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PubMed1975

Survival with mammary cancer related to the interaction of germinal center hyperplasia and sinus histiocytosis in axillary and internal mammary lymph nodes.

In a review of the histologic sections of axillary and internal mammary lymph nodes removed during surgery for invasive ductal carcinoma of the breast, we found that 16 of 17 patients in whom sinus histiocytosis was the dominant lymphoid proliferative reaction are alive with no evidence of cancer 5 or more years after operation. In contrast, 5 of 6 patients in whom germinal center hyperplasia was the only significant reaction found died of cancer in less than 5 years. Patients with both sinus histiocytosis and germinal center hyperplasia in significant amounts had survival that was intermediate; 17 of 25 of these patients are currently alive and apparently free of cancer. In addition, 5 of 6 patients in whom no evidence was found of any lymphoid proliferative reaction and 3 of 3 patients with diffuse cortical hyperplasia in their axillary lymph nodes died of cancer in less than 5 years. Germinal center hyperplasia was associated with nodal metastases anatomically in individual lymph nodes and statistically in the series of cases. The internal mammary lymph nodes of most cases showed less proliferative reaction to tumor than the axillary lymph nodes. The pattern of proliferative reactions in lymph nodes and its correlation with survival after surgery suggest that different immune reactions may either suppress or enhance the growth of carcinoma of the breast.

Axilla↗
PubMed1979

Levels of histaminase and L-DOPA decarboxylase activity in the transition from C-cell hyperplasia to familial medullary thyroid carcinoma.

The distribution of calcitonin, L-dopa decarboxylase, and histaminase is studied in sectioned total thyroid glands from patients with different stages of familial medullary thyroid carcinoma. In 5 glands with gross carcinoma and in 3 with early microscopic carcinoma the distribution of all three parameters positively correlates (p less than .01 for each correlation). In contrast, in 6 glands with C-cell hyperplasia only the distribution of calcitonin and L-dopa decarboxylase correlates (r = 0.64, p less than .01) while those for histaminase vs. calcitonin (r = .17, p = N.S.) and histaminase vs. dopa decarboxylase (r = .03, p = N.S.) do not. In the glands with microscopic carcinoma the peak levels of histaminase occur in the areas of disease as defined by immunohistochemical staining of calcitonin; mean histaminase activity is the only one of the three parameters measured that distinguishes between C-cell hyperplasia and microscopic carcinoma (p less than .005). Immunohistochemical staining of histaminase shows positive cells in glands with gross and microscopic carcinoma, but in none of the glands with hyperplasia alone. Histaminase is thus found in high amounts in some malignant C-cells only and may be a useful marker to distinguish between hyperplasia and malignancy in thyroids with early C-cell proliferative disorders.

Amine Oxidase (Copper-Containing)↗
PubMed1979

Focal nodular hyperplasia of the liver with alcoholic hyalin bodies and cytologic atypia.

Focal nodular hyperplasia is an uncommon hepatic lesion in which the component hepatocytes are usually histologically normal. A case of focal nodular hyperplasia with cytologically atypical hepatocytes is presented. Light and electron microscopic evidence is given for the presence of alcoholic hyalin in these cells. A review of cytologic changes reported in focal nodular hyperplasia by others is included. To our knowledge, the presence of alcoholic hyalin in focal nodular hyperplasia has not previously been reported.

Aged↗
PubMed1982

Immunoblastic lymphoma arising in chronic lymphoid hyperplasia of the pulmonary interstitium.

Chronic pulmonary lymphoid hyperplasia occurs alone or is associated with a variety of disorders of the immune system. It may be a diffuse or localized process and has been referred to as lymphoid interstitial pneumonitis or pseudolymphoma, respectively. Chronic lymphoid hyperplasia in other organs has been followed by the development of malignant lymphoma, particularly when associated with disorders of the immune system. This report describes two patients with chronic hyperplasia of the pulmonary interstitial lymphoid tissue who had malignant lymphoma, immunoblastic type found at autopsy. Long-term steroid usage in one patient suggests the possibility that immunosuppressive therapy may increase the risk of developing malignant lymphoma in patients with chronic pulmonary lymphoid hyperplasia.

Aged↗
PubMed1988

Preliminary report on the use of danazol in the treatment of endometrial adenomatous hyperplasia.

