Literature DB >> 26077241

Randomized Phase II Trial of Ridaforolimus in Advanced Endometrial Carcinoma.

Amit M Oza1, Sandro Pignata2, Andres Poveda2, Mary McCormack2, Andrew Clamp2, Benjamin Schwartz2, Jonathan Cheng2, Xiaoyun Li2, Kristy Campbell2, Pierre Dodion2, Frank G Haluska2.   

Abstract

PURPOSE: The prognosis for women with recurrent and metastatic endometrial cancer is poor, and improved therapies are needed. The mammalian target of rapamycin (mTOR) pathway is an important target, and mTOR inhibitors show clinical activity in endometrial cancer. PATIENTS AND METHODS: An open-label, multicenter, randomized, phase II trial of oral ridaforolimus compared with progestin or investigator choice chemotherapy (comparator) was undertaken in women with metastatic or recurrent endometrial cancer who had progressive disease following one or two lines of chemotherapy and no hormonal therapy. The primary end point was progression-free survival (PFS) assessed by independent radiologic review.
RESULTS: One hundred thirty patients were enrolled (64 received ridaforolimus and 66 received the comparator), and median age was 66 years. Treatment discontinuation as a result of adverse events was 33% with ridaforolimus versus 6% with the comparator, with common (> 10%) grade 3 toxicities being hyperglycemia, anemia, and diarrhea. Thirty-eight percent (ridaforolimus) versus 71% (comparator) of patients discontinued treatment as a result of disease progression. Median PFS at the protocol prespecified interim analysis with 58 PFS events (primary end point) was 3.6 months (95% CI, 2.7 to 7.3 months) for ridaforolimus and 1.9 months (95% CI, 1.9 to 2.3 months) for the comparator (hazard ratio, 0.53; 95% CI, 0.31 to 0.90; P = .008). PFS rate for ridaforolimus versus comparator was 48% versus 18% at 16 weeks and 38% versus 15% at 24 weeks. Objective response rate for ridaforolimus versus comparator was 0% versus 4% (P = .925), and stable disease was achieved in 35% versus 17% of patients (P = .021).
CONCLUSION: Oral ridaforolimus shows encouraging activity in advanced endometrial cancer but is associated with significant toxicity. Inhibition of the PI3K/Akt/mTOR pathway may be a viable therapeutic target.
© 2015 by American Society of Clinical Oncology.

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Year:  2015        PMID: 26077241     DOI: 10.1200/JCO.2014.58.8871

Source DB:  PubMed          Journal:  J Clin Oncol        ISSN: 0732-183X            Impact factor:   44.544


  35 in total

Review 1.  mTOR function and therapeutic targeting in breast cancer.

Authors:  Stephen H Hare; Amanda J Harvey
Journal:  Am J Cancer Res       Date:  2017-03-01       Impact factor: 6.166

Review 2.  New Targeted Agents in Endometrial Cancer: Are We Really Making Progress?

Authors:  Victor Rodriguez-Freixinos; Katherine Karakasis; Amit M Oza
Journal:  Curr Oncol Rep       Date:  2016-04       Impact factor: 5.075

Review 3.  Chemotherapy for Endometrial Cancer in Adjuvant and Advanced Disease Settings.

Authors:  Christine M Bestvina; Gini F Fleming
Journal:  Oncologist       Date:  2016-07-13

Review 4.  Hyperglycemia Associated With Targeted Oncologic Treatment: Mechanisms and Management.

Authors:  Jonathan W Goldman; Melody A Mendenhall; Sarah R Rettinger
Journal:  Oncologist       Date:  2016-07-29

Review 5.  Hyperglycaemia Induced by Novel Anticancer Agents: An Undesirable Complication or a Potential Therapeutic Opportunity?

Authors:  Rashmi R Shah
Journal:  Drug Saf       Date:  2017-03       Impact factor: 5.606

6.  Tumor mutational analysis of GOG248, a phase II study of temsirolimus or temsirolimus and alternating megestrol acetate and tamoxifen for advanced endometrial cancer (EC): An NRG Oncology/Gynecologic Oncology Group study.

Authors:  Andrea P Myers; Virginia L Filiaci; Yuping Zhang; Michael Pearl; Kian Behbakht; Vicky Makker; Parviz Hanjani; Susan Zweizig; James J Burke; Gordon Downey; Kimberly K Leslie; Paul Van Hummelen; Michael J Birrer; Gini F Fleming
Journal:  Gynecol Oncol       Date:  2016-04       Impact factor: 5.482

Review 7.  Targeting the PI3K pathway and DNA damage response as a therapeutic strategy in ovarian cancer.

Authors:  Tzu-Ting Huang; Erika J Lampert; Cynthia Coots; Jung-Min Lee
Journal:  Cancer Treat Rev       Date:  2020-04-10       Impact factor: 12.111

Review 8.  PI3K/AKT/mTOR inhibitors for advanced or recurrent endometrial cancer.

Authors:  Felicia Roncolato; Kristina Lindemann; Melina L Willson; Julie Martyn; Linda Mileshkin
Journal:  Cochrane Database Syst Rev       Date:  2019-10-07

9.  Phase II, 2-stage, 2-arm, PIK3CA mutation stratified trial of MK-2206 in recurrent endometrial cancer.

Authors:  Andrea P Myers; Panagiotis A Konstantinopoulos; William T Barry; Weixiu Luo; Russell R Broaddus; Vicky Makker; Ronny Drapkin; Joyce Liu; Austin Doyle; Neil S Horowitz; Funda Meric-Bernstam; Michael Birrer; Carol Aghajanian; Robert L Coleman; Gordon B Mills; Lewis C Cantley; Ursula A Matulonis; Shannon N Westin
Journal:  Int J Cancer       Date:  2019-12-13       Impact factor: 7.396

10.  Safety lead-in of the MEK inhibitor trametinib in combination with GSK2141795, an AKT inhibitor, in patients with recurrent endometrial cancer: An NRG Oncology/GOG study.

Authors:  Shannon N Westin; Michael W Sill; Robert L Coleman; Steven Waggoner; Kathleen N Moore; Cara A Mathews; Lainie P Martin; Susan C Modesitt; Sanghoon Lee; Zhenlin Ju; Gordon B Mills; Russell J Schilder; Paula M Fracasso; Michael J Birrer; Carol Aghajanian
Journal:  Gynecol Oncol       Date:  2019-10-15       Impact factor: 5.482

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