Inhibin and Activin Are Demonstrable by Immunohistochemistry in Ovarian Tumor Tissue

Gurusinghe, Chandan J.; Healy, D.L.; Jobling, Tom; Mamers, Pamela; Burger, Henry G.

doi:10.1006/gyno.1995.1096

Cited by 67 publications

(37 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The opposite, in fact, appears to be the case. Several reports indicate inhibin o-and S-subunit expression in gonadal sex-cord tumors (Gurusinghe et al, 1995;Flemming et al, 1995Flemming et al, ,1996Costa et al, 1997;Stewart et al, 1997;Yamashita et al, 1997;Zheng et al, 1997). In some cases, these tumors are associated with elevated circulating inhibin levels that are decreased following surgical resection (Lappohn et al, 1989;Silverman et al, 1994;Cooke et al, 1995;Yamashita et al, 1997).…”

Section: Molecular Regulation Of Inhibin Subunitsmentioning

confidence: 99%

“…Both LH and FSH are produced and stored in the same gonadotrope cells in the anterior pituitary but the two hormones (which, like the inhibins, share a common cx subunit) are differentially released. The frequency of GnRH pulses from the brain provides one mechanism governing this differential regulation of the two gonadotropins (Haisenleder et al, 1994). Future experiments need to address both the control of c@A vs. o$B assembly as well as the nature of the signals stimulating inhibin A vs. inhibin B release.…”

Section: A Differential Regulation Of Inhibin Isoformsmentioning

confidence: 99%

See 1 more Smart Citation

Mechanisms of Inhibin Signal Transduction

Bernard

Chapman²,

Woodruff³

2001

Recent Progress in Hormone Research

View full text Add to dashboard Cite

Inhibin was first identified as a gonadal hormone that potently inhibits pituitary follicle-stimulating hormone (FSH) synthesis and secretion. Although the notion of a nonsteroidal, gonadally derived inhibitory substance was realized in the early 1930s (McCullagh, 1932) identification of the hormone was not accomplished until more than 50 years later. At that time, inhibin was purified from bovine and porcine follicular fluid and was shown to be produced in two forms through dimeric assembly of an Q subunit (I 8 kDa) and one of two closely related i3 subunits (PA and PB, approximately I4 kDa) Miyamoto et al., 1985;Rivier et al., 1985;Robertson et al., 1985).

show abstract

Section: Molecular Regulation Of Inhibin Subunitsmentioning

confidence: 99%

Section: A Differential Regulation Of Inhibin Isoformsmentioning

confidence: 99%

Mechanisms of Inhibin Signal Transduction

Bernard

Chapman²,

Woodruff³

2001

Recent Progress in Hormone Research

View full text Add to dashboard Cite

show abstract

“…Inhibin is probably the most helpful marker (2,(12)(13)(14)(15)(16)(17)(18)(19). Inhibin is a dimeric glycoprotein hormone produced by normal ovarian granulosa cells and testicular Sertoli cells (20) that is involved in the regulation of pituitary folliclestimulating hormone secretion.…”

mentioning

confidence: 99%

Characteristic Pattern of Genetic Aberrations in Ovarian Granulosa Cell Tumors

Mayr¹,

Kaltz-Wittmer²,

Arbogast³

et al. 2002

Mod Pathol

View full text Add to dashboard Cite

The cytogenetic abnormalities of granulosa cell tumors (GCT) of the ovary are only partially known. Up to now, mainly numerical chromosomal aberrations have been described. Therefore we performed a comprehensive study on paraffin-embedded material of 20 GCT (17 adult, 3 juvenile; patient age between 16 and 78 y) combining comparative genomic hybridization (CGH); fluorescence in situ hybridization (FISH) using DNA-specific probes for chromosome 12, 17, 22, and X; DNA cytometry; and immunohistochemistry (inhibin, p53, Ki67).By DNA cytometry, 16 of 20 tumors (80%) were diploid. However, 6 of 16 diploid tumors (37%) showed aberrations by FISH. FISH revealed monosomy 22 in 8/18 cases (40%); trisomy 12 in 5/20 (25%); monosomy X in 2/20 (10%); and loss of chromosome 17 in one case (5%). The main findings by CGH were gains of chromosomes 12 (6 cases, 33%) and 14 (6 cases, 33%) and losses of chromosomes 22 (7 cases, 35%) and X (1 case, 5%), mostly comprising whole chromosomes or chromosome arms. Inhibin and p53 were expressed in 100% and 95% of the tumors, respectively. The Ki67 index ranged from 0% to 61%. Neither immunohistochemistry, nor DNA cytometry and molecular genetic analysis, provided statistically significant prognostic information.In summary, our study reveals a distinctive pattern of cytogenetic alterations in GCT. Our observations confirm earlier reports that trisomy 12 and 14 are frequent aberrations; however, monosomy 22 seemingly is even more prevalent. Granulosa cell tumors of the ovary (GCT) are much less common than epithelial ovarian cancer. These tumors account for 1.5% of all ovarian neoplasms and for 6% of malignant ovarian tumors. Sixty-five percent of patients are postmenopausal; Ͻ5% are prepubertal. The juvenile granulosa cell tumor is a distinctive form of GCT that occurs almost exclusively in children and young adults. More than 95% of the GCT are unilateral and confined to the ovary.

show abstract

“…22,33 The presence of NPY receptors in inhibin-expressing sex cord-stromal tumors may be indicative of an NPY action on the inhibin system; NPY may affect inhibin production and/or release and, as such, play a pathophysiological role in inhibin-producing tumors. Moreover, inhibin may have growth-suppressive functions in these tumors, since inhibin-deficient mice develop malignant sex cord-stromal tumors in very high frequency.…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y receptor expression in human primary ovarian neoplasms

Körner

Waser

Reubi

2004

Laboratory Investigation

View full text Add to dashboard Cite

Peptide hormone receptors overexpressed in human malignant neoplasms are potential targets for diagnostic scintigraphy and radiotherapy. One such receptor is the neuropeptide Y (NPY) receptor, mediating primarily feeding behavior in the brain but shown recently to play a role in breast cancer. In this study, the presence of NPY receptors was evaluated in another group of gynecological tumors, namely ovarian tumors, using in vitro receptor autoradiography with 125 I-labeled peptide YY and receptor subtype selective analogs. Remarkably, all 10 investigated inhibin-expressing granulosa cell tumors, Leydig cell tumors, and Sertoli-Leydig cell tumors expressed NPY receptors. In contrast, receptors were found in only seven of 22 ovarian adenocarcinomas (32%). Pharmacological characterization of the expressed NPY receptor subtypes in the various tumors revealed the presence of Y1, Y2, or both. In addition, Y1 receptors were observed in intra-and peritumoral blood vessels as well. NPY receptors were not expressed in three ovarian adenomas, three borderline tumors, four fibromas and fibrothecomas, and one dysgerminoma. This is the first time that NPY receptors are described in human ovarian tissue. They may play a role in the pathogenesis and also in the pathophysiology of ovarian malignancies. Moreover, the high incidence and density of NPY receptors in sex cord-stromal tumors suggest that these receptors represent a new potential target for the diagnostic and therapeutic administration of NPY analogs in these tumors.

show abstract

Inhibin and Activin Are Demonstrable by Immunohistochemistry in Ovarian Tumor Tissue

Cited by 67 publications

References 0 publications

Mechanisms of Inhibin Signal Transduction

Mechanisms of Inhibin Signal Transduction

Characteristic Pattern of Genetic Aberrations in Ovarian Granulosa Cell Tumors

Neuropeptide Y receptor expression in human primary ovarian neoplasms

Contact Info

Product

Resources

About