Immunohistological Analysis of Mast Cell Numbers in the Intratumoral and Peritumoral Regions of Prostate Carcinoma Compared to Benign Prostatic Hyperplasia

Aydın, Özlem; Düşmez, Duygu; Cinel, Leyla; Doruk, Erdal; Kanık, Arzu

doi:10.1078/0344-0338-00253

Cited by 23 publications

(27 citation statements)

References 18 publications

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“…Gupta (1970) first reported the presence of mast cells around PCas. In our study, we observed mast cell aggregation at the periphery of PCas, similar to previous reports (Sari et al, 1999;Aydin et al, 2002). However, this is the first report that mast cell infiltration around prostate tumours is a significant prognostic factor for PCa.…”

Section: Discussionsupporting

confidence: 92%

“…In contrast, in a heterocyclic amine-induced rat PCa model, Nakai et al (2007) reported increased infiltration of stromal mast cell in the ventral prostate, with increased prostatic epithelial proliferation, suggesting that mast cells may have beneficial roles in progression of PCa (Nakai et al, 2007). The significance of mast cell accumulation around PCa has not been investigated extensively (Gupta, 1970;Sari et al, 1999;Aydin et al, 2002). In the present study, the viability of mast cell accumulation around PCa as a prognostic factor was examined.…”

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confidence: 81%

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Decreased number of mast cells infiltrating into needle biopsy specimens leads to a better prognosis of prostate cancer

et al. 2007

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Mast cell infiltration is often observed around human tumours. Inflammatory cells such as macrophages, neutrophils and mast cells infiltrating around tumours are known to contribute to tumour growth; however, the clinical significance of mast cell invasion in prostate cancer (PCa) has not been investigated. Mast cell infiltration was evaluated in 104 patients (age range, 45 -88 years; median, 72 years), who underwent needle biopsy of the prostate and were confirmed to have PCa. Needle biopsy specimens of prostate were sliced into 5-mm-thick sections and immunostained for mast cells with monoclonal antibody against mast cell-specific tryptase. Mast cells were counted systematically under a microscope ( Â 400 magnification), and the relations between mast cell numbers and clinicopathologic findings were evaluated. The mast cell count was evaluated for prognostic value by multivariate analysis. Mast cells were immunostained around the cancer foci. The median number of mast cells in each case was 16. The mast cell count was higher around cancer foci in patients with higher Gleason scores than in those with low Gleason scores. The mast cell number correlated well with clinical stage (Po0.001). Prostate-specific antigen-free survival of patients with higher mast cell counts was better than that in patients with lower mast cell counts (Po0.001). Multivariate analysis revealed that mast cell count was a significant prognostic factor (Po0.005). The number of mast cells infiltrating around cancer foci in prostate biopsy specimens can be a significant prognostic factor of PCa.

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Section: Discussionsupporting

confidence: 92%

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confidence: 81%

Decreased number of mast cells infiltrating into needle biopsy specimens leads to a better prognosis of prostate cancer

et al. 2007

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“…Such functional complexity may explain the discrepancy emerging from different studies, showing opposite correlations of MC accumulation with prognosis in different settings (8). In this scenario, prostate cancer is no exception; several studies on human prostate tumor samples have tried to address this issue (9)(10)(11)(12)(13), but no conclusive data exist about the actual role of MCs in promoting or suppressing cancer at this site. In a recent work, peritumoral MCs were shown to enhance angiogenesis and tumor growth in the orthotopic AT-1 rat prostate tumor model and MCs were seen recruited in the peritumoral compartment in men during the formation of androgenindependent prostate cancer (14), recommending MCs as a novel target for prostate tumor therapy.…”

Section: Introductionmentioning

confidence: 86%

Mast Cell Targeting Hampers Prostate Adenocarcinoma Development but Promotes the Occurrence of Highly Malignant Neuroendocrine Cancers

et al. 2011

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Mast cells (MC) are c-Kit-expressing cells, best known for their primary involvement in allergic reactions, but recently reappraised as important players in either cancer promotion or inhibition. Here, we assessed the role of MCs in prostate tumor development. In prostate tumors from both tumor-prone transgenic adenocarcinoma of the mouse prostate (TRAMP) mice and human patients, MCs are specifically enriched and degranulated in areas of well-differentiated (WD) adenocarcinoma but not around poorly differentiated (PD) foci that coexist in the same tumors. We derived novel TRAMP tumor cell lines, representative of WD and PD variants, and through pharmacologic stabilization or genetic ablation of MCs in recipients mice, we showed that MCs promote WD adenocarcinoma growth but are dispensable for PD tumors. WD tumors rely on MCs for matrix metalloprotease 9 (MMP-9) provision, as reconstitution of MC-deficient mice with wild-type but not MMP-9 À/À MCs was sufficient to promote their growth. In contrast, PD tumors are MMP-9 self-competent, consistently with epithelial-to-mesenchymal transition. Such a dual source of MMP-9 was confirmed in human tumors, suggesting that MCs could be a good target for early-stage prostate cancer. Interestingly, in testing whether MC targeting could block or delay tumorigenesis in tumor-prone TRAMP mice, we observed a high incidence of early and aggressive tumors, characterized by a neuroendocrine (NE) signature and c-Kit expression. Taken together, these data underscore the contribution of MCs in tumor progression and uncover a new, opposite role of MCs in protecting against the occurrence of aggressive NE variants in prostate cancer. Cancer Res; 71(18); 5987-97. Ó2011 AACR.

