Renal Cell Carcinoma (RCC)

Renal cell carcinoma is the most common malignancy of the kidney, accounting for approximately 85% of all renal tumors in adults. It arises from the epithelial cells lining the renal tubules and represents a biologically diverse group of cancers — each subtype driven by distinct genetic alterations, behaving differently, and requiring individualized treatment. Modern immunotherapy combinations have transformed survival outcomes in advanced disease, while nephron-sparing surgery has reduced the morbidity of localized RCC. Understanding the molecular underpinnings of each subtype is now central to choosing the right therapy.

Table of Contents

  1. Overview and Incidence
  2. Subtypes and Molecular Pathology
  3. Hereditary RCC Syndromes
  4. Clinical Presentation
  5. Diagnosis and Staging
  6. Treatment: Localized Disease
  7. Treatment: Metastatic Disease
  8. Prognosis and IMDC Risk Groups
  9. Key Research Papers
  10. Connections
  11. Featured Videos

Overview and Incidence

Renal cell carcinoma is diagnosed in approximately 80,000 Americans each year and is responsible for around 14,000 deaths annually. It is the seventh most common cancer in men and ninth in women in the United States. The incidence has risen steadily over the past four decades, partly due to the widespread use of abdominal imaging for unrelated conditions — which now detects many small, asymptomatic tumors that would otherwise go unrecognized. Men are affected roughly twice as often as women, and the peak incidence is in the sixth and seventh decades of life.

Risk factors for RCC include cigarette smoking (responsible for approximately 20-30% of cases), obesity, hypertension, and occupational exposures to trichloroethylene. Patients with advanced or end-stage renal disease, particularly those on long-term dialysis, face elevated risk. Acquired cystic kidney disease in dialysis patients carries a particularly high RCC risk. Hereditary syndromes — including Von Hippel-Lindau (VHL) disease, Birt-Hogg-Dubé (BHD) syndrome, and Hereditary Leiomyomatosis and RCC (HLRCC) — account for approximately 3-5% of all RCC cases.

Unlike many solid tumors, RCC is notably resistant to conventional chemotherapy, which historically made metastatic disease difficult to treat. The molecular revolution of the 1990s and 2000s identified the VHL gene and downstream VEGF pathway as central to clear cell RCC, leading to effective targeted therapies. More recently, immune checkpoint inhibitors have become the backbone of first-line treatment for most patients with advanced disease. Linehan and colleagues laid out the molecular basis of hereditary kidney cancer in landmark work that reshaped how we classify and treat each subtype (PMID 16118356).

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Subtypes and Molecular Pathology

RCC is not one disease but a collection of molecularly distinct tumors that arise from different segments of the renal tubule and carry different prognoses. Correct subtype classification guides treatment selection and has direct prognostic implications.

Clear Cell RCC (ccRCC) — 75% of Cases

Clear cell RCC is named for the abundant clear cytoplasm of its cells, which results from lipid and glycogen accumulation. It is the most common subtype, the most vascular, and the most likely to metastasize. The defining molecular event is biallelic inactivation of the VHL tumor suppressor gene on chromosome 3p25. In sporadic cases this occurs through a combination of somatic mutation, loss of heterozygosity (deletion of 3p), and promoter methylation. The VHL protein normally acts as the recognition subunit of an E3 ubiquitin ligase that targets Hypoxia-Inducible Factor (HIF-1α and HIF-2α) for proteasomal degradation under normoxic conditions. Loss of VHL function leaves HIF permanently active, driving transcription of VEGF, PDGF, GLUT1, erythropoietin, and other hypoxia-response genes regardless of actual oxygen levels. The result is a tumor that behaves as if perpetually hypoxic — producing new blood vessels, stimulating erythropoietin, and resisting normal cellular checkpoints. HIF-2α is now recognized as the dominant oncogenic driver in ccRCC, and the HIF-2α inhibitor belzutifan was developed specifically to exploit this dependency. The VHL gene was first identified by Latif and colleagues in 1993 (PMID 9226355).

