions are the glandular hyperplasias, ciliated and squamous cell metaplasias in the case of hyperestrogenism, and the mucinous and clear cell meta- and hyperplasias in the case of gestagen excess. In 1994, the WHO established a new classification of endometrial hyperplasias. This classification takes into account the profound differences in cancer risk, and accordingly demands a clearcut distinction between simple and complex (steroid sensitive, almost always reversible) hyperplasias without atypia, and simple and complex (partial steroid resistant and potential progressive) hyperplasias with atypia. The conclusion drawn from clinical experience is, that the atypical endometrial hyperplasia--and this alone--is the precancerous lesion of the ordinary endometroid carcinoma. In contrast, it is still not clear which biological significance accounts to all the complex squamous, mucinous, clear cell and ciliated cell meta- and hyperplasias. Yet, it is good pathological and clinical practice, to upgrade any metaplastic lesion with nuclear atypia, and to remove the uterus as it is done in almost all atypical endometrial hyperplasias.

Algorithms↗
PubMed2004

Mucin core protein expression by colorectal mucinous carcinomas with or without mucus hyperplasia.

BACKGROUND: In the categorization of colorectal mucinous carcinomas, much attention has been paid to the amount of extracellular mucin, but little to that of intracellular mucin. Perhaps this factor would be useful in further categorization. METHODS: We estimated the amount of intracellular mucin morphologically, and classified colorectal tumors (tubular adenomas, mucinous carcinomas, and nonmucinous carcinomas) into two categories each, those with and without intracellular mucus hyperplasia. From preliminary results, we chose a range of 50% or more for the ratio of intracellular mucus to the total area of tumor cells for our definition of such hyperplasia. Then, mucin expression in the different categories was examined immunochemically with antibodies to the mucin core proteins MUC1, MUC2, MUC5AC, and MUC6. RESULTS: MUC1 expression was found in none of the 40 adenomas, 8 (17%) of the 48 mucinous carcinomas (with little difference in those with and without mucus hyperplasia), and 4 (16%) of the 25 nonmucinous carcinomas. MUC2 was found in all mucinous carcinomas. MUC5AC was found in 18 (86%) of the 21 mucinous carcinomas with mucus hyperplasia and 18 (90%) of the 20 adenomas with mucus hyperplasia, but in only 9 (33%) of the 27 mucinous carcinomas without mucus hyperplasia, 5 (20%) of the 25 nonmucinous carcinomas, and 2 (10%) of the 20 adenomas without mucus hyperplasia. CONCLUSIONS: Mucinous carcinomas with and without mucus hyperplasia may arise from adenomas with and without mucus hyperplasia, respectively. The amount of intracellular mucin may be a morphologic reflection of the origin of colorectal mucinous carcinomas.

Adenocarcinoma, Mucinous↗
PubMed1995

Overexpression of P-glycoprotein in adenomatous hyperplasia of human liver with cirrhosis.

Adenomatous hyperplasia in the human liver with cirrhosis is similar to the hyperplastic nodule in rat hepato-carcinogenesis in that the mdr gene or its product P-glycoprotein is overexpressed. We immunohistochemically stained archival formalin-fixed, paraffin-embedded sections of 15 adenomatous hyperplasias with or without hepatocellular carcinoma in livers with cirrhosis, using the avidin-biotin-complex method and the JSB-1 monoclonal antibody which specifically binds the cytoplasmic epitope of P-glycoprotein. Of 15 cases with adenomatous hyperplasia, four were found solely in livers with cirrhosis. In six cases, adenomatous hyperplasia and hepatocellular carcinoma were found in the same liver separately. Hepatocellular carcinoma was discovered within adenomatous hyperplasia in five cases. All 15 livers with cirrhosis and those with adenomatous hyperplasia were positively stained for P-glycoprotein. When the grade of staining was compared between adenomatous hyperplasia and the surrounding liver, P-glycoprotein was overexpressed in 12 of 15 cases with adenomatous hyperplasia. P-glycoprotein was also stained more strongly in well-differentiated hepatocellular carcinoma than in the liver, but the staining grade of hepatocellular carcinoma was weaker than that of adenomatous hyperplasia. Moreover, the glycoprotein expression was less when the tumor was less differentiated.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Thyroid epithelial cell hyperplasia in IFN-gamma deficient NOD.H-2h4 mice.

The role of inflammatory cells in thyroid epithelial cell (thyrocyte) hyperplasia is unknown. Here, we demonstrate that thyrocyte hyperplasia in IFN-gamma-/- NOD.H-2h4 mice has an autoimmune basis. After chronic exposure to increased dietary iodine, 60% of IFN-gamma-/- mice had severe thyrocyte hyperplasia with minimal or moderate lymphocyte infiltration, and thyroid dysfunction with reduced serum T4. All mice produced anti-thyroglobulin autoantibody. Some wild-type NOD.H-2h4 mice had isolated areas of thyrocyte hyperplasia with predominantly lymphocytic infiltration, whereas IL-4-/- and 50% of wild-type NOD.H-2h4 mice developed lymphocytic thyroiditis but no thyrocyte hyperplasia. Both thyroid infiltrating inflammatory cells and environmental factors (iodine) were required to induce thyrocyte hyperplasia. Splenocytes from IFN-gamma-/- mice with thyrocyte hyperplasia, but not splenocytes from naïve IFN-gamma-/- mice, induced hyperplasia in IFN-gamma-/- NOD.H-2h4.SCID mice. These results may provide clues for understanding the mechanisms underlying development of epithelial cell hyperplasia not only in thyroids but also in other tissues and organs.

Animals↗