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Incidence and Mortality
Estimated new cases and deaths from renal cell (kidney and renal pelvis) cancer in the United States in 2023:
Follow-up and Survivorship
Renal cell cancer, also called renal adenocarcinoma or hypernephroma, can often be cured if it is diagnosed and treated when still localized to the kidney and the immediately surrounding tissue. The probability of cure is directly related to the stage or degree of tumor dissemination. Even when regional lymphatics or blood vessels are involved with tumor, a significant number of patients can achieve prolonged survival and probable cure. When distant metastases are present, disease-free survival is poor; however, some patients will survive after surgical resection of all known tumor. Because most patients are diagnosed when the tumor is still relatively localized and amenable to surgical removal, approximately 75% of all patients with renal cell cancer survive for 5 years. Occasionally, patients with locally advanced or metastatic disease may exhibit indolent courses lasting several years. Late tumor recurrence many years after initial treatment also occasionally occurs.
Renal cell cancer is one of the few tumors in which well-documented cases of spontaneous tumor regression in the absence of therapy exist, but this regression occurs rarely and may not lead to long-term survival.
Surgical resection is the mainstay of treatment of this disease. Even in patients with disseminated tumor, locoregional forms of therapy may play an important role in palliating symptoms of the primary tumor or of ectopic hormone production. Systemic therapy has demonstrated only limited effectiveness.
Approximately 85% of renal cell cancers are adenocarcinomas, mostly of proximal tubular origin. Most of the remainder are transitional cell carcinomas of the renal pelvis. For more information, see Transitional Cell Cancer of the Renal Pelvis and Ureter Treatment. Adenocarcinomas may be separated into clear cell and granular cell carcinomas; however, the two cell types may occur together in some tumors. Some investigators have found that granular cell tumors have a worse prognosis, but this finding is not universal. Distinguishing between well-differentiated renal adenocarcinomas and renal adenomas can be difficult. The diagnosis is usually made arbitrarily on the basis of the size of the mass, but size alone should not influence the treatment approach because metastases can occur with lesions as small as 0.5 centimeter.
The staging system for renal cell cancer is based on the degree of tumor spread beyond the kidney.[1,2,3] Involvement of blood vessels may not be a poor prognostic sign if the tumor is otherwise confined to the substance of the kidney. Abnormal liver function test results may be caused by a paraneoplastic syndrome that is reversible with tumor removal, and these types of results do not necessarily represent metastatic disease. Except when computed tomography (CT) examination is equivocal or when iodinated contrast material is contraindicated, CT scanning is as good as or better than magnetic resonance imaging for detecting renal masses.
AJCC Stage Groupings and TNM Definitions
The American Joint Committee on Cancer (AJCC) has designated staging by TNM (tumor, node, metastasis) classification to define renal cell cancer.
Current treatment cures more than 50% of patients with stage I renal cell cancer, but patients with stage IV disease have very poor outcomes. All patients with newly diagnosed renal cell cancer are candidates for clinical trials, when possible.
Treatment Options for Stage I Renal Cell Cancer
Treatment options for stage I renal cell cancer include the following:
Surgical resection is the accepted, often curative, therapy for patients with stage I renal cell cancer. Resection may be simple or radical. Radical resection includes removal of the kidney, adrenal gland, perirenal fat, and Gerota's fascia, with or without a regional lymph node dissection. Some, but not all, surgeons believe radical surgery yields superior results.
In patients with bilateral stage I neoplasms (concurrent or subsequent), bilateral partial nephrectomy or unilateral partial nephrectomy with contralateral radical nephrectomy, when technically feasible, may be a preferred alternative to bilateral nephrectomy with dialysis or transplantation. Increasing evidence suggests that a partial nephrectomy is curative in selected cases. A pathologist should examine the gross specimen as well as the frozen section from the parenchymal margin of excision.
In patients who are not candidates for surgery, EBRT or arterial embolization can provide palliation.
Current Clinical Trials
Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.
Treatment Options for Stage II Renal Cell Cancer
Treatment options for stage II renal cell cancer include the following:
Radical resection is the accepted, often curative, therapy for patients with stage II renal cell cancer. The operation includes removal of the kidney, adrenal gland, perirenal fat, and Gerota's fascia, with or without a regional lymph node dissection. Lymphadenectomy is commonly used, but its effectiveness has not been definitively proven. Postoperative systemic therapy with the anti-programmed death-1 (PD-1) antibody pembrolizumab has been shown to prolong disease-free survival (DFS), but not overall survival (OS), in patients with high-risk pT2 tumors. EBRT has been given before or after nephrectomy, without conclusive evidence that this improves survival compared with the results of surgery alone. However, it may benefit selected patients with more extensive tumors.
