Active cell death in hormone-dependent tissues

Tenniswood, Martin; Guenette, R. Sean; Lakins, Johnathon N.; Mooibroek, Marilyn J.; Wong, Paul; Welsh, JoEllen

doi:10.1007/bf00048064

Cited by 255 publications

(148 citation statements)

References 217 publications

(227 reference statements)

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“…During tumor promotion by NAF, the excess of cell proliferation over apoptosis increased with advancing only in a few models using hormone-dependent tumors. [29][30][31] Here we provide-to our knowledge, for the first time-funcmalignancy (Fig. 5), as shown above for spontaneous carcinogenesis.…”

Section: Effects Of Naf Treatment On Normal Liver and On Tumormentioning

confidence: 89%

Inherent increase of apoptosis in liver tumors: Implications for carcinogenesis and tumor regression

et al. 1997

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In the past few years, scientific interest has focused on We quantitatively assessed rates of cell replication and the process of apoptosis. Like cell replication, apoptosis is of apoptosis during the development and regression of controlled by the networks of positive and negative growth liver cancer. In rats, apoptotic activity gradually insignals. 3,[6][7][8][9][10][11] Currently prevailing views assume that maligcreased from normal liver to putative preneoplastic foci nant cells are incapable of apoptosis and/or are not responsive (PPF), to hepatocellular adenoma (HCA), and to hepatoto death signals, thereby allowing unrestrained growth of cellular carcinoma (HCC). At all stages, rates of cell replicancer. cation were higher than of apoptosis, allowing a prefer-We studied the role of apoptosis for carcinogenesis and ential net gain of (pre)neoplastic cells. As in rats, in tumor reversion in rat and human liver. Liver cancer is human HCC, birth and death rates were increased maniamong the eight leading causes of cancer death worldwide; fold, indicating a species-independent phenomenon. Imtherapeutic possibilities are very limited and prognosis is plications of the increasing cell turnover were studied usually poor. 12 Etiologic factors include genotoxic agents such in rats using the administration and withdrawal of naas certain mycotoxins or hepatitis B virus, and numerous fenopin (NAF), a liver mitogen and nongenotoxic carcinnongenotoxic exposures, e.g., ethanol, cytotoxic and inflamogen. Prolonged NAF treatment enhanced cell number matory events, steroid hormones, as well as overnutrition, in normal liver by 25%, while PPF and liver tumors were dietary constituents and some drugs, all of which may enamplified at least 100-fold. After stopping NAF treathance the growth rate of precancerous and cancerous lesions ment, cell replication ceased, while cell elimination by in the liver. 12,13 Experimental results on cancer prestages apoptosis was increased in normal and (pre)neoplastic (putative preneoplastic foci [PPF]) in this organ were not liver. HCA and HCC showed the most pronounced shifts consistent with the concept of failure of apoptosis during carfrom replication toward apoptosis. As a result, 5 weeks cinogenesis. Rather, PPF showed rates of apoptosis much after halting NAF, 20% of cells in normal liver, but about higher than normal liver; thus, the high rate of cell replica-85% of (pre)neoplastic lesions including HCC, were elimtion in PPF was largely counteracted and net growth was inated. The implications of these findings include that impeded. 11,14,15 Tumor promotion by liver mitogens or overnongenotoxic carcinogens can act as survival factors feeding inhibited apoptosis and enhanced survival of cells even for malignant cells. Furthermore, tumor cells not preferentially in PPF, thereby allowing their selective only exhibit excessive proliferation, but also undergo growth; conversely, withdrawal of these survival/growth facapoptosis at rates that far exceed those in normal tissue.tors enhanced apopt...