Since the authors recently reported that danazol inhibits the growth of human endometrial cancer cells in vitro, a clinical trial was initiated to examine whether danazol can regress adenomatous hyperplasia, a precursor of endometrial adenocarcinoma. Danazol was used for 3 months in the treatment of five patients with a history of hypermenorrhea and irregular uterine bleeding. Within a 9-month follow-up period, all patients were symptom-free, and none of the specimens obtained by endometrial biopsy showed the presence of adenomatous hyperplasia. These findings suggest that danazol has a potential application in the treatment of patients with endometrial adenomatous hyperplasia. A possible mechanism of action of the compound in adenomatous hyperplasia is also discussed.

Adenoma↗
PubMed1990

Clinical effects of danazol on endometrial hyperplasia in menopausal and postmenopausal women.

Much evidence has been suggested that cystic, adenomatous, and atypical hyperplasia as well as adenocarcinoma in situ of the endometrium may ultimately progress to invasive cancer. Consequently, these lesions should be considered to be precursors of endometrial cancer. Twelve postmenopausal and three perimenopausal women with vaginal bleeding due to endometrial hyperplasia received 400 mg/d of danazol orally for 3 months. After 15 to 30 days of continuous danazol therapy, the endometrial glands ceased to grow and became smaller and rounder. The lumina of glands were narrow and contained no secretion. The nucleic mitosis of the glands disappeared. All women showed regression of hyperplastic endometrium within 2 to 3 months of initial treatment. In the 15 cases treated, endometrial hyperplasia could be controlled successfully with danazol without further recurrence and/or progression of the disease. In summary, danazol should be an effective and safe alternative therapy to progesterone for the treatment of endometrial hyperplasia.

Aged↗
PubMed1994

p53 expression in pseudoepitheliomatous hyperplasia, keratoacanthoma, and squamous cell carcinoma of skin.

BACKGROUND: Expression of p53 protein has been described in a variety of human malignant tumors. Recent reports have also demonstrated its presence in benign and reactive lesions. The significance of p53 expression is unclear. METHODS: This study examines the p53 expression in proliferative lesions of skin, including 6 pseudoepitheliomatous hyperplasia, 33 keratoacanthoma, and 45 squamous cell carcinoma, and to evaluate its significance. RESULTS: p53 expression was observed in all of the six cases of pseudoepitheliomatous hyperplasia, 78.8% of keratoacanthoma, and 75.5% of squamous cell carcinoma. The staining pattern of pseudoepitheliomatous hyperplasia and keratoacanthoma was generally less intense and extensive compared with that of squamous cell carcinoma. A keratoacanthoma with nuclear atypia that showed strong and extensive p53 staining was also encountered. The perilesional skin in sun-exposed sites often showed the presence of p53-positive keratinocytes. Control skin taken from the buttock was negative for p53 protein. Conversely, p53 was often expressed in carcinomas arising from sun-exposed as well as sun-protected sites. p53 positivity involved mainly the undifferentiated cells at the base of the epidermis or periphery of tumor cords. Differentiated keratinized cells were not stained. p53-positive fibroblasts were also noted in the inflammatory and granulation tissues of pseudoepitheliomatous hyperplasia. CONCLUSIONS: p53 expression in skin is common and appears to be an early event in a series of genetic alterations reflecting underlying actinic damage, which may lead to but does not necessarily indicate neoplastic or malignant transformation. Because p53 staining is seen in proliferative and undifferentiated cells and ceases to be expressed when the cells differentiate, it appears that the expression of p53 protein, mutant or wild-type, is an indicator of immaturity and proliferative capacity of the cell rather than one of neoplasia or malignancy.

Carcinoma, Squamous Cell↗
PubMed2001

The role of hyperplasia in multiple parathyroid adenomas.

