Cynthia A. Zerillo
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Cynthia A. Zerillo has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Debbie C Koay
Department of Internal Medicine (Section of Medical Oncology), Yale Cancer Center and Smilow Cancer Hospital at Yale-New-Haven Hospital, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA
1 shared publication - Ibrahim Sandokji
Pediatric Department, College of Medicine, Taibah University, Madinah 42353, Saudi Arabia
1 shared publication - Jillian K. Warejko
Pediatric Nephrology, Department of Pediatrics, Yale University School of Medicine, New Haven, USA
1 shared publication - Jonathan Marquez
Division of Genetic Medicine, Department of Pediatrics, University of Washington and Seattle Children's Hospital, Seattle, WA, USA
1 shared publication - Lyndsay N. Harris
Yale Comprehensive Cancer Center
1 shared publication - Michael P. DiGiovanna
Yale University School of Medicine
1 shared publication
Latest Publications
- Open Access
- 17 July 2019
- Published by Springer Nature in BMC Nephrology
- Vol. 20 (1) , 1-5
Identification of novel mutations and phenotype in the steroid resistant nephrotic syndrome gene NUP93: a case report
Monogenic mutations may be a significant cause of steroid-resistant nephrotic syndrome. NUP93 is a gene previously reported to cause isolated steroid-resistant nephrotic syndrome. Here we describe a case of recessive, syndromic, steroid-resistant nephrotic syndrome caused by NUP93 mutation. NUP93 may convey a phenotype that has not only SRNS, but also other syndromic features.
- 17 July 2019
- Published by Springer Nature in BMC Nephrology
- Vol. 20 (1) , 1-5
Open AccessIdentification of novel mutations and phenotype in the steroid resistant nephrotic syndrome gene NUP93: a case report
Monogenic mutations may be a significant cause of steroid-resistant nephrotic syndrome. NUP93 is a gene previously reported to cause isolated steroid-resistant nephrotic syndrome. Here we describe a case of recessive, syndromic, steroid-resistant nephrotic syndrome caused by NUP93 mutation. NUP93 may convey a phenotype that has not only SRNS, but also other syndromic features.
- Open Access
- 9 August 2010
- Published by Springer Nature in Breast Cancer Research
- Vol. 12 (4) , R62
Anti-tumor effects of retinoids combined with trastuzumab or tamoxifen in breast cancer cells: induction of apoptosis by retinoid/trastuzumab combinations
Introduction: HER2 and estrogen receptor (ER) are important in breast cancer and are therapeutic targets of trastuzumab (Herceptin) and tamoxifen, respectively. Retinoids inhibit breast cancer growth, and modulate signaling by HER2 and ER. We hypothesized that treatment with retinoids and simultaneous targeting of HER2 and/or ER may have enhanced anti-tumor effects. Methods: The effects of retinoids combined with trastuzumab or tamoxifen were examined in two human breast cancer cell lines in culture, BT474 and SKBR3. Assays of proliferation, apoptosis, differentiation, cell cycle distribution, and receptor signaling were performed. Results: In HER2-overexpressing/ER-positive BT474 cells, combining all-trans retinoic acid (atRA) with tamoxifen or trastuzumab synergistically inhibited cell growth, and altered cell differentiation and cell cycle. Only atRA/trastuzumab-containing combinations induced apoptosis. BT474 and HER2-overexpressing/ER-negative SKBR3 cells were treated with a panel of retinoids (atRA, 9-cis-retinoic acid, 13-cis-retinoic acid, or N-(4-hydroxyphenyl) retinamide (fenretinide) (4-HPR)) combined with trastuzumab. In BT474 cells, none of the single agents except 4-HPR induced apoptosis, but again combinations of each retinoid with trastuzumab did induce apoptosis. In contrast, the single retinoid agents did cause apoptosis in SKBR3 cells; this was only modestly enhanced by addition of trastuzumab. The retinoid drug combinations altered signaling by HER2 and ER. Retinoids were inactive in trastuzumab-resistant BT474 cells. Conclusions: Combining retinoids with trastuzumab maximally inhibits cell growth and induces apoptosis in trastuzumab-sensitive cells. Treatment with such combinations may have benefit for breast cancer patients.
- 9 August 2010
- Published by Springer Nature in Breast Cancer Research
- Vol. 12 (4) , R62
Open AccessAnti-tumor effects of retinoids combined with trastuzumab or tamoxifen in breast cancer cells: induction of apoptosis by retinoid/trastuzumab combinations
Introduction: HER2 and estrogen receptor (ER) are important in breast cancer and are therapeutic targets of trastuzumab (Herceptin) and tamoxifen, respectively. Retinoids inhibit breast cancer growth, and modulate signaling by HER2 and ER. We hypothesized that treatment with retinoids and simultaneous targeting of HER2 and/or ER may have enhanced anti-tumor effects. Methods: The effects of retinoids combined with trastuzumab or tamoxifen were examined in two human breast cancer cell lines in culture, BT474 and SKBR3. Assays of proliferation, apoptosis, differentiation, cell cycle distribution, and receptor signaling were performed. Results: In HER2-overexpressing/ER-positive BT474 cells, combining all-trans retinoic acid (atRA) with tamoxifen or trastuzumab synergistically inhibited cell growth, and altered cell differentiation and cell cycle. Only atRA/trastuzumab-containing combinations induced apoptosis. BT474 and HER2-overexpressing/ER-negative SKBR3 cells were treated with a panel of retinoids (atRA, 9-cis-retinoic acid, 13-cis-retinoic acid, or N-(4-hydroxyphenyl) retinamide (fenretinide) (4-HPR)) combined with trastuzumab. In BT474 cells, none of the single agents except 4-HPR induced apoptosis, but again combinations of each retinoid with trastuzumab did induce apoptosis. In contrast, the single retinoid agents did cause apoptosis in SKBR3 cells; this was only modestly enhanced by addition of trastuzumab. The retinoid drug combinations altered signaling by HER2 and ER. Retinoids were inactive in trastuzumab-resistant BT474 cells. Conclusions: Combining retinoids with trastuzumab maximally inhibits cell growth and induces apoptosis in trastuzumab-sensitive cells. Treatment with such combinations may have benefit for breast cancer patients.