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Section: Effects Of Naf Treatment On Normal Liver and On Tumormentioning

confidence: 89%

Inherent increase of apoptosis in liver tumors: Implications for carcinogenesis and tumor regression

et al. 1997

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“…It was suggested that clusterin protects the apoptotic cell from complement fixation during the time of membrane blebbing and cytoplasmic condensation (Tenniswood et al, 1992). Lack of correlation between clusterin expression and apoptosis was demonstrated in other systems, such as neural death during development (Garden et al, 1991), and several inducible models of apoptosis (Pearse et al, 1992;reviewed in Rosenberg et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Clusterin expression within skin correlates with hair growth

Seiberg¹,

Marthinuss²

1995

Developmental Dynamics

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Clusterin/T'RPM-2 is a sulfated glycoprotein that is expressed in many tissues. Independently cloned and isolated by several laboratories, it bears many names, and has been shown to be involved in many processes. These include cell-cell adhesion and aggregation, inhibition of complement cytolysis, programmed cell death and apoptosis, tissue remodeling, and terminal differentiation. The hair follicle undergoes cycles of growth, regression, and rest, which involve both tissue remodeling and programmed cell death. To identify whether clusterin expression is involved in hair growth and cycling, we studied the expression of clusterin throughout the hair cycle. We demonstrate that clusterin is expressed during the growth phase of the hair cycle. We found no correlation between clusterin expression and the apoptotic regression of the hair follicle. Using immunohistochemistry we localized clusterin to the inner root sheath of the follicle. This suggests that clusterin might be involved in the morphogenesis and differentiation of the hair follicle. We propose that clusterin has a role in the maintenance of the layered structure of the hair follicle, and in the interactions between the inner root sheath and both the outer root sheath and the hair shaft. o 1995 Wiley-Liss, Inc.

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“…2 Because it has been studied independently by a number of laboratories and in different systems, it has been given various names, such as SGP-2, clusterin, apolypoprotein J, SP 40 -40, complement lysis inhibitor, gp80, glycoprotein III, and T64. 3 The human homologue of clusterin is comprised of 449 amino acids with two 40-kd subunits (␣ and ␤) joined by a unique five disulfide bond motif. 4 The protein precursor is encoded on a single 2 kb mRNA that is transcribed from a single copy gene located on chromosome 8 (8p21).…”

mentioning

confidence: 99%

“…6 Thus, clusterin mRNA has been widely used as a genetic marker of apoptotic cell death. 3 In hormone-dependent tissues, such as the prostate and the mammary gland, clusterin expression is induced after hormone ablation. 10,11 However, these studies did not analyze which cells account for the rise in clusterin gene expression, the cells undergoing apoptosis or those destined to survive.…”

mentioning

confidence: 99%

Overexpression of Clusterin in Human Breast Carcinoma

Redondo

Villar

Torres-Muñoz

et al. 2000

The American Journal of Pathology

229

181

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Clusterin has been implicated in numerous processes including active cell death, immune regulation, cell adhesion and morphological transformation. The purpose of this study was to examine clusterin expression in a large series of breast carcinomas by immunohistochemistry and in situ hybridization. The study included 40 samples of non-neoplastic glandular epithelia, 42 benign lesions, 15 atypical intraductal hyperplasias, 35 carcinomas in situ, 114 invasive carcinomas, and lymph node metastases from 40 patients. Epithelial normal cells were always negative for clusterin expression and only 19% of the benign lesions presented positive staining. In contrast to the benign lesions, however, the frequency of clusterin positive samples increased in atypical hyperplasias (47%, P ‫؍‬ 0.08), intraductal carcinomas (49%, P ‫؍‬ 0.01) and invasive carcinomas (53%, P < 0.001). Positive staining presented a cytoplasmic pattern, except in 3 cases of invasive carcinomas which had nuclear staining. Clusterin mRNA by in situ hybridization confirmed the specific cellular pattern of clusterin expression by immunohistochemistry. Clusterin expression was associated with large tumor size (P ‫؍‬ 0.04), estrogen and progesterone receptor negative status (P ‫؍‬ 0.02 and P ‫؍‬ 0.001, respectively) and with the progression from primary carcinoma to metastatic carcinoma in lymph nodes (80% metastatic nodes had positive expression) (P ‫؍‬ 0.004). Ten of 15 (67%) primary carcinomas without clusterin expression became positive in lymph node metastases, while most (

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Active cell death in hormone-dependent tissues

Cited by 255 publications

References 217 publications

Inherent increase of apoptosis in liver tumors: Implications for carcinogenesis and tumor regression

Inherent increase of apoptosis in liver tumors: Implications for carcinogenesis and tumor regression

Clusterin expression within skin correlates with hair growth

Overexpression of Clusterin in Human Breast Carcinoma

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