eMedicine Specialties > Oncology > Carcinomas of the Genitourinary Tract

Renal Cell Carcinoma: Treatment & Medication

Author: Kush Sachdeva, MD, Southern Oncology and Hematology Associates, South Jersey Healthcare, Fox Chase Cancer Center Partner
Coauthor(s): Bagi RP Jana, MD, Assistant Professor, University of Central Florida College of Medicine; Attending Physician, Department of Medicine, Florida Hospital Cancer Institute, Orlando; Mansoor Javeed, MD, FACP, Clinical Assistant Professor of Medicine, University of California Davis; Consultant, Sierra Hematology-Oncology Medical Center; Issam Makhoul, MD, Associate Professor, Department of Medicine, Division of Hematology/Oncology, University of Arkansas for Medical Sciences; Brendan Curti, MD, Director, Genitourinary Oncology Research, Robert W Franz Cancer Research Center, Earle A Chiles Research Institute, Providence Cancer Center
Contributor Information and Disclosures

Updated: Jun 25, 2009

Treatment

Medical Care

More than 50% of patients with renal cell carcinoma are cured in early stages, but outcome for stage IV disease is poor. The probability of cure is related directly to the stage or degree of tumor dissemination, so the approach is curative for early stage disease. Selected patients with metastatic disease respond to immunotherapy, but many patients can be offered only palliative therapy for advanced disease.