BACKGROUND: Parathyroid adenoma is the most common cause of primary hyperparathyroidism (pHPT). Adenomas usually involve only a single gland, and the remaining glands are normal or suppressed. Multiple parathyroid adenomas have been reported to occur in as high as 11% of patients with pHPT. The significant incidence of multiple adenomas with histologic similarities to hyperplasia has raised the possibility that adenoma is a continuation of the hyperplasia state. To test this theory, we used molecular genetics to compare clonality and proliferative activity of parathyroid adenoma with its corresponding normal glandular tissue. Furthermore, we devised a scheme to definitively distinguish between the different parathyroid states on a molecular level, because histologic distinction is unreliable. METHODS: The study included three patients with a diagnosis of singular parathyroid adenoma and three with double parathyroid adenomas. Paraffin-embedded surgical specimens of both adenomas and normal glands were retrieved from each patient. Clonal analysis of the phosphoglycerolkinase (PGK) gene has suggested that parathyroid adenomas are monoclonal. Clonality of parathyroid adenomas and normal parathyroid glands was studied by polymerase chain reaction-based restriction fragment length polymorphic analysis for the PGK gene. Proliferative activity of the specimens was also analyzed using the immunohistochemical markers PCNA and Ki-67. RESULTS: All adenomas were monoclonal and all normal parathyroid glands were polyclonal for the PGK gene in both the single and double adenoma specimens. All adenomas stained positive for proliferative activity. In the three patients with singular adenoma, proliferative activity was not detected in the normal parathyroid tissue. However, in the double adenoma group, two of the three patients showed hyperproliferative activity in the normal glands. CONCLUSION: Proliferative activity consistent with hyperplasia was present in some normal glands of multiple adenoma patients. Our observation supports the theory that multiple adenomas may be a continuation of the hyperplasia state.

Adenoma↗
PubMed1998

Platelet-derived growth factor, intimal hyperplasia, and ischemic complications in giant cell arteritis.

OBJECTIVE: To explore whether vasoocclusion in giant cell (temporal) arteritis (GCA) is related to intimal hyperplasia and in situ production of platelet-derived growth factor (PDGF). METHODS: Temporal artery biopsy specimens from patients with GCA were analyzed for the presence of intimal hyperplasia. Expression of PDGF-A and PDGF-B was assessed by immunohistochemistry and digitized image analysis. RESULTS: PDGF-A and PDGF-B were widely expressed in inflamed arteries. CD68+ macrophages, smooth muscle cells, and multinucleated giant cells produced PDGF, whereas hyperplastic intimal tissue did not. Arteries with marked luminal narrowing and those with no or minimal luminal narrowing differed in the extent and distribution of PDGF expression. Concentric intimal hyperplasia was associated with the accumulation of PDGF-A- and PDGF-B-producing CD68+ macrophages at the media-intima junction. PDGF+,CD68+ macrophages in close proximity to the internal elastic lamina frequently coproduced matrix metalloproteinase 2. Intimal hyperplasia of the temporal artery correlated with ischemic complications of GCA, such as ocular involvement, jaw claudication, and aortic arch syndrome. CONCLUSION: Production of PDGF has a role in arterial occlusion in GCA. The excessive fibroproliferative response leading to luminal narrowing can be distinguished from the stenosing process in atherosclerosis and postangioplasty restenosis, suggesting that there are different response patterns to arterial injury. In GCA, macrophages at the media-intima border are the dominant source of PDGF. Since vasoocclusion is associated with a number of serious complications in GCA, inhibition of intimal proliferation should be a major goal of treatment.

Brain Ischemia↗
PubMed2003

Hypertrichosis terminalis, gingival hyperplasia, and a characteristic face: a new distinct entity.

Congenital generalized hypertrichosis terminalis has been described in association with other features as gingival hyperplasia, osteochondrodysplasia, and a dysmorphic face. Bondeson and Miles [1993: Am J Med Genet 47:198-212] described a woman with universal congenital hypertrichosis terminalis associated with gingival hyperplasia; the face of this patient was coarse and different from other forms of hypertrichosis described before. We present an 11-year, 6-month-old girl with universal congenital hypertrichosis terminalis, gingival hyperplasia, and a characteristic coarse face resembling the patient described by Bondeson and Miles [1993: Am J Med Genet 47:198-212]. We propose that this type of congenital generalized hypertrichosis terminalis, associated with gingival hyperplasia and a coarse face, is a distinctive new entity.

Abnormalities, Multiple↗
PubMed1989

Role for prazosin in reducing the development of rabbit intimal hyperplasia after endothelial denudation.