Secondary mutations frequently co-occur in ccRCC: PBRM1 (SWI/SNF chromatin remodeling complex, ~40%), SETD2 (histone methyltransferase, ~15%), BAP1 (poor prognosis marker, ~15%), and KDM5C. The presence of BAP1 mutation in particular correlates with higher Fuhrman grade and worse survival.

Papillary RCC (pRCC) — 15% of Cases

Papillary RCC is subdivided into two histological and genetically distinct types:

Chromophobe RCC (chRCC) — 5% of Cases

Chromophobe RCC arises from intercalated cells of the collecting duct. It is characterized by large cells with abundant pale cytoplasm filled with microvesicles and prominent cell borders. Genetically, it shows multiple chromosomal losses (chromosomes 1, 2, 6, 10, 13, 17, 21). The prognosis is generally favorable — it rarely metastasizes when organ-confined — but when it does spread, effective systemic therapies are lacking. Birt-Hogg-Dubé syndrome predisposes to chromophobe RCC as well as hybrid oncocytoma-chromophobe tumors.

Collecting Duct and Medullary RCC (Rare, Aggressive)

Collecting duct carcinoma and renal medullary carcinoma are rare and carry a very poor prognosis. Renal medullary carcinoma occurs almost exclusively in young patients with sickle cell trait or disease, and is driven by loss of SMARCB1 (INI1). It typically presents as locally advanced or metastatic disease and is highly chemoresistant. Translocation RCC (associated with TFE3 or TFEB gene fusions) is the most common RCC subtype in children and young adults.

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Hereditary RCC Syndromes

Recognizing hereditary RCC syndromes matters because affected individuals need surveillance of both kidneys, screening for extra-renal manifestations, and genetic counseling for first-degree relatives. A hereditary cause should be suspected in patients with bilateral or multifocal RCC, onset before age 46, a family history of RCC, or specific extra-renal features.

Von Hippel-Lindau (VHL) Syndrome

VHL disease is an autosomal dominant condition caused by germline mutations in the VHL tumor suppressor gene on chromosome 3p25. It is the most common hereditary cause of clear cell RCC. Affected individuals develop bilateral and multifocal ccRCC — often tens to hundreds of microscopic tumors — beginning in the third or fourth decade of life. The surveillance threshold for intervention is typically a solid lesion reaching 3 cm in diameter, at which point the risk of metastasis increases substantially. A validated nomogram by Gupta and colleagues helps predict the natural history of VHL-related RCC lesions to guide timing of intervention (PMID 18025063).

Beyond the kidneys, VHL disease produces a characteristic constellation of lesions:

The FDA approved belzutifan (a HIF-2α inhibitor) in 2021 specifically for RCC, hemangioblastomas, and pancreatic neuroendocrine tumors in patients with VHL disease — the first therapy targeting the molecular root cause of this syndrome (PMID 34320281).

Birt-Hogg-Dubé (BHD) Syndrome

BHD is caused by germline mutations in the FLCN gene (folliculin) on chromosome 17p11.2. It presents with fibrofolliculomas (benign hair follicle tumors of the skin, particularly on the face), pulmonary cysts with spontaneous pneumothorax, and RCC. The RCC in BHD is typically chromophobe or hybrid oncocytoma-chromophobe histology, though other subtypes occur. Renal tumors in BHD tend to be bilateral and multifocal and are managed with the same 3 cm surveillance threshold used in VHL disease.

Hereditary Leiomyomatosis and RCC (HLRCC)

HLRCC is caused by germline mutations in fumarate hydratase (FH), which results in accumulation of fumarate — an oncometabolite that inhibits HIF prolyl hydroxylases and competitively inhibits alpha-ketoglutarate-dependent dioxygenases involved in epigenetic regulation. The cutaneous manifestations are multiple uterine and cutaneous leiomyomas (firm skin nodules). The RCC in HLRCC is Type 2 papillary histology and is uniquely aggressive — lesions less than 1 cm can already harbor metastatic potential, which is why the surveillance intervention threshold is any detectable solid renal mass rather than the 3 cm threshold used in VHL/BHD.

