F-18 FDG PET/CT Imaging in Small Cell Prostate Cancer

Flamini, Rodrigo de Carvalho; Yamaga, Lilian Yuri Itaya; Mello, Maria Eduarda; Wagner, Jairo; Cunha, Marcelo Livorsi da; Osawa, Akemi; Campos, Guilherme C.; Funari, Marcelo Buarque de Gusmão

doi:10.1097/rlu.0b013e3181db4ce9

Cited by 12 publications

(7 citation statements)

References 9 publications

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“…The Warburg effect, initially described in 1924, has received renewed attention recently in the field of cancer metabolism due to the widespread clinical application of Fluorodeoxyglucose (FDG) – Positron Emission Tomography (PET) imaging which is based on increased glucose uptake by cancer cells. Unlike most tumors, however, FDG-PET imaging cannot detect localized, untreated PCa 5 , but can image SCNC 6 , suggesting that metabolic differences may be an underlying mechanism for the vastly different biologic behaviors of AdenoCa and SCNC. Additionally, literature has shown that prostatic AdenoCa utilizes mitochondrial respiration which is unique to the metabolism displayed in other tumor cells 7 .…”

Section: Introductionmentioning

confidence: 99%

The Role of CD44 in Glucose Metabolism in Prostatic Small Cell Neuroendocrine Carcinoma

Cohen

Sun

et al. 2016

Molecular Cancer Research

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While prostatic adenocarcinomas are relatively indolent, some patients with advanced adenocarcinomas recur with small cell neuroendocrine carcinoma which is highly aggressive and lethal. Because glycolysis is a feature of malignancy and the degree of glycolysis generally correlates with tumor aggressiveness, we wanted to compare the metabolic differences and the molecular mechanisms involved between the two tumor types. In this study, and based on previous characterization, LNCaP and PC-3 prostate cancer cell lines were selected as models of prostatic adenocarcinoma and small cell neuroendocrine carcinoma, respectively. In addition to measuring glucose consumption, lactate secretion, and ROS levels we performed metabolic profiling in these two model systems. The role of CD44 was studied by RNA interference (RNAi) and lentivirus-mediated overexpression. Expression of key enzymes in glycolysis was studied using human tissue microarrays containing benign prostate, adenocarcinoma, and small cell neuroendocrine carcinoma. Results showed that glycolytic features of PC-3 cells were higher than that of LNCaP cells. PFKFB4 was overexpressed in human small cell carcinoma tissue vs. adenocarcinoma tissue. CD44 regulated glucose metabolism, intracellular ROS, and cell proliferation in PC-3 cells. Inhibition of CD44 also sensitized PC-3 cells to carboplatin. In conclusion, this study suggests different pathways of glucose metabolism contribute to the disparate biological behaviors of these two tumor types. Implications CD44 is an important regulator of glucose metabolism in small cell neuroendocrine carcinoma and may be an important therapeutic target.

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Section: Introductionmentioning

confidence: 99%

The Role of CD44 in Glucose Metabolism in Prostatic Small Cell Neuroendocrine Carcinoma

Cohen

Sun

et al. 2016

Molecular Cancer Research

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“…Small cell prostate carcinoma (SCPC) is a rare, aggressive form of prostate cancer with a poor prognosis, comprising approximately 0.5% to 1% of all prostate cancers. 1 Median survival in patients with SCPC is 12 months. 2,3 Small cell prostate carcinoma is commonly diagnosed in the setting of clinical progression of PCA patients on long-term androgen deprivation therapy.…”

Section: Figurementioning

confidence: 99%

Mismatched Lesions on 18F-FDG PET and 18F-Fluciclovine PET Images in a Patient With Metastatic Prostate Small Cell Carcinoma

2021

Clin Nucl Med

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A 65-year-old man with fluciclovine-avid metastatic prostate small cell carcinoma with prostate-specific antigen (PSA) 19.4 ng/mL at diagnosis underwent system therapy and subsequent surgery and achieved hormonal response with PSA <0.1 ng/mL. An 18 F-fluciclovine PET/CT scan 3 months after surgery was negative for disease. Although PSA remained <0.1 ng/mL, the rising carcinoembryonic antigen prompted an 18 F-FDG PET/CT 6 weeks later. It showed multiple hypermetabolic lesions in the prostatectomy bed, liver, and right iliac bone, suggestive of malignant disease. The FDG-avid prostatectomy lesions were further confirmed on MRI. This case demonstrates that FDG PET/CT has a role in suspected metastatic prostate small cell carcinoma with negative fluciclovine PET examination.

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“…This resulted in the higher rate of glucose uptake and lactate production in presence of oxygen (Vander Heiden et al, 2009 ). Early clinical studies have shown that fluorodeoxyglucose (FDG)-PET imaging which is based on increased glucose uptake by cancer cells failed to detect naïve localized PCa (Effert et al, 1996 ), but can detect the advanced stage small cell prostate cancer (SCPC) (de Carvalho Flamini et al, 2010 ), highlighting the metabolic differences underlying the adenocarcinoma and SCPC. Moreover, the higher uptake of glucose has been associated with the elevated expression of Glucose Transporter 1 (GLUT1) in poorly differentiated hormone-independent PCa (Effert et al, 2004 ).…”

Section: Factors Governing Cellular Plasticitymentioning

confidence: 99%

Dynamics of Cellular Plasticity in Prostate Cancer Progression

Tiwari

Manzar

Ateeq

2020

Front. Mol. Biosci.

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Despite the current advances in the treatment for prostate cancer, the patients often develop resistance to the conventional therapeutic interventions. Therapy-induced drug resistance and tumor progression have been associated with cellular plasticity acquired due to reprogramming at the molecular and phenotypic levels. The plasticity of the tumor cells is mainly governed by two factors: cell-intrinsic and cell-extrinsic. The cell-intrinsic factors involve alteration in the genetic or epigenetic regulators, while cell-extrinsic factors include microenvironmental cues and drug-induced selective pressure. Epithelial-mesenchymal transition (EMT) and stemness are two important hallmarks that dictate cellular plasticity in multiple cancer types including prostate. Emerging evidence has also pinpointed the role of tumor cell plasticity in driving anti-androgen induced neuroendocrine prostate cancer (NEPC), a lethal and therapy-resistant subtype. In this review, we discuss the role of cellular plasticity manifested due to genetic, epigenetic alterations and cues from the tumor microenvironment, and their role in driving therapy resistant prostate cancer.

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F-18 FDG PET/CT Imaging in Small Cell Prostate Cancer

Cited by 12 publications

References 9 publications

The Role of CD44 in Glucose Metabolism in Prostatic Small Cell Neuroendocrine Carcinoma

The Role of CD44 in Glucose Metabolism in Prostatic Small Cell Neuroendocrine Carcinoma

Mismatched Lesions on 18F-FDG PET and 18F-Fluciclovine PET Images in a Patient With Metastatic Prostate Small Cell Carcinoma

Dynamics of Cellular Plasticity in Prostate Cancer Progression

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