Neuroendocrine tumor cells in prostate cancer: Evaluation of the neurosecretory products serotonin, bombesin, and gastrin – impact on angiogenesis and clinical follow‐up

Heinrich, Elmar; Trojan, Lutz; Friedrich, David A.; Voß, Martin; Weiß, Christel; Michel, Maurice Stephan; Grobholz, Rainer

doi:10.1002/pros.21392

Cited by 28 publications

(20 citation statements)

References 23 publications

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“…Moreover, we also nin in cholangiocarcinoma, which stimulate cholangiocarcinoma cell growth, and this condition is responsive to the blockade by the inhibition of serotonin synthesis (50,52). In contrast, serotonin by itself plays a marginal role in regulating the growth of PCa cells in general (53), and there was no significant clinical correlation of serotonin levels with PCa disease progression (54,55). The different effects of serotonin in diverse cancers therefore also provide insights into the differential functions of MAOA in PCa and other cancers.…”

Section: Figure 11mentioning

confidence: 91%

Monoamine oxidase A mediates prostate tumorigenesis and cancer metastasis

Wu¹,

Shao²,

Li³

et al. 2014

J. Clin. Invest.

196

249

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Section: Figure 11mentioning

confidence: 91%

Monoamine oxidase A mediates prostate tumorigenesis and cancer metastasis

Wu¹,

Shao²,

Li³

et al. 2014

J. Clin. Invest.

196

249

View full text Add to dashboard Cite

“…For patients with known CRPC and clinical suspicion of SCC, treatment can be selected on the basis of clinical features if tissue is not readily accessible or if it is unsafe to wait for a pathological diagnosis. Increased expression of plasma CgA—along with other plasma markers, such as CEA, Ca19.9, neuron-specific enolase, bombesin, 5-hydroxytryptamine, and gastrin—might provide supporting evidence for the diagnosis of prostatic SCC, 40,54,59,60 and could have a role in monitoring response to therapy. Many questions relating to the optimal use of serum neuroendocrine and epithelial markers remain unanswered and there is no consensus regarding their use in routine clinical practice.…”

Section: Diagnostic Work-upmentioning

confidence: 99%

Small cell carcinoma of the prostate

et al. 2014

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Pure small-cell carcinoma (SCC) of the prostate is a rare entity and one of the most aggressive malignancies of the prostate. Histologically, prostatic SCCs of the prostate are part of a spectrum of anaplastic tumours of the prostate and are similar to SCCs of the lungs. In most cases, SCC of the prostate is associated with conventional prostatic adenocarcinoma. Both components of these mixed tumours frequently share molecular alterations such as ERG gene rearrangements or AURKA and MYCN amplifications, suggesting a common clonal origin. The clinical behaviour of small-cell prostate carcinomas is characterized by extensive local disease, visceral disease, and low PSA levels despite large metastatic burden. Commonly, the emergence of the SCC occurs in patients with high-grade adenocarcinoma who are often treated with androgen deprivation treatment (ADT). However, SCCs do not usually benefit from ADT. A biopsy of accessible lesions is strongly recommended to identify those with SCC pathological features, as management is undoubtedly affected by this finding. Chemotherapy is the standard approach for treating patients with either localized or advanced prostatic SCC. Despite the emergence of more-aggressive treatment modalities, the prognosis of men with prostatic SCC remains dismal.

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“…Current work has shown that patients with Gleason score 8–10 prostate cancer that have >1% NE positive diseases have inferior clinical outcomes when they are treated with radiotherapy due to an increase in distant disease failure [26]. The number of NE positive cells was correlated with the Gleason score and high numbers of NE positive cells were associated with early treatment failure [27]. As noted above obesity has been associated with increased risk of more aggressive prostate cancer, higher rates of biochemical relapse, and prostate cancer-specific death.…”

Section: Introductionmentioning

confidence: 99%

Growth and Progression of TRAMP Prostate Tumors in Relationship to Diet and Obesity

et al. 2012

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To clarify effects of diet and body weight on prostate cancer development, three studies were undertaken using the TRAMP mouse model of this disease. In the first experiment, obesity was induced by injection of gold thioglucose (GTG). Age of prostate tumor detection (~33 wk) and death (~43 wk) was not significantly different among the groups. In the second study, TRAMP-C2 cells were injected into syngeneic C57BL6 mice and tumor progression was evaluated in mice fed either high-fat or low-fat diets. The high fat fed mice had larger tumors than did the low-fat fed mice. In the third study, tumor development was followed in TRAMP mice fed a high fat diet from 6 weeks of age. There were no significant effects of body weight status or diet on tumor development among the groups. When the tumors were examined for the neuroendocrine marker synaptophysin, there was no correlation with either body weight or diet. However, there was a significant correlation of the expression of synaptophysin with earlier age to tumor detection and death. In summary, TRAMP-C2 cells grew faster when the mice were fed a high-fat diet. Further synaptophysin may be a marker of poor prognosis independent of weight and diet.

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Neuroendocrine tumor cells in prostate cancer: Evaluation of the neurosecretory products serotonin, bombesin, and gastrin – impact on angiogenesis and clinical follow‐up

Abstract: NETC have an influence on angiogenesis and are correlated with the clinical-pathological parameters. A high expression of NETC is associated with an early failure of treatment. Our study underlines the importance of NETC in prostate cancer.

Cited by 28 publications

References 23 publications

Monoamine oxidase A mediates prostate tumorigenesis and cancer metastasis

Monoamine oxidase A mediates prostate tumorigenesis and cancer metastasis

Small cell carcinoma of the prostate

Growth and Progression of TRAMP Prostate Tumors in Relationship to Diet and Obesity

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