• The treatment options for renal cell cancer are surgery, radiation therapy, chemotherapy, hormonal therapy, immunotherapy, or combinations of these.
  • Options for chemotherapy and endocrine-based approaches are limited, and no hormonal or chemotherapeutic regimen is accepted as a standard of care. Objective response rates, either for single or combination chemotherapy, usually are lower than 15%. Therefore, various biologic therapies have been evaluated.
  • Renal cell carcinoma is an immunogenic tumor, and spontaneous regressions have been documented. Many immune modulators, such as interferon, IL-2 (aldesleukin [Proleukin]), bacillus Calmette-Guérin (BCG) vaccination, lymphokine-activated killer (LAK) cells plus IL-2, tumor-infiltrating lymphocytes, and nonmyeloablative allogeneic peripheral blood stem-cell transplantation, have been tried.
• Multikinase inhibitors
  • Sorafenib
    • On December 20, 2005, the US Food and Drug Administration granted approval for sorafenib (Nexavar), a small molecule Raf kinase and vascular endothelial growth factor (VEGF) multireceptor kinase inhibitor, for the treatment of patients with advanced renal cell carcinoma. This indication is based on the demonstration of improved progression-free survival in a large, multinational, randomized double-blind, placebo-controlled phase 3 study and a supportive phase 2 study. Overall survival results from the phase 3 study are preliminary at this time.
    • The sorafenib phase 3 study was conducted in patients with advanced (unresectable or metastatic) renal cell carcinoma who had received one prior systemic treatment. Study endpoints included overall survival, progression-free survival, and response rate.
      • Among 769 patients randomized, the median age was 59 years and 70% were male.
      • Baseline patient and disease characteristics were well balanced. Regarding prior therapies, 93% had prior nephrectomies; 99% had received prior systemic therapies, including interleukin 2 (44%) and an interferon (68%).
      • The median progression-free survival was 167 days in the sorafenib group versus 84 days in the placebo control group (HR 0.44; 95% CI for HR: 0.35-0.55, logrank p <0.000001). Time-to-progression was similarly improved. Tumor response was determined by independent radiologic review according to Response Evaluation Criteria in Solid Tumors (RECIST) criteria. Overall, of 672 patients who were able to be evaluated for response, 7 (2%) sorafenib patients and 0 (0%) placebo patients had confirmed partial responses.
    • Sorafenib toxicities (based on an updated phase 3 study database of 902 patients) included reversible skin rashes in 40% and hand-foot skin reaction in 30%. Diarrhea was reported in 43%, treatment-emergent hypertension in 17%, and sensory neuropathic changes in 13%. Alopecia, oral mucositis, and hemorrhage also were reported more commonly on the sorafenib arm. The incidence of treatment-emergent cardiac ischemia/infarction events was higher in the sorafenib group (2.9%) compared with the placebo group (0.4%).
    • Grade 3 and 4 adverse events were unusual; only hand-foot skin reaction occurred at 5% or greater frequency in the sorafenib arm. Laboratory findings included asymptomatic hypophosphatemia in 45% versus 12% and serum lipase elevations in 41% versus 30% of sorafenib versus placebo patients, respectively. Grade 4 pancreatitis was reported in 2 sorafenib patients, although both patients subsequently resumed sorafenib, one at full dose.
    • Physicians should be aware of the importance of frequent blood pressure monitoring and management, especially during the first 6 weeks after starting sorafenib, and the unusual laboratory alterations on sorafenib therapy. The recommended dose is 400 mg (two 200-mg tab) twice daily taken either 1 hour before or 2 hours after meals. Adverse events were accommodated by temporary dose interruptions or reductions to 400 mg once daily or 400 mg every other day.
    • Sorafenib targets serine/threonine and receptor tyrosine kinases, including those of RAF; VEGFR-2,3; PDGFR-b; KIT; FLT-3; and RET.
    • Further clinical studies evaluating the role of sorafenib in the first-line setting, in combination with other immunomodulators, are underway. Preliminary results appear promising.
  • Sunitinib (Sutent)
    • Sunitinib is another multi-kinase inhibitor approved by the FDA in January 2006 for the treatment of metastatic kidney cancer that has progressed after a trial of immunotherapy. The approval was based on the high response rate (40% partial responses) and a median time to progression of 8.7 months and an overall survival of 16.4 months.
    • The receptor tyrosine kinases inhibited by sunitinib include VEGFR 1-3 and PDGFR a and b.
    • Major toxicities (grade II or higher) include fatigue (38%), diarrhea (24%), nausea (19%), dyspepsia (16%), stomatitis (19%), and decline in cardiac ejection fraction (11%). Dermatitis occurred in 8%, and hypertension occurred in 5% of patients.
    • A recent phase 3 study evaluating sunitinib in the first-line setting, compared against IFN-a, in patients with metastatic renal cell carcinoma demonstrated significant improvement in PFS and response rates compared against the control arm. These results are considered to be preliminary, and longer-term follow-up is necessary for conclusive results.
  • Temsirolimus (Torisel)
    • Temsirolimus inhibits mTOR (mammalian target of rapamycin), which is a serine/threonine kinase important in the regulation of cell growth and division.  Genes involved with the response to hypoxia (HIF pathway described above) are also upregulated by mTOR and are believed to be central to the pathogenesis of kidney cancers.