Intimal hyperplasia is the universal response to endothelial denudation and occurs after a variety of vascular procedures. In a proportion of cases the smooth muscle cell proliferation may lead to stenosis of the blood vessels. These vessels exhibit increased sensitivity to noradrenaline that can be reduced by the alpha 1-adrenergic antagonist prazosin. Because the alpha 1-adrenergic receptor and platelet-derived growth factor (which promotes vascular smooth muscle cell proliferation) act through the same metabolic pathway, it was postulated that alpha 1-adrenergic blockade might reduce the development of intimal hyperplasia. Twenty-eight New Zealand White rabbits underwent endothelial denudation of the aorta using a Fogarty balloon catheter. Test rabbits were treated with prazosin from the day of operation until they were killed. All rabbits were killed either 1 or 4 weeks after endothelial denudation. Intimal hyperplasia in cross-sections of the aorta was measured using an X-Y digitizer and was standardized in terms of percentage luminal reduction. Prazosin-treated rabbits had significantly less luminal reduction at 1 week (0.75(1.8) versus 9.7(3.1) per cent, mean (s.d.), P less than 0.001) and at 4 weeks (14.7(4.4) versus 25.3(12.8) per cent, P less than 0.05) than control rabbits. It is concluded that prazosin caused a major reduction in the development of intimal hyperplasia.

Animals↗
PubMed2003

Expression of steroid receptor coactivators and corepressors in human endometrial hyperplasia and carcinoma with relevance to steroid receptors and Ki-67 expression.

BACKGROUND: To examine the steroid hormone dependent growth mechanism of human endometrial hyperplasia and carcinoma, expression levels of steroid receptor cofactors, such as coactivators (steroid receptor coactivator 1 [SRC-1] and p300/cyclic AMP-response element-binding protein (p300/CBP]) and corepressors (nuclear receptor corepressor [NCoR] and silencing mediator for retinoid and thyroid-hormone receptors [SMRT]), were investigated. METHODS: The expression levels of cofactors were examined immunohistochemically using 20 samples of normal endometria, 36 samples of hyperplastic endometria, and 58 of malignant endometria and were compared with the expression levels of estrogen receptor (ER), progesterone receptor (PR), and a proliferation marker, Ki-67. RESULTS: In samples of normal endometria, the expression of coactivators was observed diffusely in glandular cells in the proliferative phase, with a mean positivity index (PI) of 81.8 for SRC-1 and 91.3 for p300/CBP, whereas expression levels decreased in endometrial hyperplasia (PI: SRC-1, 58.9; p300/CBP, 83.8) and endometrial carcinoma (PI: SRC-1, 45.0; p300/CBP, 55.4). In endometrial hyperplasia, there was a significant correlation between the expression of ER and SRC-1 or p300/CBP. In contrast, there were no significant statistical or topologic correlations between the expression of coactivators and the expression of ER/PR in endometrial carcinoma. The expression of corepressors generally was limited, except for elevated expression of NCoR in endometrial hyperplasia (PI, 23.8). CONCLUSIONS: The current study showed that expression levels of the steroid receptor coactivators SRC-1 and p300/CBP were reduced in endometrial carcinoma compared with normal and hyperplastic endometrium. In addition, topologic coexpression of both coactivators and ER/PR was lost in endometrial carcinoma. Accordingly, limited response to sex steroids in patients with endometrial carcinoma may be ascribed to the dissociation of cofactors and ER/PR.

Carcinoma↗
PubMed1983

Hyperplasia in the spinal sensory system of the frog. II. Central and peripheral connectivity patterns.

