Response to paclitaxel, gemcitabine, and cisplatin in renal medullary carcinoma

Bell, Moshe D.

doi:10.1002/pbc.20780

Cited by 19 publications

(14 citation statements)

References 2 publications

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“…8 Our results suggest that repeated administration of oxycodone not only causes upregulation of P-gp, but also significantly affects the transport of paclitaxel across the BBB, liver, and kidney. These findings have potentially important implications on the therapeutic activity of paclitaxel especially in the treatment of brain, hepatic and renal tumors [19][20][21]39,40 when coadministered with oxycodone. It should be noted that oxycodone levels would have been quantified in the oxycodone tolerant animals if radiolabelled oxycodone was available.…”

Section: Discussionmentioning

confidence: 97%

Oxycodone induces overexpression of P‐glycoprotein (ABCB1) and affects paclitaxel's tissue distribution in Sprague Dawley rats

Hassan

Myers

Lee

et al. 2007

Journal of Pharmaceutical Sciences

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Previous studies suggest that P-glycoprotein (P-gp) modulates the PK/PD of many compounds including opioid agonists and chemotherapeutic agents. The objective of this study was to assess the P-gp affinity status of oxycodone, the P-gp expression, and the paclitaxel's tissue distribution in oxycodone-treated rats. P-gp ATPase assay, Caco-2 transepithelial permeability studies, and mdr1a/b (−/−) mice were used to assess the P-gp affinity status of oxycodone. P-gp expression was determined by Western blot analysis while [ 14 C] paclitaxel's distributions in the liver, kidney, brain, and plasma tissues were determined by liquid scintillation counter. Oxycodone stimulated the P-gp ATPase activity in a concentration-dependant manner. The Caco-2 secretory transport of oxycodone was reduced from 3.64 ×10 −5 to 1.96 × 10 −5 cm/s (p <0.05) upon preincubation with the P-gp inhibitor, verapamil. The brain levels of oxycodone in mdr1a/b (+/+) were not detectable (<15 ng/mL) while in mdr1a/b (−/−) the average levels were 115 ± 39 ng/mL. The P-gp protein levels were increased by 1.3-4.0 folds while paclitaxel's tissue distributions were decreased by 38-90% (p <0.05) in oxycodone-treated rats. These findings display that oxycodone is a P-gp substrate, induces overexpression of P-gp, and affects paclitaxel's tissue distribution in a manner that may influence its chemotherapeutic activity.

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Section: Discussionmentioning

confidence: 97%

Oxycodone induces overexpression of P‐glycoprotein (ABCB1) and affects paclitaxel's tissue distribution in Sprague Dawley rats

Hassan

Myers

Lee

et al. 2007

Journal of Pharmaceutical Sciences

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“…Most RMCs do not respond to chemotherapy or radiation therapy. However, two recent publications reported three adolescent and young adult patients who responded to cisplatin or carboplatin in combination with gemcitabine and paclitaxel [7,8]. Although the prognosis is dismal, rare cases of longterm survival have been reported, raising the question of whether young patients with sickle cell traits should be surveyed closely to detect and treat RMC early [6].…”

Section: Renal Medullary Carcinomamentioning

confidence: 94%

The changing face of renal cell carcinoma pathology

Aydın¹,

Zhou

2008

Curr Oncol Rep

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“…As this did not turn out to be effective to our patient, we eventually added paclitaxel to his regimen, as PCG has shown good response in previous reports. 33,44,45 Newer targeted therapeutic options are being considered recently: In a phase II study evaluating "bortezomib," a proteasome inhibitor, in patients with advanced RCC, one of those patients actually had an RMC. An updated follow-up on this specific patient revealed that after receiving a total of 7 months of bortezomib therapy, he achieved complete remission, and remained without evidence of disease after more than 27 months.…”

Section: Pathophysiologymentioning

confidence: 99%

“…We chose the third option, the "standard therapy," as this is what has been mainly described in the literature. The 2 most commonly used standard regimens have been the high-dose intensity MVAC (methotrexate, vinblastine, doxorubicin, and cisplatin) 31 and PCG (paclitaxel, carboplatin, and gemcitabine), 33,44,45 with the latter considered by most as the preferred regimen. On the basis of global gene expression profiling, Yang et al 46 found that RMC resembled transitional cell carcinoma, and suggested that it should not be treated as a conventional RCC.…”

Section: Pathophysiologymentioning

confidence: 99%

Renal Medullary Carcinoma in a White Adolescent With Sickle Cell Trait

Daher

Bourgi²,

Riachy³

et al. 2014

Journal of Pediatric Hematology/Oncology

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Renal medullary carcinoma (RMC) is a rare neoplasm of the kidney that has been recently described. It is almost exclusive to young patients of African descent and associated with sickle cell hemoglobinopathy, mainly sickle cell trait and hemoglobin sickle cell disease. The prognosis of RMC is very poor because of the highly aggressive behavior of this neoplasm and its resistance to conventional chemotherapy. Metastatic disease is almost universal at the time of presentation, and the malignancy is minimally responsive to a variety of regimens and/or modalities, including surgery, radiotherapy, chemotherapy, and biological immune-modulation therapy. We report the seventh case of a left RMC occurring in a white child with sickle cell trait, but with a localization of the tumor in the left kidney, considered a nonpredominant side for this type of tumor.

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Response to paclitaxel, gemcitabine, and cisplatin in renal medullary carcinoma

Cited by 19 publications

References 2 publications

Oxycodone induces overexpression of P‐glycoprotein (ABCB1) and affects paclitaxel's tissue distribution in Sprague Dawley rats

Oxycodone induces overexpression of P‐glycoprotein (ABCB1) and affects paclitaxel's tissue distribution in Sprague Dawley rats

The changing face of renal cell carcinoma pathology

Renal Medullary Carcinoma in a White Adolescent With Sickle Cell Trait

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