    • Temsirolimus has been tested alone and in conjunction with interferon in patients with poor prognosis advanced renal cell carcinoma. Temsirolimus monotherapy at a dose of 25 mg IV weekly showed longer overall and progression-free survival compared to interferon (median survival 10.9 months versus 7.3 months, p = 0.008).  There was no significant additive effect of interferon combined with temsirolimus. A second study combining the temsirolimus and interferon over a range of dose levels showed overall survival of 18.8 months and progression-free survival of 9.1 months for the combination. Partial response was observed in 8% and stable disease in 36% of patients.
    • Common toxicities of temsirolimus include asthenia, rash, anemia, hypophosphatemia and hyperlipidemia.  
    • FDA approval for temsirolimus was given in May 2007 for the treatment of advanced renal cell carcinoma at a dose of 25 mg weekly IV until progression.     
    • The novel combination of bevacizumab (a neutralizing monoclonal antibody to VEGF, which binds to and inhibits it) and interferon has been shown to have activity against metastatic RCC.⁵
  • Everolimus (Afinitor)
    • RAD001 (everolimus [Afinitor]) is a serine-threonine kinase inhibitor of mTOR, an important regulatory protein in cell signaling. A recent phase 2 trial in patients with metastatic RCC demonstrated promising preliminary clinical results. Everolimus was approved by the US Food and Drug Administration in March 2009 for advanced renal cell carcinoma after failure of treatment with sunitinib or sorafenib.
  • Other multikinase inhibitors undergoing investigation for renal cell carcinoma
    • Lapatinib is an EGFR and ErbB-2 dual tyrosine kinase inhibitor, which appears to have efficacy in the treatment of tumors, including RCC, which overexpress EGFR. This was recently reported in a phase 3 study in advanced RCC evaluating lapatinib against hormonal therapy in patients who had failed prior therapy.
  • Future treatment strategies for advanced renal cell carcinoma will likely incorporate a combination of molecular approaches, using multidrug regimens consisting of small-molecule kinase inhibitors with biologic therapies, immunomodulatory therapies, or both.
  • For early stage renal cell carcinoma, current and future treatment strategies would utilize these molecular approaches earlier in the adjuvant setting in order to improve overall survival rates. Indeed, a randomized phase 3 trial of sunitinib versus sorafenib versus placebo as adjuvant therapy in patients with resected renal cell carcinoma is currently ongoing and open for patient enrollment.
  • The optimal sequence or combination of active agents in advanced renal cell carcinoma is not yet defined. Based on decisions arrived at from considering level 1 evidence, the following may be considered as reasonable targeted therapy choices in metastatic renal cell carcinoma not eligible for high-dose IL-2 therapy.
    • For previously untreated patients with clear cell renal cell cancer of low or intermediate risk, sunitinib or the combination of bevacizumab and interferon alpha
    • For patients with previously untreated clear cell renal cell cancer with poor prognostic (high-risk) characteristics, temsirolimus
    • Sorafenib for patients with previously treated clear cell renal cell cancer; an increase in dose of sorafenib may give responses in patients in whom standard doses initially fail; patients in whom sorafenib is failing may be treated with sunitinib if that drug had not been previously used.
    • The treatment of metastatic renal cell carcinoma is problematic, and, wherever possible, patients should be directed to approved and controlled clinical trials. This applies as well in the adjuvant treatment of surgically resected renal cell carcinoma, for which no therapy to the present has been found to be of survival benefit.
  • High-dose interleukin-2 must be considered for robust patients with excellent cardiopulmonary reserve, as it remains the only treatment known to induce complete and durable remissions, albeit in a minority of patients. Prospective studies are underway to identify patients more likely to respond to interleukin-2 immunotherapy based on carbonic anhydrase IX expression in the primary tumor and other assessments of immune function and regulation.  This study may help to resolve the sequence and selection of available agents for individual patients with metastatic disease.
• Chemotherapy
  • A recent phase 2 trial of weekly intravenous gemcitabine (600 mg/m² on days 1, 8, and 15) with continuous infusion fluorouracil (150 mg/m²/d for 21 d in 28-d cycle) in patients with metastatic renal cell cancer produced a partial response rate of 17%. No complete responses were noted. Eighty percent of patients had multiple metastases, and 83% had received previous treatment. The mean progression-free survival duration of 28.7 weeks was significantly longer than that of historic controls.
  • Floxuridine (5-fluoro 2'-deoxyuridine [FUDR]), 5-fluorouracil (5-FU), and vinblastine, paclitaxel (Taxol), carboplatin, ifosfamide, gemcitabine, and anthracycline (doxorubicin) all have been used. Floxuridine infusion has a mean response rate of 12%, while vinblastine infusion yielded an overall response rate of 7%. 5-FU alone has a response rate of 10%, but when used in combination with interferon, it had a 19% response rate in some studies.
  • Renal cell carcinoma is refractory to most chemotherapeutic agents because of multidrug resistance mediated by p -glycoprotein. Normal renal proximal tubules and renal cell carcinoma both express high levels of p -glycoprotein. Calcium channel blockers or other drugs that interfere with the function of p -glycoprotein can diminish resistance to vinblastine and anthracycline in human renal cell carcinoma cell lines.
• Biologic therapies