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“…Specifically, it has been reported that mast cell numbers are increased within prostate tumors, 50 and that low mast cell numbers in PCa may lead to a better prognosis. 51 This evidence, however, is largely anecdotal and does not define the role of the mast cells in PCa.…”

Section: Estrogens Prostatitismentioning

confidence: 99%

Increased Endogenous Estrogen Synthesis Leads to the Sequential Induction of Prostatic Inflammation (Prostatitis) and Prostatic Pre-Malignancy

Ellem

Wang

Poutanen

et al. 2009

The American Journal of Pathology

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Prostatitis causes substantial morbidity to men, through associated urinary symptoms, sexual dysfunction, and pelvic pain; however, 90% to 95% of cases have an unknown etiology. Inflammation is associated with the development of carcinoma, and, therefore, it is imperative to identify and study the causes of prostatitis to improve our understanding of this disease and its role in prostate cancer. As estrogens cause prostatic inflammation, here we characterize the murine prostatic phenotype induced by elevated endogenous estrogens due to aromatase overexpression (AROM؉). Early-life development of the AROM؉ prostate was normal; however, progressive changes culminated in chronic inflammation and pre-malignancy. The AROM؉ prostate was smaller at puberty compared with wild-type controls. Mast cell numbers were significantly increased at puberty and preceded chronic inflammation, which emerged by 40 weeks of age and was characterized by increased mast cell, macrophage, neutrophil, and T-lymphocyte numbers. The expression of key inflammatory mediators was also significantly altered, and premalignant prostatic intraepithelial neoplasia lesions emerged by 52 weeks of age. Taken together, these data link estrogens to prostatitis and premalignancy in the prostate, further implicating a role for estrogen in prostate cancer. These data also establish the AROM؉ mouse as a novel, non-bacterial model for the study of prostatitis. Prostatitis, an exceedingly common condition in the male population worldwide, has an incidence of ϳ9% and a prevalence of ϳ14%, and, unlike benign prostatic hyperplasia and prostate cancer (PCa), which are predominantly diseases of older men, prostatitis afflicts men of all ages. It is also the most common outpatient condition seen in men under 50 years of age and accounts for more clinical visits than either PCa and/or benign prostatic hyperplasia.1,2 At present our knowledge of prostatitis is lacking, with 90% to 95% of cases having an unknown etiology. This represents a significant problem, particularly as prostatitis has also been implicated in the development of PCa.3-5 Given the prevalence of prostatitis and this putative link to PCa, it is vitally important to identify the unknown causes of prostatitis.Several causes of prostatitis have been postulated, including hormonal variation or exposure, infection due to sexually transmitted disease, 6 dietary factors, and physical trauma from urine reflux. 7 However, of particular interest is an apparent link between estrogen and prostatic inflammation, 8 which has emerged mainly from the administration of pharmacological levels of exogenous estrogen to rodents.9 Additional data obtained from further rodent studies show that the prostate gland is particularly sensitive to estrogenic exposure during development in fetal and neonatal life; transient estrogen exposure before puberty results in inflammation later in life, well after the exposure has occurred.10,11 Several decades of research from various laboratories, including our own, has demonstrated that...

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Immunohistological Analysis of Mast Cell Numbers in the Intratumoral and Peritumoral Regions of Prostate Carcinoma Compared to Benign Prostatic Hyperplasia

Cited by 23 publications

References 18 publications

Decreased number of mast cells infiltrating into needle biopsy specimens leads to a better prognosis of prostate cancer

Decreased number of mast cells infiltrating into needle biopsy specimens leads to a better prognosis of prostate cancer

Mast Cell Targeting Hampers Prostate Adenocarcinoma Development but Promotes the Occurrence of Highly Malignant Neuroendocrine Cancers

Increased Endogenous Estrogen Synthesis Leads to the Sequential Induction of Prostatic Inflammation (Prostatitis) and Prostatic Pre-Malignancy

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