Prevention and early detection of prostate cancer

Cuzick, Jack; Thorat, Mangesh A.; Andriole, Gerald L.; Brawley, Otis W.; Brown, Powel H.; Čulig, Zoran; Eeles, Rosalind; Ford, Leslie G.; Hamdy, Freddie C.; Holmberg, Lars; Ilić, Dragan; Key, Timothy J.; Vecchia, Carlo La; Lilja, Hans; Marberger, Michael; Meyskens, Frank L.; Minasian, Lori M.; Parker, Christopher; Parnes, Howard L.; Perner, Sven; Rittenhouse, Harry G.; Schalken, Jack A.; Schmid, Hans Peter; Schmitz‐Dräger, Bernd J.; Schröder, Fritz H.; Stenzl, Arnulf; Tombal, Bertrand; Wilt, Timothy J; Wolk, Alicja

doi:10.1016/s1470-2045(14)70211-6

Cited by 398 publications

(304 citation statements)

References 85 publications

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“…Indeed, it is currently not possible to accurately distinguish high-risk prostate tumors, which require extensive therapeutic intervention, from low-risk indolent tumors, many of which do not require any therapy (Draisma et al 2009, Cuzick et al 2014, Tombal et al 2014, Weiner et al 2015. Therefore, most men with clinically localized PCa undergo radical prostatectomy or radiotherapy with curative intent (Boorjian et al 2012, Heidenreich et al 2014).…”

mentioning

confidence: 99%

Regulation of vascular endothelial growth factor in prostate cancer

Brot¹,

Ntekim²,

Cardenas³

et al. 2015

Endocrine-Related Cancer

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Prostate cancer (PCa) is the most common malignancy affecting men in the western world. Although radical prostatectomy and radiation therapy can successfully treat PCa in the majority of patients, up to w30% will experience local recurrence or metastatic disease. Prostate carcinogenesis and progression is typically an androgen-dependent process. For this reason, therapies for recurrent PCa target androgen biosynthesis and androgen receptor function. Such androgen deprivation therapies (ADT) are effective initially, but the duration of response is typically %24 months. Although ADT and taxane-based chemotherapy have delivered survival benefits, metastatic PCa remains incurable. Therefore, it is essential to establish the cellular and molecular mechanisms that enable localized PCas to invade and disseminate. It has long been accepted that metastases require angiogenesis. In the present review, we examine the essential role for angiogenesis in PCa metastases, and we focus in particular on the current understanding of the regulation of vascular endothelial growth factor (VEGF) in localized and metastatic PCa. We highlight recent advances in understanding the role of VEGF in regulating the interaction of cancer cells with tumor-associated immune cells during the metastatic process of PCa. We summarize the established mechanisms of transcriptional and post-transcriptional regulation of VEGF in PCa cells and outline the molecular insights obtained from preclinical animal models of PCa. Finally, we summarize the current state of anti-angiogenesis therapies for PCa and consider how existing therapies impact VEGF signaling.

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mentioning

confidence: 99%

Regulation of vascular endothelial growth factor in prostate cancer

Brot¹,

Ntekim²,

Cardenas³

et al. 2015

Endocrine-Related Cancer

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“…Finally, PSA is a well-recognized tool to elucidate the prostatic origin of metastatic malignancy [11,12].…”

Section: Discussionmentioning

confidence: 99%

Bone Marrow Metastases as an Initial Presentation of Gastrointestinal Adenocarcinoma: A Case Report

Molina-Arrebola¹

2017

CMR

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Bone marrow metastases as the initial presentation of a solid tumour are uncommon, especially if the primary neoplasm site cannot be identified during the diagnosis presentation despite laboratory testing and imaging techniques. In these situations, bone marrow examination can lead to a final diagnosis of the primary malignancy. We report an unusual case of osteoblastic metastases from an unknown primary site -this was because no relevant lesions were found from either imaging or endoscopic examination. The patient was sent for a bone marrow biopsy, revealing a morphology replaced by glandular structures and an immunohistochemistry consistent with a gastrointestinal origin. Bone marrow examination was the clue to the final diagnosis and led to specific treatment.

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“…However, other evidence suggest that mTOR may also play a positive role in cancer patients. It has been demonstrated that physical exercise stimulates the mTOR pathway and this is correlated with the prevention of certain type of cancers [34][35][36]. mTOR can also increase tolerability of chemotherapy and can protect against autophagy (frequently associate with cancer resistance to therapy) and improve prognosis [37][38][39].…”

Section: Amino Acids Supplementation As a Cancer Fighting Weaponmentioning

confidence: 99%

Nutrition, Nitrogen Requirements, Exercise and Chemotherapy-Induced Toxicity in Cancer Patients. A puzzle of Contrasting Truths?

Flati¹,

Corsetti²,

Pasini³

et al. 2015

ACAMC

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Amino acids can modulate cell metabolism and control cell fate by regulating cell survival and cell death. The molecular mechanisms involved are mediated by the mTOR complexes mTORC1 and mTORC2 activity. These complexes are finely regulated and the continuous advancement of the knowledge on their composition and function is revealing that their balance may represent the condition that determines the cell fate. This is important for normal healthy cells but it is becoming clear, and it is even more important, that the balance of the mTORCs activity may also condition the cell fate of cancer cells. Here, we discuss the evidences supporting the amino acids supplementation as a cancer fighting weapon and a possible strategy to counteract the myocyte toxicity associated with chemotherapy, possibly by tipping the balance of mTORCs activity.

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Prevention and early detection of prostate cancer

Cited by 398 publications

References 85 publications

Regulation of vascular endothelial growth factor in prostate cancer

Regulation of vascular endothelial growth factor in prostate cancer

Bone Marrow Metastases as an Initial Presentation of Gastrointestinal Adenocarcinoma: A Case Report

Nutrition, Nitrogen Requirements, Exercise and Chemotherapy-Induced Toxicity in Cancer Patients. A puzzle of Contrasting Truths?

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