  • The interferons are natural glycoproteins with antiviral, antiproliferative, and immunomodulatory properties. The interferons have a direct antiproliferative effect on renal tumor cells in vitro, stimulate host mononuclear cells, and enhance expression of major histocompatibility complex molecules. Interferon-alpha, which is derived from leukocytes, has an objective response rate of approximately 15% (range 0-29%).
  • Preclinical studies have shown synergy between interferons and cytotoxic drugs. In several prospective randomized trials, combinations do not appear to provide major advantages over single-agent therapy. Many different types and preparations of interferons have been used without any difference in efficacy.
  • IL-2 is a T-cell growth factor and activator of T cells and natural killer cells. IL-2 affects tumor growth by activating lymphoid cells in vivo without affecting tumor proliferation directly.
    • In the initial study by the National Cancer Institute, bolus intravenous infusions of high-dose IL-2 combined with LAK cells produced objective response rates of 33%. In subsequent multicenter trials, the response rate was 16%. Subsequent studies also showed that LAK cells add no definite therapeutic benefit and can be eliminated from the treatment. A high-dose regimen (600,000-720,000 IU/kg q8h for a maximum of 14 doses) resulted in a 19% response rate with 5% complete responses. The majority of responses to IL-2 were durable, with median response duration of 20 months. Eighty percent of patients who responded completely to therapy with IL-2 were alive at 10 years.
    • Most patients responded after the first cycle, and those who did not respond after the second cycle did not respond to any further treatment. Therefore, the current recommendation is to continue treatment with high-dose IL-2 to best response (up to 6 cycles) or until toxic effects become intolerable. Treatment should be discontinued after 2 cycles if the patient has had no regression. Combinations of IL-2 and interferon or other chemotherapeutic agents such as 5-FU have not been shown to be more effective than high-dose IL-2 alone.
    • Toxic effects associated with high-dose IL-2 are related to increased vascular permeability and secondary cytokine secretion (eg, IL-1, interferon gamma, tumor necrosis factor, nitric oxide). The management of high-dose IL-2 toxicities requires inpatient monitoring, often in an intensive care unit.
      • The major toxic effect of high-dose IL-2 is a sepsislike syndrome, which includes a progressive decrease in systemic vascular resistance and an associated decrease in intravascular volume due to capillary leak.
      • Other toxic effects are fever, chills, fatigue, infection, and hypotension.
      • High-dose IL-2 has been associated with a 1-4% incidence of treatment-related death and should be offered only to patients with no cardiac ischemia or significant impairment of renal or pulmonary functions. Management includes judicious use of fluids and vasopressor support to maintain blood pressure and intravascular volume and at the same time to avoid pulmonary toxicity due to noncardiogenic pulmonary edema from the capillary leak. This syndrome is normally reversible.
• Other experimental approaches for treatment include immunomodulatory drugs, vaccines, and nonmyeloablative allogeneic peripheral blood stem-cell transplantation.
  • The immunomodulator, lenalidomide (Revlimid), a derivative of thalidomide, inhibits VEGF, stimulates T and NK cells, and inhibits inflammatory cytokines. It has been evaluated extensively in hematologic malignancies and recently was reported to demonstrate efficacy in renal cell carcinoma regression and delayed time to progression in a phase 2 study of metastatic renal cell carcinoma.
  • Vaccine trials are in early stages of development. Few antigens have been identified that induce T-cell responses from renal cell carcinoma. One example of vaccine strategy is to induce the gene for granulocyte-macrophage colony-stimulating factor (GM-CSF) into autologous cultured renal cell cancer lines by retroviral transduction. Patients then are immunized with irradiated tumor cells secreting large amounts of GM-CSF and are evaluated for immune responses and clinical tumor regression. Other approaches to vaccination include tumor lysates and dendritic cells. Autologous vaccine therapy is now being tried in combination with cytokine therapy.
  • Nonmyeloablative allogeneic stem-cell transplantation is another research approach. This can induce sustained regression of metastatic renal cell carcinoma in patients who have had no response to conventional immunotherapy. In one recent trial, 19 patients with refractory metastatic renal cell carcinoma who had suitable donors received a preparative regimen of cyclophosphamide and fludarabine, followed by an infusion of peripheral blood stem cells from a human leukocyte antigen (HLA)-identical sibling or a sibling with a mismatch of a single HLA antigen. Patients with no response received as many as 3 infusions of donor lymphocytes. Two patients died of transplantation-related causes, and 8 died from progressive disease. In 10 patients (53%), metastatic disease regressed; 3 patients had a complete response, and 7 had a partial response. The durations of these responses continue to be assessed. Further trials are needed to confirm these findings and to evaluate long-term benefits.
• Multiple studies have been conducted using megestrol (Megace) in the treatment of renal cell carcinoma. No benefit has been shown except for appetite stimulation, so megestrol is currently not recommended. Antiestrogens such as tamoxifen (100 mg/m²/d or more) and toremifene (300 mg/d) also have been tried, with a response rate as low as that of most chemotherapeutic agents.

