Advances in treatment of metastatic renal cell carcinoma

Gong, Jun; Gerendash, Benjamin; Dizman, Nazlı; Khan, Abrar Ahmad; Pal, Sumanta K.

doi:10.1097/mou.0000000000000319

Cited by 9 publications

(7 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…c-KIT, FLT-3 and RET are located on the tumour cell surface. Targeting these receptors will inhibit tumour growth [24,26,46]. RAF is an intracellular enzyme involved in all RTK pathways.…”

Section: Renal Cell Carcinomamentioning

confidence: 99%

Drug-Induced Hypertension Caused by Multikinase Inhibitors (Sorafenib, Sunitinib, Lenvatinib and Axitinib) in Renal Cell Carcinoma Treatment

Møller

Budolfsen

Grimm

et al. 2019

IJMS

View full text Add to dashboard Cite

This paper reviews current treatments for renal cell carcinoma/cancer (RCC) with the multikinase inhibitors (MKIs) sorafenib, sunitinib, lenvatinib and axitinib. Furthermore, it compares these drugs regarding progression-free survival, overall survival and adverse effects (AE), with a focus on hypertension. Sorafenib and sunitinib, which are included in international clinical guidelines as first- and second-line therapy in metastatic RCC, are now being challenged by new-generation drugs like lenvatinib and axitinib. These drugs have shown significant clinical benefits for patients with RCC, but all four induce a variety of AEs. Hypertension is one of the most common AEs related to MKI treatment. Comparing sorafenib, sunitinib and lenvatinib revealed that sorafenib and sunitinib had the same efficacy, but sorafenib was safer to use. Lenvatinib showed better efficacy than sorafenib but worse safety. No trials have yet been completed that compare lenvatinib with sunitinib. Although axitinib promotes slightly higher hypertension rates compared to sunitinib, the overall discontinuation rate and cardiovascular complications are favourable. Although the mean rate of patients who develop hypertension is similar for each drug, some trials have shown large differences, which could indicate that lifestyle and/or genetic factors play an additional role.

show abstract

“…c-KIT, FLT-3 and RET are located on the tumour cell surface. Targeting these receptors will inhibit tumour growth [24,26,46]. RAF is an intracellular enzyme involved in all RTK pathways.…”

Section: Renal Cell Carcinomamentioning

confidence: 99%

Drug-Induced Hypertension Caused by Multikinase Inhibitors (Sorafenib, Sunitinib, Lenvatinib and Axitinib) in Renal Cell Carcinoma Treatment

Møller

Budolfsen

Grimm

et al. 2019

IJMS

View full text Add to dashboard Cite

show abstract

“…The use of immune checkpoint inhibitors for the treatment of advanced melanoma [1] and other solid tumour entities [2] , [3] , [4] , [5] is establishing immunotherapy as a fourth pillar besides systemic anticancer treatments (conventional chemotherapy and targeted therapies), surgery and radiotherapy. Numerous clinical trials and preclinical projects have been started and CTLA4 (cytotoxic T-lymphocyte-associated protein 4) and PD-1 (Programmed cell death protein 1 receptor)/PD-L1 (PD-1 ligand) antibodies have been FDA approved for the treatment of malignant melanoma and non-small cell lung cancer as well as other cancer types.…”

Section: Immune Checkpoint Inhibitionmentioning

confidence: 99%

Beyond checkpoint inhibition – Immunotherapeutical strategies in combination with radiation

Eckert¹,

Gaipl

Niedermann

et al. 2017

Clinical and Translational Radiation Oncology

View full text Add to dashboard Cite

show abstract

“…The National Cancer Data Base revealed 5-year survival rates of 80.9% in stage I, 73.7% in stage II, 53.3% in stage III and 8.2% in stage IV kidney cancer patients [4] . Various aspects of the treatment for advanced RCC and metastatic RCC have been studied, and target therapy and immunotherapy have showed considerable improvement in patient survival [5] , [6] , [7] .…”

Section: Introductionmentioning

confidence: 99%

Molecular Characterization and Putative Pathogenic Pathways of Tuberous Sclerosis Complex–Associated Renal Cell Carcinoma

Park

Lee

Chang

et al. 2018

Translational Oncology

View full text Add to dashboard Cite

Tuberous sclerosis complex–associated renal cell carcinoma (TSC-RCC) has distinct clinical and histopathologic features and is considered a specific subtype of RCC. The genetic alterations of TSC1 or TSC2 are responsible for the development of TSC. In this study, we assessed the mTOR pathway activation and aimed to evaluate molecular characteristics and pathogenic pathways of TSC-RCC. Two cases of TSC-RCC, one from a 31-year-old female and the other from an 8-year-old male, were assessed. The mTOR pathway activation was determined by immunohistochemistry. The mutational spectrum of both TSC-RCCs was evaluated by whole exome sequencing (WES), and pathogenic pathways were analyzed. Differentially expressed genes were analyzed by NanoString Technologies nCounter platform. The mTOR pathway activation and the germline mutations of TSC2 were identified in both TSC-RCC cases. The WES revealed several cancer gene alterations. In Case 1, genetic alterations of CHD8, CRISPLD1, EPB41L4A, GNA11, NOTCH3, PBRM1, PTPRU, RGS12, SETBP1, SMARCA4, STMN1, and ZNRF3 were identified. In Case 2, genetic alterations of IWS1 and TSC2 were identified. Further, putative pathogenic pathways included chromatin remodeling, G protein–coupled receptor, Notch signaling, Wnt/β-catenin, PP2A and the microtubule dynamics pathway in Case 1, and mRNA processing and the PI3K/AKT/mTOR pathway in Case 2. Additionally, the ALK and CRLF2 mRNA expression was upregulated and CDH1, MAP3K1, RUNX1, SETBP1, and TSC1 mRNA expression was downregulated in both TSC-RCCs. We present mTOR pathway activation and molecular characteristics with pathogenic pathways in TSC-RCCs, which will advance our understanding of the pathogenesis of TSC-RCC.

show abstract

Advances in treatment of metastatic renal cell carcinoma

Cited by 9 publications

References 33 publications

Drug-Induced Hypertension Caused by Multikinase Inhibitors (Sorafenib, Sunitinib, Lenvatinib and Axitinib) in Renal Cell Carcinoma Treatment

Drug-Induced Hypertension Caused by Multikinase Inhibitors (Sorafenib, Sunitinib, Lenvatinib and Axitinib) in Renal Cell Carcinoma Treatment

Beyond checkpoint inhibition – Immunotherapeutical strategies in combination with radiation

Molecular Characterization and Putative Pathogenic Pathways of Tuberous Sclerosis Complex–Associated Renal Cell Carcinoma

Contact Info

Product

Resources

About