In patients who are not candidates for surgery, arterial embolization can provide palliation.
Pembrolizumab is an immune checkpoint inhibitor and a monoclonal antibody targeting the PD-1 protein.
Evidence (adjuvant pembrolizumab):
Treatment Options for Stage III Renal Cell Cancer
Treatment options for stage III renal cell cancer include the following:
Adjuvant systemic therapy
Surgical resection is the standard treatment for patients with clinical stage III renal cell cancer. Several different studies have investigated whether adjuvant (postoperative) systemic therapy improves outcomes. None of these trials have demonstrated any impact on overall survival (OS). However, two agents are associated with longer relapse-free survival.
Pembrolizumab is an immune checkpoint inhibitor and a monoclonal antibody targeting the programmed death-1 (PD-1) protein.
Sunitinib is an oral tyrosine kinase inhibitor targeting the vascular endothelial growth factor pathway.
Treatment options for patients with T3a, N0, M0 disease
Radical resection is the accepted, often curative therapy for patients with this stage of renal cell cancer. The operation includes removal of the kidney, adrenal gland, perirenal fat, and Gerota's fascia, with or without a regional lymph node dissection. Lymphadenectomy is commonly used, but its effectiveness has not been definitively proven. EBRT has been given before or after nephrectomy, without conclusive evidence that it improves survival compared with the results of surgery alone. However, it may benefit selected patients with more extensive tumors.
In patients with bilateral stage T3a neoplasms (concurrent or subsequent), bilateral partial nephrectomy or unilateral partial nephrectomy with contralateral radical nephrectomy, when technically feasible, may be a preferred alternative to bilateral nephrectomy with dialysis or transplantation.
Treatment options for patients with T3b, N0, M0 disease
Radical resection is the accepted, often curative therapy for patients with this stage of renal cell cancer. The operation includes removal of the kidney, adrenal gland, perirenal fat, and Gerota's fascia, with or without a regional lymph node dissection. Lymphadenectomy is commonly used, but its effectiveness has not been definitively proven. Surgery is extended to remove the entire renal vein and caval thrombus and a portion of the vena cava as necessary. EBRT has been given before or after nephrectomy, without conclusive evidence that it improves survival compared with the results of surgery alone. However, it may benefit selected patients with more extensive tumors.
In patients with stage T3b neoplasms who manifest concurrent or subsequent renal cell cancer in the contralateral kidney, a partial nephrectomy, when technically feasible, may be a preferred alternative to bilateral nephrectomy with dialysis or transplantation.[7,8,9]
Treatment options for patients with T1, N1, M0; T2, N1, M0; or T3, N1, M0 disease
This stage of renal cell cancer is curable with surgery in a small minority of patients. A radical nephrectomy and lymph node dissection is necessary. The value of preoperative and postoperative EBRT has not been demonstrated, but EBRT may be used for palliation in patients who are not candidates for surgery. Arterial embolization of the tumor with Gelfoam or other materials may be used preoperatively to reduce blood loss at nephrectomy or for palliation in patients with inoperable disease.
Treatment Options for First-Line Therapy for Stage IV Renal Cell Cancer
Treatment options for first-line therapy for stage IV renal cell cancer include the following:
Treatment Options for Second-Line Therapy for Stage IV Renal Cell Cancer
Treatment options for second-line therapy for stage IV renal cell cancer include the following:
Treatment Options for Third- and Fourth-Line Therapy for Stage IV Renal Cell Cancer
Treatment options for third- and fourth-line therapy for stage IV renal cell cancer include the following:
The prognosis is poor for any patients with renal cell cancer that is progressing, recurring, or relapsing after treatment, regardless of cancer cell type or stage of disease. Almost all patients with stage IV renal cell cancer are incurable. The use and selection of further treatment depends on many factors, including previous treatment and site of recurrence, as well as individual patient considerations. Carefully selected patients may benefit from surgical resection of localized metastatic disease, particularly if they have had a prolonged disease-free interval since their primary therapy.
Immune checkpoint inhibitors
Immune checkpoint inhibitors are drugs that block certain proteins that inhibit the immune system's response to cancer. These proteins down-regulate T-lymphocyte activity and can prevent these cells from killing cancer cells. By reducing the activity of these inhibitory proteins, immune checkpoint inhibitors increase the immune response to cancer. Immune checkpoint proteins that are targeted by this class of drugs include programmed death-1 (PD-1), programmed cell death-ligand-1 (PD-L1), and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4).
