Clinical Review on the Management of Metastatic Renal Cell Carcinoma

Renal cell carcinomas vary considerably in their tumor biology and disease course, which is reflected in the range of treatment paradigms in localized and metastatic renal cell carcinoma (mRCC). Active surveillance remains an important component of all renal cell carcinoma management. In mRCC, the rapid evolution from cytokine-based therapy to targeted therapy to immunotherapy with checkpoint blockade has revolutionized the field and drastically altered treatment outcomes. More recently, combination therapies have become a standard of care for most patients with mRCC. In this review, we highlight recent critical data that led to changes in treatment paradigms and provide a practical framework for the management of patients with mRCC.

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Paradigm towards Tailored Therapies and Complete Responses in the Treatment of Metastatic Renal Cell Carcinoma

Oncology & Hematology Review (US) ◽

10.17925/ohr.2012.08.1.30 ◽

2012 ◽

Vol 08 (01) ◽

pp. 30

Author(s):

Mayer Fishman ◽

Thomas Hutson ◽

Neeraj Agarwal ◽

Eric Jonasch ◽

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Keyword(s):

Renal Cell Carcinoma ◽

Cell Carcinoma ◽

Metastatic Renal Cell Carcinoma ◽

Renal Cell ◽

Kinase Inhibitors ◽

Mammalian Target Of Rapamycin ◽

Interleukin 2 ◽

Standard Of Care ◽

Complete Response ◽

High Dose

In recent years, the management of metastatic renal cell carcinoma (mRCC) has been revolutionized by the advent of targeted therapies. Multitargeted kinase inhibitors (such as sunitinib, sorafenib, pazopanib, and axitinib), the vascular endothelial growth factor inhibitor bevacizumab, and mammalian target of rapamycin inhibitors (such as everolimus and temsirolimus) have become the standard of care for the palliation of metastatic disease. Unfortunately, cumulative toxicities and the lack of marked benefits have prevented the combined use of most molecularly targeted agents. Selected patients with mRCC benefit from immunotherapy, as subsets of patients can experience long-term disease remission or complete response with high-dose interleukin-2. In order to optimize the value of immunotherapy, improvements in the selection of drugs and combinations with novel immunomodulatory agents must be pursued.

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The spinal distribution of metastatic renal cell carcinoma: Support for locoregional rather than arterial hematogenous mode of early bony dissemination.

Journal of Clinical Oncology ◽

10.1200/jco.2020.38.6_suppl.742 ◽

2020 ◽

Vol 38 (6_suppl) ◽

pp. 742-742

Author(s):

Kyrollis Attalla ◽

Cihan Duzgol ◽

Lily McLaughlin ◽

Jessica Flynn ◽

Irina Ostrovnaya ◽

...

Keyword(s):

Renal Cell Carcinoma ◽

Cell Carcinoma ◽

Metastatic Renal Cell Carcinoma ◽

Tumor Size ◽

Renal Cell ◽

Spinal Metastasis ◽

Tumor Biology ◽

Molecular Features ◽

Metastatic Involvement ◽

Distant Spread

742 Background: To investigate the distribution of spinal metastasis in metastatic renal cell carcinoma (mRCC) and to explore relationships between biological and clinical factors and patterns of spinal spread. Methods: An institutional database was queried to identify patients with mRCC and spinal metastatic involvement from June 2005 – November 2018. A blinded radiologist examined all cross-sectional imaging involving the spine and scored each level for absence or presence of disease. Clinical and biologic features including primary tumor size and degree of spinal and non-bony metastatic involvement (including regional lymph node and distant deposits) were collected. Spinal distributions were evaluated by the Kolmogorov Smirnov test and compared across radiographic and clinical parameters. Results: One-hundred patients with 685 spinal levels involved by mRCC were evaluated. A nonuniform spatial distribution was observed across the cohort; a preponderance of thoracolumbar involvement was noted with the mode at L3 (p<0.001). No difference in metastatic distribution was observed in right versus left-sided tumors. Tumors <4cm compared to >7cm, patients who had distant spread versus bone-only disease, and patients with increasing number of spine levels involved (1 versus >5 levels) had a significantly different distribution (p<0.001 for all comparisons). Smaller tumor size, distant spread, and greater number of involved levels appeared to have a more uniform distribution of spinal metastasis. Conclusions: These data support a dominant locoregional as opposed to arterial hematogenous mechanism for the early dissemination of mRCC to the spine. This is concordant with the theory of the valveless Batson plexus acting as a conduit for such spread, as the kidneys are compartmentally distinct from, but reside just anterior to the spine at L1-L3. Characterizations of the biologic molecular features contributing to osseous tropism and aggressive tumor biology (as seen in the subset of patients with uniform spread, such as outlier patients with small tumors), have implications for surveillance and are an area of active investigation.

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