Publications by authors named "Joseph Carbone"

3 Publications

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Prostate minimally invasive procedures: complications and normal vs. abnormal findings on multiparametric magnetic resonance imaging (mpMRI).

Abdom Radiol (NY) 2021 May 11. Epub 2021 May 11.

Department of Radiological Sciences, University of California, Irvine, Orange, CA, 92868-3201, USA.

Minimally invasive alternatives to traditional prostate surgery are increasingly utilized to treat benign prostatic hyperplasia and localized prostate cancer in select patients. Advantages of these treatments over prostatectomy include lower risk of complication, shorter length of hospital stay, and a more favorable safety profile. Multiparametric magnetic resonance imaging (mpMRI) has become a widely accepted imaging modality for evaluation of the prostate gland and provides both anatomical and functional information. As prostate mpMRI and minimally invasive prostate procedure volumes increase, it is important for radiologists to be familiar with normal post-procedure imaging findings and potential complications. This paper reviews the indications, procedural concepts, common post-procedure imaging findings, and potential complications of prostatic artery embolization, prostatic urethral lift, irreversible electroporation, photodynamic therapy, high-intensity focused ultrasound, focal cryotherapy, and focal laser ablation.
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http://dx.doi.org/10.1007/s00261-021-03097-6DOI Listing
May 2021

Inhibition of gap junctional intercellular communication and activation of mitogen-activated protein kinase by tumor-promoting organic peroxides and protection by resveratrol.

Nutr Cancer 2007 ;57(1):38-47

Department of Pediatrics & Human Development and the National Food Safety & Toxicology Center, Michigan State University, East Lansing 48824-1302, USA.

Dicumyl peroxide (di-CuOOH) and benzoyl peroxide (BzOOH) act as tumor promoters in SENCAR mice, whereas di-tert-butylhydroperoxide does not. Tumor promotion requires the removal of growth suppression by inhibition of gap junctional intercellular communication (GJIC) and the induction of mitogenic intracellular pathways. We showed that di-CuOOH and BzOOH both reversibly inhibited GJIC and transiently activated mitogen-activated protein kinase, specifically, the extracellular receptor kinase at noncytotoxic conditions in WB-F344 rat liver epithelial cells, whereas the non-tumor-promoting di-tert-butylhydroperoxide did not inhibit GJIC or activate extracellular receptor kinase. di-CuOOH but not BzOOH inhibited GJIC through a phosphatidylcholine-specific phospholipase C-dependent mechanism. N-acetylcysteine (NAC) was needed to prevent a cytotoxic, glutathione-depleting effect of BzOOH, whereas di-CuOOH was noncytotoxic and did not alter glutathione levels at all doses and times tested. Pretreatment of WB-F344 cells with resveratrol, a polyphenolic antioxidant present in red wine, prevented at physiological doses the inhibition of GJIC by di-CuOOH but not from BzOOH and was effective in significantly preventing extracellular receptor kinase activation by both peroxides. NAC did not prevent any of the peroxide effects on either GJIC or extracellular receptor kinase, suggesting a specific antioxidant effect of resveratrol.
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http://dx.doi.org/10.1080/01635580701268188DOI Listing
July 2007

Cannabinoids inhibit gap junctional intercellular communication and activate ERK in a rat liver epithelial cell line.

Int J Cancer 2003 Mar;104(1):12-8

Department of Pediatrics and Human Development, Michigan State University, East Lansing, MI 48824-1302,USA.

Many tumor promoters suppress the immune system; however, the direct effect of immunosuppressants on the tumorigenic pathways of nonimmune cells in solid tissue has not been well documented. Cannabinoids were chosen to explore this question further. Cannabinoids are immune modulators that affect specific intracellular signaling pathways in leukocytes. Since these compounds are nongenotoxic, any tumorigenic effect that might be associated with these compounds would need to occur through an epigenetic mechanism. Therefore, we determined the effect of Delta(9)-THC and CBN, 2 plant-derived cannabinoids, on 2 key epigenetic markers of tumor promotion: inhibition of GJIC, which is essential in removing a cell from growth suppression, and activation of the ERK-MAPK pathway, which is crucial in activating the appropriate genes for mitogenesis. Both Delta(9)-THC and CBN reversibly inhibited GJIC at noncytotoxic doses (15 microM) in a normal diploid WB rat liver epithelial oval cell line within 20 min and activated ERK1 and ERK2 within 5 min. Inhibition of MEK with PD98059 prevented the inhibition of GJIC by either cannabinoid, suggesting that inhibition of GJIC was MEK-dependent. Based on RT-PCR analysis and employment of an antagonist of CB1 and CB2, the effects on GJIC and MAPK were independent of both cannabinoid receptors. Cannabinoids affected crucial epigenetic pathways associated with cell proliferation in a rodent liver epithelial cell model system.
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http://dx.doi.org/10.1002/ijc.10899DOI Listing
March 2003