Surgical Care

Surgical resection remains the only known effective treatment for localized renal cell carcinoma, and it also is used for palliation in metastatic disease.

• Radical nephrectomy, which remains the most commonly performed standard surgical procedure today for treatment of localized renal carcinoma, involves complete removal of the Gerota fascia and its contents, including a resection of kidney, perirenal fat, and ipsilateral adrenal gland, with or without ipsilateral lymph node dissection. Radical nephrectomy provides a better surgical margin than simple removal of the kidney, since perinephric fat may be involved in some patients. Twenty to thirty percent of patients with clinically localized disease develop metastatic disease after nephrectomy. Some surgeons believe that the adrenal gland should not be removed because of the low probability of ipsilateral adrenal metastasis and the morbidity associated with adrenalectomy. In the absence of distant metastatic disease with locally extensive and invasive tumors, adjacent structures such as bowel, spleen, or psoas muscle may be excised en bloc during radical nephrectomy.
  • Lymph nodes may be involved in 10-25% of patients. The 5-year survival rate in patients with regional node involvement is substantially lower than in patients with stage I or II disease. Regional lymphadenectomy adds little in terms of operative time or risk and should be included in conjunction with radical nephrectomy.
  • Approximately 5% of patients with renal cell carcinoma have inferior vena caval involvement. Tumor invasion of the renal vein and inferior vena cava usually occurs as a well-vascularized thrombus covered with its own intimal surface. In patients with renal vein involvement without metastases, radical nephrectomy is performed with early ligation of the renal artery but no manipulation of the renal vein. If the inferior vena cava is involved, then vascular control of the inferior vena cava is obtained both above and below the tumor thrombus, and the thrombus is resected intact, with subsequent closure of the vena cava. Patients with actual invasion of the inferior vena caval wall have poor prognoses, despite aggressive surgical approaches.
  • At least 3 common approaches exist for removal of kidney cancer, as follows: (1) the transperitoneal approach, (2) the flank approach, and (3) the thoracoabdominal approach. Approach depends on tumor location and size and the body habitus of the patient. The thoracoabdominal approach offers the advantage of palpation of the ipsilateral lung cavity and mediastinum, as well as the ability to resect solitary pulmonary metastases.
• Laparoscopic nephrectomy is a less invasive procedure, incurs less morbidity, and is associated with shorter recovery time and less blood loss. The need for pain medications is reduced, but operating room time and costs are higher. Disadvantages include concerns about spillage and technical difficulties in defining surgical margins. Laparoscopic partial nephrectomy can be considered at centers with experience in this procedure for early stage renal cell cancer.
• Palliative nephrectomy should be considered in patients with metastatic disease for alleviation of symptoms such as pain, hemorrhage, malaise, hypercalcemia, erythrocytosis, or hypertension. Several randomized studies are now showing improved overall survival in patients presenting with metastatic kidney cancer who have nephrectomy followed by either interferon or IL-2. If the patient has good physiological status, then nephrectomy should be performed prior to immunotherapy. Reports have documented regression of metastatic renal cell carcinoma after removal of the primary tumor. Adjuvant nephrectomy is not recommended for inducing spontaneous regression; rather, it is performed to decrease symptoms or to decrease tumor burden for subsequent therapy in carefully controlled environments.
• About 25-30% of patients have metastatic disease at diagnosis, and fewer than 5% have solitary metastasis. Surgical resection is recommended in selected patients with metastatic renal carcinoma. This procedure may not be curative in all patients but may produce some long-term survivors. The possibility of disease-free survival increases after resection of primary tumor and isolated metastasis excision.
• Radiation therapy may be considered as the primary therapy for palliation in patients whose clinical condition precludes surgery, either because of extensive disease or poor overall condition.
  • A dose of 4500 centigray (cGy) is delivered, with consideration of a boost up to 5500 cGy.
  • Preoperative radiation therapy yields no survival advantage.
  • Controversies exist concerning postoperative radiation therapy, but it may be considered in patients with perinephric fat extension, adrenal invasion, or involved margins. A dose of 4500 cGy is delivered, with consideration of a boost.
  • Palliative radiation therapy is often used for local or symptomatic metastatic disease, such as painful osseous lesions or brain metastasis, to halt potential neurological progression. Surgery also should be considered for solitary brain or spine lesions, followed by postoperative radiotherapy.
• About 11% of patients develop brain metastasis during the course of illness. Renal cell carcinoma is a radioresistant tumor, but radiation treatment of brain metastasis improves quality of life, local control, and overall survival duration. Patients with untreated brain metastasis have a median survival time of 1 month, which can be improved with glucocorticoid therapy and brain irradiation. Stereotactic radiosurgery is more effective than surgical extirpation for local control and can be performed on multiple lesions.