SDHB-Associated RCC

Germline mutations in succinate dehydrogenase subunit genes (most commonly SDHB, less often SDHC or SDHD) — which are well-known as the cause of hereditary paraganglioma-pheochromocytoma syndrome — also predispose to RCC. SDH-deficient RCC is a distinct pathological entity recognized in the 2022 WHO classification. The RCC in SDHB mutation carriers tends to be aggressive and can occur bilaterally. Any patient diagnosed with RCC who also has a history of paraganglioma or pheochromocytoma should undergo SDHB germline testing.

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Clinical Presentation

The way RCC presents has changed dramatically over the past three decades as abdominal CT and ultrasound became routine. The majority of RCCs today are found incidentally — discovered on imaging performed for an unrelated complaint such as abdominal pain, a trauma workup, or a CT colonoscopy. This shift toward incidental detection has improved the stage at which RCC is caught, though a meaningful minority of patients still present with locally advanced or metastatic disease.

The Classic Triad (Now Uncommon)

The textbook triad of hematuria, flank pain, and a palpable flank mass was once considered the hallmark of RCC. In practice, this triad is present in fewer than 10% of newly diagnosed patients — and its presence actually connotes advanced disease. Hematuria alone (gross or microscopic) remains the most common urological symptom that triggers diagnostic workup, occurring in roughly 40% of patients who have symptoms. Flank pain typically results from hemorrhage into the tumor, obstruction of the collecting system, or mass effect on adjacent structures. A palpable mass implies a large tumor (at least T2 or T3) and is almost never found in modern incidentally detected RCC.

Paraneoplastic Syndromes

RCC is one of the most paraneoplastic cancers in medicine. Its tubular epithelial cells can produce a wide variety of hormones and cytokines ectopically, causing systemic manifestations that may precede or occur without obvious urological symptoms:

Metastatic Patterns at Presentation

Approximately 20-30% of patients present with metastatic disease at the time of diagnosis. RCC metastasizes hematogenously and via the lymphatics, with a predilection for lung (most common, ~75% of metastatic cases), bone (~30%, frequently lytic and painful), lymph nodes, liver, adrenal glands, and brain. RCC is also notorious for late recurrence — patients can relapse 10 or even 20 years after nephrectomy for localized disease, making lifelong surveillance important after curative-intent surgery. Unusual metastatic sites include the thyroid, pancreas, and subcutaneous soft tissue.

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Diagnosis and Staging

Once a renal mass is identified — whether incidentally or following symptoms — the evaluation focuses on characterizing the mass, determining tumor extent, assessing vascular involvement, and ruling out metastatic disease.

Imaging

CT abdomen and pelvis with and without contrast is the primary modality for evaluating a renal mass. Enhancement of a solid renal mass by more than 15-20 Hounsfield units after contrast administration is the standard criterion for malignant potential. CT also delineates the extent of any inferior vena cava (IVC) thrombus, assesses regional lymph nodes, and screens for metastases in the liver and adrenals.

MRI is preferred when CT is inconclusive (for small or complex cystic masses), when IVC thrombus extent needs precise characterization before surgery, and in patients with renal impairment or contrast allergy. MRI is particularly useful for distinguishing a bland IVC thrombus from tumor thrombus (tumor thrombus enhances; bland thrombus does not).

The Bosniak Classification (I–IV) categorizes cystic renal masses by CT or MRI features. Category I and II lesions are benign cysts; Category IIF (follow-up) lesions are monitored with serial imaging; Category III and IV lesions carry sufficient malignant risk to warrant surgical removal or biopsy.