Ipilimumab plus nivolumab
In a randomized controlled trial, the combination of ipilimumab and nivolumab prolonged overall survival (OS) when compared with sunitinib as first-line systemic therapy for patients with advanced-stage renal cell carcinoma. Both drugs are immune checkpoint inhibitors. Ipilimumab is an antibody that targets CTLA-4. Nivolumab is an antibody that targets PD-1.
Evidence (ipilimumab plus nivolumab):
Nivolumab is the only treatment that has shown prolonged OS in patients who have previously received antiangiogenic therapy. Nivolumab is a fully human antibody that blocks ligand activation of the PD-1 protein. By blocking the interaction between PD-1 and PD-1 ligands 1 and 2, nivolumab blocks a pathway that inhibits the cellular immune response and restores cellular immunity.
It is not clear whether the dose of 3 mg/kg every 2 weeks used in the phase III trial offers any advantage over the dose of 2 mg/kg every 3 weeks used in the phase II trial; however, the latter dose offers substantial cost savings.
Interferon-alpha and IL-2
Cytokine therapy with interferon-alpha or IL-2 has been shown to induce objective responses. Interferon-alpha appears to have a modest impact on survival in selected patients. Interferon-alpha has approximately a 15% objective response rate in appropriately selected individuals. In general, these patients have nonbulky pulmonary or soft tissue metastases with excellent performance status ratings of 0 or 1, according to the Eastern Cooperative Oncology Group (ECOG) rating scale, and the patients show no weight loss. The interferon-alpha doses used in studies reporting good response rates have been in an intermediate range (6–20 million units administered 3 times weekly). A Cochrane analysis of six randomized trials, with a total of 963 patients, indicated an HR for survival of 0.78 (CI, 0.67–0.90) or a weighted average improvement in survival of 2.6 months.[Level of evidence A1]
High-dose IL-2 produces an overall response rate similar to that of interferon-alpha, but approximately 5% of the patients have shown durable complete remissions.[27,38,39,40,41,42] No randomized controlled trial of IL-2 has ever shown a longer survival result. High-dose IL-2 is used because it is the only systemic therapy that has been associated with inducing durable complete remissions, albeit in a small fraction (about 5%) of patients who are eligible for this treatment. The optimum dose of IL-2 is unknown. High-dose therapy appears to be associated with higher response rates but with more toxic effects. Low-dose inpatient regimens show activity against renal cell carcinoma with fewer toxic effects, especially hypotension, but have not been shown to be superior to placebo or any alternative regimen in terms of survival or quality of life (QOL). Outpatient subcutaneous administration has also demonstrated responses with acceptable toxic effects but, again, with unclear survival or QOL benefit. Combinations of IL-2 and interferon-alpha have been studied, but outcomes have not been better than with high-dose or low-dose IL-2 alone.[24,44]
Combined Immune Checkpoint Inhibitors and Antiangiogenic Targeted Therapies
After immune checkpoint inhibitors and antiangiogenic targeted therapies were found to improve outcomes, clinical trials of the combination of these two approaches showed longer OS when compared with monotherapy.
Pembrolizumab plus axitinib
Evidence (pembrolizumab plus axitinib):
Pembrolizumab plus lenvatinib
Evidence (pembrolizumab plus lenvatinib):
Nivolumab plus cabozantinib
Evidence (nivolumab plus cabozantinib):
Avelumab plus axitinib
Evidence (avelumab plus axitinib):
In patients without metastatic disease, resection of the primary tumor, when feasible, is standard practice. In patients with unresectable and/or metastatic cancers, tumor embolization, EBRT, and nephrectomy can aid in the palliation of symptoms caused by the primary tumor or related ectopic hormone or cytokine production.
In the era before targeted antiangiogenic therapies and immune checkpoint inhibitors, two randomized studies demonstrated an OS benefit in selected patients who underwent initial cytoreductive nephrectomy before the administration of interferon-alpha.[5,6] However, there is evidence that undergoing cytoreductive nephrectomy before antiangiogenic therapy does not provide a survival benefit to patients with intermediate- and poor-risk disease. Cytoreductive nephrectomy for good-risk patients has not been studied in a randomized controlled trial in the era of targeted therapies and immunotherapy. The limited data available from retrospective nonrandomized studies suggest a benefit in good-risk patients in the current era of targeted therapies.