Central and peripheral connectivity patterns of hyperplastic dorsal root ganglia (DRGs) in Rana pipiens are examined in order to determine the relative roles of peripheral and central contacts in the production of DRG hyperplasias. The hyperplasias are produced in the intact hindlimb DRGs after the removal in tadpoles and young postmetamorphic frogs of neighboring DRGs (Davis and Constantine-Paton, '83). The peripheral target zones of the hyperplastic DRGs, determined by physiological recordings of sensory receptive fields, are found to undergo a significant degree of expansion relative to controls. Peripheral expansion is most pronounced in caudalmost DRG 10, and this effect occurs in experimental animals operated during larval and postmetamorphic stages. Further, anatomical labelling of peripheral sensory fibers coursing to the hindlimb reveals that the hyperplastic DRG 10 actually contains additional fibers projecting to the denervated regions. The central projection of the hyperplastic DRG 10 does not show corresponding increases in longitudinal arborization after the application of horseradish peroxidase to the appropriate dorsal roots. These observations are made on some of the same experimental animals in which peripheral fields are shown to have vastly expanded. We conclude that the peripheral processes of the hyperplastic DRGs are less rigidly specified than the central terminations, and that it is the periphery which plays the primary role in controlling the cell numbers increases. A second aim of this investigation is to identify whether sexually dimorphic connectivity patterns in normal frogs explain the production of DRG 10 hyperplasias exclusively in male experimental animals (Davis and Constantine-Paton, '83). We apply the same techniques used in our connectivity studies of hyperplastic DRGs to the investigation of connectivity patterns of DRG 10s in normal males and females. No sex-dependent differences in peripheral and central connectivity are found. Thus, since normal male and female frogs possess an equivalent amount of target space for DRG 10, the unique production of hyperplasias in male experimental animals cannot be explained solely on the basis of connectivity. We speculate on what other factors may be involved.

Animals↗
PubMed1991

Cytologic findings in microglandular hyperplasia of the cervix.

A case of florid microglandular hyperplasia of the uterine cervix that contained cells with severe atypia suggesting malignancy on a Papanicolaou smear is reviewed. Findings from 25 additional smears from patients with microglandular hyperplasia are reported. These sometimes contained glandular cells with varying degrees of atypia, but demonstrated no features specific for microglandular hyperplasia. The distinction between markedly atypical endocervical cells sometimes exfoliated from microglandular hyperplasia and those of adenocarcinoma is discussed.

Adult↗
PubMed2006

Imbalance in liver homeostasis leading to hyperplasia by overexpressing either one of the Bcl-2-related genes, zfBLP1 and zfMcl-1a.

Apoptosis is an essential part of normal embryonic development in vertebrates, and it is involved in sculpturing organs and controlling cell populations. In previous studies, we identified two novel proteins, zfBLP1 and zfMcl-1a, which are similar to those of the Bcl-2 family as a group of evolutionarily conserved proteins that regulate cellular anti-apoptosis. To evaluate the effect of dysregulated hepatocyte apoptosis during zebrafish hepatogenesis, we demonstrate the transgenic overexpression of either zfBLP1 or zfMcl-1a in zebrafish larval liver. Results showed that 18%-43% of larvae overexpressed zfBLP1 and that 16%-37% of larvae overexpressed zfMc1-1a in the liver leading to liver hyperplasia in 5-day postfertilization (dpf) zebrafish larvae. Histologically, zebrafish larvae exhibiting liver hyperplasia displayed a normal type of hepatocyte and the same cell numbers in their two liver buds compared with only one liver bud of wild-type larvae. Of interest, the expression of cyclin genes (A2, B, D1, and E), hepatocyte nuclear factor genes (HNF-1alpha, beta, -3beta, and 4alpha), and oncogenic markers (P53, c-myc, beta-catenin, N-ras, and gankyrin) were up-regulated, while the expression of C/EBP-alpha was down-regulated in a zfMcl-1a-mediated anti-apoptotic process of the liver. Increased cell death and proliferation was found in both hepatic cells of zebrafish larvae overexpressing either zfBLP1 or zfMcl-1a. However, those zebrafish larvae with liver hyperplasia only lived approximately 10 days. (This finding may have been due to liver abnormalities that led to failure of liver function.) In conclusion, transgenic overexpression of zfBLP1 or zfMcl-1a in zebrafish larvae interrupts regulation of the homeostatic balance between cell proliferation and programmed cell death during hepatogenesis and leads to liver hyperplasia.

Animals↗
PubMed2004

Serum concentrations of IGF-I, IGFBP-3 and c-peptide and risk of hyperplasia and cancer of the breast in postmenopausal women.