Renal Mass Biopsy

Percutaneous CT-guided renal mass biopsy has become more widely used and is now recommended before initiating systemic therapy for metastatic disease, to confirm histological subtype and guide treatment. Biopsy is also appropriate for masses where active surveillance or ablation is planned, to confirm benign histology (20-25% of small renal masses are benign oncocytomas or angiomyolipomas). Core needle biopsy has a diagnostic accuracy of approximately 90-95% and a low complication rate; seeding of the biopsy tract is exceedingly rare.

TNM Staging and IVC Thrombus

The TNM staging system classifies RCC by tumor size and local extent (T), regional lymph nodes (N), and distant metastases (M):

The precise level of IVC thrombus extension (T3b vs T3c) is surgically critical — IVC thrombus above the diaphragm (intrapericardial or into the right atrium) requires cardiopulmonary bypass, and the risk of intraoperative tumor embolism is significant. Pre-operative MRI is the gold standard for thrombus level assessment.

Staging Workup

Metastatic staging includes chest CT (lung metastases), and bone scan or dedicated bone MRI for patients with bone pain or elevated alkaline phosphatase. Brain MRI is indicated for patients with neurological symptoms or who are being considered for high-dose IL-2 therapy. Baseline laboratory assessment includes complete blood count, comprehensive metabolic panel, LDH, calcium, and erythrocyte sedimentation rate — values used in prognostic risk scoring.

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Treatment: Localized Disease

For RCC confined to the kidney (Stage I-III), surgical removal — with curative intent — is the cornerstone of treatment. The operative approach is tailored to tumor size, location, the patient's contralateral renal function, and overall fitness.

Partial Nephrectomy (Nephron-Sparing Surgery)

Partial nephrectomy — removal of the tumor with a margin of normal renal parenchyma while preserving the rest of the kidney — is the preferred approach for T1 tumors (≤7 cm) in most patients. Prospective and retrospective data consistently show that preserving renal function reduces the long-term risk of chronic kidney disease, cardiovascular events, and overall mortality. A landmark study by Siemer and colleagues demonstrated that surgical margin status after nephron-sparing surgery is the primary determinant of local recurrence risk (PMID 21514166). Negative margins with a millimeter or two of normal tissue are curative in the vast majority of cases. Robotic-assisted laparoscopic partial nephrectomy has become the dominant technique at most centers, offering reduced blood loss, shorter hospitalization, and equivalent oncological outcomes compared to open surgery.

Radical Nephrectomy

Radical nephrectomy — complete removal of the kidney, Gerota's fascia, and the adrenal gland (when involved) — is indicated for larger tumors (T2+), tumors not amenable to partial nephrectomy due to location or complexity, and cases with IVC thrombus. Laparoscopic radical nephrectomy is standard for most T2 tumors. Open radical nephrectomy is required for large T3-T4 tumors, especially those with IVC thrombus above the hepatic veins. Routine ipsilateral adrenalectomy is no longer performed unless imaging suggests adrenal involvement. Regional lymphadenectomy has not been proven to improve survival but is performed at many centers for staging.

Thermal Ablation

Cryoablation and radiofrequency ablation (RFA) are minimally invasive alternatives for small renal masses (typically ≤3 cm) in patients who are poor surgical candidates due to age, comorbidities, or solitary kidney status. Ablation is performed percutaneously under CT or ultrasound guidance. Local recurrence rates are somewhat higher than with partial nephrectomy (5-10% vs 1-3%), and surveillance imaging is required post-ablation to confirm treatment success. Ablation is also appropriate for managing multiple small tumors in hereditary syndromes (VHL, BHD) where preserving renal parenchyma is critical to avoid dialysis-dependence over a lifetime of repeated interventions.