The CARMENA trial (NCT00930033) evaluated the effectiveness of cytoreductive nephrectomy before targeted therapy. The study reported no benefit for patients who underwent cytoreductive nephrectomy before receiving treatment with sunitinib, an oral antiangiogenic tyrosine kinase inhibitor. This study enrolled only patients with intermediate- (57%) and poor-risk (43%) disease, whereas a previous retrospective study found that cytoreductive nephrectomy only benefited good- and intermediate-risk patients in the sunitinib era. Similarly, the positive trials in the interferon era were restricted to patients who were asymptomatic or minimally symptomatic, with a performance status rating of 0 or 1, according to the ECOG rating scale; these patients were also considered candidates for postoperative immunotherapy.
A multicenter analysis of 351 patients with metastatic renal cell carcinoma was conducted to assess the impact of cytoreductive nephrectomy. The study evaluated patients who received systemic therapy and compared outcomes of those who underwent cytoreductive nephrectomy with those who did not. The median OS was 38.1 months for patients who underwent nephrectomy compared with 16.4 months for those treated with systemic therapy alone (P = .03). However, the survival benefit was limited to patients with an ECOG performance status rating of 0 to 1 and good- or intermediate-risk disease. Interpretation of the study is limited by selection bias because patients were not randomly assigned to the nephrectomy group. Whether there is a benefit from cytoreductive nephrectomy for patients who are not subsequently treated with systemic therapy has not been tested.
Randomized controlled trials of cytoreductive nephrectomy:
A randomized, controlled, noninferiority trial of 450 patients compared the outcomes of patients who received sunitinib alone with those who received cytoreductive nephrectomy followed by sunitinib. The trial was designed to enroll 576 individuals; therefore it was underpowered. In this study, 43% of the patients had poor-risk disease and 57% had intermediate-risk disease.
Randomized controlled trials of interferon with or without preceding cytoreductive nephrectomy:
Two randomized studies demonstrated an OS benefit in selected patients who underwent initial cytoreductive nephrectomy before the administration of interferon-alpha.[5,6]
Resection of oligometastatic disease
Selected patients with solitary or a limited number of distant metastases can achieve prolonged survival with nephrectomy and surgical resection of the metastases.[45,46,47,48,49,50] Even patients with brain metastases had similar results. The likelihood of achieving therapeutic benefit with this approach appears enhanced in patients with a long disease-free interval between the initial nephrectomy and the development of metastatic disease.
Antiangiogenic and Other Targeted Therapy
A growing understanding of the biology of cancer in general, and renal cell cancer in particular, has led to the development and U.S. Food and Drug Administration (FDA) approval of six new agents that target specific growth pathways. Two of the approved targeted therapies block the mammalian target of rapamycin (mTOR), a serine/threonine protein kinase that regulates cell growth, division, and survival.
Anti-vascular endothelial growth factor (VEGF) and multitargeted tyrosine kinase inhibitors (TKIs)
Based on research showing that most clear cell renal cell carcinomas carried a mutation resulting in constitutive production of cytokines stimulating angiogenesis, several agents that targeted VEGF-mediated pathways were developed. Several of these agents have been shown in randomized, controlled trials to significantly delay progression of clear cell renal cell carcinoma, but none has resulted in a statistically significant increase in OS as conventionally assessed. Many of these trials allowed crossover upon progression and, in some instances, other agents with similar biological activity were available to patients after they withdrew from the clinical trial. These circumstances may have made it more difficult to detect an OS benefit. For the clinician, this makes it challenging to determine the real benefit of these drugs to the patient. The four FDA-approved anti-VEGF agents include three oral TKIs: pazopanib, sorafenib, and sunitinib; and an anti-VEGF monoclonal antibody, bevacizumab. Axitinib is a newer, highly selective, and more potent inhibitor of VEGF receptors 1, 2, and 3. The FDA approved axitinib for the treatment of advanced renal cell carcinoma after the failure of one previously received systemic therapy.
Sunitinib and the combination of bevacizumab plus interferon-alpha have each been associated with longer PFS than interferon-alpha alone in randomized, controlled trials. Sunitinib is an orally available multikinase inhibitor (VEGFR-1, VEGFR-2, PDGFR, c-Kit).
Bevacizumab, a monoclonal antibody that binds to and neutralizes circulating VEGF protein, delayed progression of clear-cell renal cell carcinoma when compared with placebo in patients with disease refractory to biological therapy. Similarly, bevacizumab plus interferon-alpha as first-line therapy resulted in longer PFS but not OS compared with interferon-alpha alone in two similarly designed, randomized, controlled trials.[20,21]
Pazopanib is an orally available multikinase inhibitor (VEGFR-1, VEGFR-2, VEGFR-3, PDGFR, and c-KIT) and has also been approved for the treatment of patients with advanced renal cell carcinoma.