Experimental evidence suggests that insulin and insulin-related growth factors may play a role in breast pathology through their mitogenic and anti-apoptotic effects on breast cells. Our objective was to assess the relationship between serum concentrations of insulin-like growth factor-I (IGF-I), its major binding protein (IGFBP-3), the ratio IGF-I:IGFBP-3, c-peptide (a marker of insulin secretion) and the ratio c-peptide:fructosamine (a marker of insulin resistance) and the risk of epithelial hyperplasia (an established breast cancer risk factor) and localized breast cancer among postmenopausal women. Study subjects were patients who provided serum before breast biopsy or mastectomy in 3 hospitals in Grand Rapids, MI between 1977 and 1987. Two case groups, 186 subjects with epithelial hyperplasia of the breast and 185 subjects with localized breast cancer, were compared to 159 subjects with nonproliferative breast changes that have not been associated with increased breast cancer risk. Serum concentrations of IGF-I, IGFBP-3 and the ratio IGF-I:IGFBP-3 were not related to risk of either hyperplasia or breast cancer. For women in the highest quartile of c-peptide or of c-peptide:fructosamine compared to those in the lowest quartile, the odds ratios (ORs) for hyperplasia were 3.0 (95% confidence interval [CI] 1.4-6.5) and 3.3 (95% CI 1.5-7.3), respectively (p trend = 0.02 and 0.02, respectively). The corresponding ORs for breast cancer were 1.5 (95% CI 0.7-3.0) and 1.6 (95% CI 0.8-3.2), respectively (p trend = 0.35 and 0.25, respectively). Our results suggest that insulin and insulin resistance may play a role in breast pathology in postmenopausal women.

Adult↗
PubMed1992

Harderian gland hyperplasia in c-mos transgenic mice.

Transgenic mice carrying the mouse mos proto-oncogene linked to a retroviral LTR develop hyperplasia of the Harderian glands. Enlargement of the glands is evident as early as 18 weeks after birth, with glands reaching up to 10 times their normal weight. Approximately 65% of the cases of hyperplasia occur bilaterally, and the majority of mice affected are male (66%). Elevated levels of mos expression are found in all Harderian glands of mice from the affected transgenic line, but not in glands of normal mice or a non-affected transgenic line, indicating that hyperplasia is dependent on mos expression. Histological examination of the tissue reveals a general involvement of the entire gland epithelium in hyperplastic growth, with no evidence of focal or malignant tumours. These observations show that in addition to neu, myc, ras and ret transgenes, mos, a member of the protein-serine/threonine kinase family of oncogenes, can induce Harderian gland hyperplasia, thus revealing an unusual response by this organ to various classes of oncogenes. Analysis of fos, jun, myc and ets oncogene RNA in mos-induced hyperplastic Harderian glands shows that there are no consistent changes in the level of expression of these oncogenes, suggesting that mos acts via a mechanism other than by increasing the expression of these genes.

Animals↗
PubMed1994

Di(2-ethylhexyl)phthalate-induced changes in liver estrogen metabolism and hyperplasia.

Exposure to a common phthalate, di(2-ethylhexyl)phthalate (DEHP), is associated with liver hyperplasia prior to the development of hepatocellular carcinoma in rodents. The exact mechanism of liver hyperplasia as well as tumorigenesis by this agent is not known. Since other lines of evidence point to estrogens as mediators of liver hyperplastic changes, we investigated whether DEHP exposure might alter hepatic estrogen metabolism and induce hyperplasia. Male Fischer 344 rats were fed either control or 1.2% DEHP-containing diets and sacrificed after 4, 8 and 16 weeks of exposure; activities of several sex hormone-responsive markers were measured. Rats fed DEHP had significantly increased serum estradiol levels, but hepatic activity of both cytosolic and nuclear estrogen receptor (ER) was significantly reduced. The serum content of ceruloplasmin, an estrogen-responsive protein synthesized by the liver, was also reduced, perhaps as a consequence of loss of ER activity. The rise in serum estradiol in DEHP-treated rats may be explained by the observation that these rats showed significant losses in hepatic activity of both a major male estrogen-metabolizing enzyme, estrogen 2-hydroxylase, and a male-specific estrogen-sequestering protein. In contrast to reductions in these activities, the expression of proliferating cell nuclear antigen and mRNAs for both ER and fos increased significantly as a result of exposure to DEHP. Our results suggest that changes in estrogen metabolism, receptor activity and activation of genes for cell proliferation are among the earliest metabolic alterations induced by DEHP. These changes together with the induced hyperplasia could play a crucial role in hepatocellular carcinoma development as a result of continuous exposure to DEHP.

Animals↗