Consultations

• Urology
• Oncology
• Radiation oncology

Medication

The goals of pharmacotherapy are to induce remission, reduce morbidity, and prevent complications.

Antineoplastic agents

Few options are available for the systemic therapy of renal cell carcinoma, and no hormonal or chemotherapeutic regimen is accepted as a standard of care to treat renal cell carcinoma. Objective response rates, either for single or combination chemotherapy, usually are lower than 15%. The recently approved multikinase inhibitors induce objective responses in up to 40% of patients, but they are not known to cure patients with metastatic disease.

Aldesleukin (Proleukin)

IL-2; T-cell growth factor and activator of T cells and natural killer cells. Affects tumor growth by activating lymphoid cells in vivo, without affecting tumor proliferation directly.

Vinblastine (Velban, Alkaban-AQ)

Vinca alkaloid with cytotoxic effect via mitotic arrest. Binds to specific site on tubulin, prevents polymerization of tubulin dimers, and inhibits microtubule formation.

Gemcitabine (Gemzar)

Cytidine analog. After intracellular metabolism to active nucleotide, inhibits ribonucleotide reductase and competes with deoxycytidine triphosphate for incorporation into DNA.

5-fluorouracil (Adrucil)

Fluorinated pyrimidine antimetabolite that inhibits thymidylate synthase (TS) and interferes with RNA synthesis and function. Has cell-cycle specificity with activity in S phase. Inhibits thymidylate synthase by 5-FU metabolite F-dUMP. Metabolite FUTMP incorporates into RNA and F-dUTP incorporates into DNA, resulting in alteration of RNA processing and inhibition of DNA synthesis.

Sorafenib (Nexavar)

First oral multikinase inhibitor that targets serine/threonine and tyrosine receptor kinases in both the tumor cell and the tumor vasculature. Targets kinases involved in tumor cell proliferation and angiogenesis, thereby decreasing tumor cell proliferation. These kinases included RAF kinase, VEGFR-2, VEGFR-3, PDGFR-beta, KIT, and FLT-3. Indicated for advanced renal cell carcinoma.

Sunitinib (Sutent)

Mulitkinase inhibitor that targets several tyrosine kinase inhibitors implicated in tumor growth, pathologic angiogenesis, and metastatic progression. Inhibits platelet-derived growth factor receptors (ie, PDGFR-alpha, PDGFR-beta), vascular endothelial growth factor receptors (ie, VEGFR1, VEGFR2, VEGFR3), stem cell factor receptor (KIT), Fms-like tyrosine kinase-3 (FLT3), colony-stimulating factor receptor type 1 (CSF-1R), and the glial cell-line–derived neurotrophic factor receptor (RET). Indicated for advanced renal cell carcinoma.

Temsirolimus (Torisel)

Water soluble ester of sirolimus. Binds with high affinity to immunophilin FKBP (FK506 binding protein). This complex inhibits mammalian target of rapamycin (mTOR) kinase, a key protein in cells that regulates gene translation responsible for cell cycle regulation. mTOR also reduces cell growth factors (eg, vascular endothelial growth factor) involved in new blood vessel development. Indicated for advanced renal cell carcinoma.

Everolimus (Afinitor)

Rapamycin-derivative kinase inhibitor. Indicated for advanced renal cell carcinoma after failure of treatment with sunitinib or sorafenib. Reduces cell proliferation and angiogenesis by inhibition of mTOR pathway.

Interferon alfa 2a (Roferon A) and 2b (Intron A)

Interferons are natural glycoproteins with antiviral, antiproliferative, and immunomodulatory properties.
They have direct antiproliferative effect on renal tumor cells, stimulate host mononuclear cells, and enhance expression of major histocompatibility complex molecules.

Pazopanib (Votrient)

Multityrosine kinase inhibitor. Indicated for advanced renal cell carcinoma.

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