Although the typical regimen for administering sunitinib is a 6-week cycle of 4 weeks on the drug and 2 weeks off the drug, the Patient Preference Study of Pazopanib Versus Sunitinib in Advanced or Metastatic Kidney Cancer (PISCES [NCT01064310]) chose a treatment period of 10 weeks rather than 12 weeks. Because of this treatment-period change, the 10 weeks of sunitinib treatment included 4 weeks on the drug, followed by 2 weeks off the drug, followed by 4 more weeks on the drug. Patients assigned to pazopanib followed by sunitinib had their preference for treatment assessed at the end of the second 4-weeks-on-the-drug period during which they took sunitinib daily for 28 days. At that point, the sunitinib side effects became the most severe. The expected result from an assessment conducted at the end of a 6-week treatment cycle versus the 4-week treatment cycle would be greatly abated side effects.
In addition, the 2-week washout period that occurred between the two 10-week treatment periods was a true break from treatment for patients assigned to take pazopanib first; however, for the patients taking sunitinib, the 2-week washout period was just the completion of their second 6-week treatment cycle. In other words, patients assigned to pazopanib first had a true 2-week break from treatment, and their drug preference was assessed at the peak period of toxic effects from sunitinib; however, the patients assigned to sunitinib first had no true treatment break before starting pazopanib and may have had less opportunity to recover from the side effects of sunitinib.
Cabozantinib is an oral TKI of the MET, AXL, and VEGF receptors. After a phase I trial showed activity against renal cell carcinoma, a phase III trial assessed the activity of cabozantinib in the second-line setting in a randomized controlled trial.
Axitinib has been shown to prolong PFS when used as second-line systemic therapy.
Comparing the toxicity of the axitinib and sorafenib regimens is complicated because the axitinib arm included a dose-escalation component, and only those patients who tolerated the lower dose were subsequently given the higher doses. Hypertension, nausea, dysphonia, and hypothyroidism were more common with axitinib, whereas palmar-plantar erythrodysesthesia, alopecia, and rash were more common with sorafenib.[32,52]
Tivozanib is a TKI that is selective for the VEGF receptor. A phase III randomized controlled trial compared tivozanib with sorafenib for first-line treatment of patients with metastatic renal cell cancer. The study reported that tivozanib was associated with a longer median PFS, but OS favored sorafenib. A subsequent phase III randomized controlled trial compared the two drugs in patients who had at least two prior systemic treatments, including at least one prior VEGF inhibitor. This second trial reported a longer median PFS for patients treated with tivozanib and no difference in OS. In the United States, the FDA has approved tivozanib for patients who have had two or more prior systemic therapies.
Sorafenib is an orally available multikinase inhibitor (CRAF, BRAF, KIT, FLT-3, VEGFR-2, VEGFR-3, and PDGFRB) and has also been approved for the treatment of patients with advanced renal cell carcinoma.
Mammalian target of rapamycin (mTOR) inhibitors
Temsirolimus is an intravenously administered mTOR inhibitor.
Everolimus is an orally administered mTOR inhibitor.
Combined Therapy With Multitargeted TKIs and mTOR Inhibitors
Lenvatinib plus everolimus
Lenvatinib is a multitargeted tyrosine kinase inhibitor with activity against VEGFR-1, VEGFR-2, and VEGFR-3, with inhibitory activity against fibroblast growth factor receptors (FGFR1, FGFR2, FGFR3, and FGFR4), PDGFRA, RET, and KIT.
Evidence (lenvatinib plus everolimus):
Responses to cytotoxic chemotherapy generally have not exceeded 10% for any regimen that has been studied in adequate numbers of patients.
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
General Information About Renal Cell Cancer
Updated statistics with estimated new cases and deaths for 2023 (cited American Cancer Society as reference 1).
This summary is written and maintained by the PDQ Adult Treatment Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ® Cancer Information for Health Professionals pages.
Purpose of This Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of renal cancer. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.
Reviewers and Updates
This summary is reviewed regularly and updated as necessary by the PDQ Adult Treatment Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
The lead reviewer for Renal Cell Cancer Treatment is:
Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
Levels of Evidence
Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Adult Treatment Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
Permission to Use This Summary
PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as "NCI's PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary]."
The preferred citation for this PDQ summary is:
PDQ® Adult Treatment Editorial Board. PDQ Renal Cell Cancer Treatment. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: https://www.cancer.gov/types/kidney/hp/kidney-treatment-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389256]
Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.
Based on the strength of the available evidence, treatment options may be described as either "standard" or "under clinical evaluation." These classifications should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.
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Last Revised: 2023-02-16
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