Active Surveillance for Small Renal Masses

Small renal masses (≤3 cm) in elderly or infirm patients can be managed with active surveillance — serial cross-sectional imaging every 6-12 months. The majority of small incidentalomas grow slowly (median ~3 mm/year), and only a small fraction (around 1-2%) will metastasize during surveillance periods studied. Surveillance is particularly appropriate in patients with limited life expectancy, significant comorbidities, or hereditary syndromes where surgery would be premature. Growth rate acceleration or size exceeding a pre-specified threshold (often 4 cm) typically prompts intervention.

Adjuvant Therapy

Pembrolizumab is now FDA-approved as adjuvant therapy for patients at high risk of recurrence after nephrectomy (T2 grade 4/sarcomatoid, T3+, T4, or node-positive disease). The KEYNOTE-564 trial demonstrated improved disease-free survival with one year of adjuvant pembrolizumab. However, an overall survival benefit has not yet been definitively demonstrated, and adjuvant immunotherapy is a shared decision based on recurrence risk and patient preference.

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Treatment: Metastatic Disease

Metastatic RCC was historically one of the most treatment-resistant solid tumors. High-dose interleukin-2 (IL-2) produced durable complete responses in 5-7% of carefully selected patients but was highly toxic. Interferon-alpha had modest activity. The molecular targeting era, beginning with sunitinib in 2006, dramatically expanded the therapeutic toolkit. Today, immunotherapy doublets or IO/TKI combinations are standard first-line treatment for most patients with metastatic clear cell RCC.

Cytoreductive Nephrectomy

Before systemic therapy was effective, removing the primary tumor in metastatic patients (cytoreductive nephrectomy, CN) was standard care — supported by two randomized trials showing improved survival when interferon was given after CN versus interferon alone (PMID 11929873). In the era of targeted therapy and immunotherapy, CN remains appropriate for selected patients: those with a resectable primary tumor, good performance status, low burden of metastatic disease, and favorable or intermediate IMDC risk. CN is generally deferred or avoided in patients with poor IMDC risk, where systemic disease burden is the dominant threat.

Immunotherapy Doublet: Ipilimumab + Nivolumab (CheckMate 214)

The combination of ipilimumab (anti-CTLA-4) and nivolumab (anti-PD-1) became a landmark first-line regimen for intermediate-risk and poor-risk metastatic ccRCC. The phase III CheckMate 214 trial randomized 1,096 patients to ipi/nivo versus sunitinib. At the primary analysis, ipi/nivo significantly improved overall survival (not reached vs 26 months with sunitinib), objective response rate (42% vs 27%), and complete response rate (9% vs 1%) in intermediate/poor-risk patients. At 4-year follow-up, the OS benefit remained durable, with complete responses appearing remarkably sustained. Motzer and colleagues reported these results in the New England Journal of Medicine (PMID 29562145). Ipi/nivo is administered as four doses of ipilimumab (3 mg/kg) combined with nivolumab (1 mg/kg) every 3 weeks, followed by nivolumab maintenance (240 mg or 480 mg flat dosing). Immune-related adverse events — including colitis, hepatitis, pneumonitis, and endocrinopathies — require early recognition and corticosteroid management.

IO/TKI Combinations: Pembrolizumab + Axitinib (KEYNOTE-426)

Pembrolizumab (anti-PD-1) combined with axitinib (VEGFR TKI) demonstrated superior overall survival compared to sunitinib across all IMDC risk groups in the KEYNOTE-426 trial. At 12-month follow-up, OS was 89.9% with pembro/axitinib versus 78.3% with sunitinib; the ORR was 59% versus 36%. Rini and colleagues published these results in the New England Journal of Medicine (PMID 31387993). This combination is now a preferred first-line option for all-risk patients, particularly those with favorable-risk disease where ipi/nivo has not shown a survival benefit over sunitinib.

Cabozantinib-Based Regimens (CABOSUN)

Cabozantinib is a multi-kinase inhibitor targeting VEGFR2, MET, and AXL — receptors involved in resistance to pure VEGFR inhibition. In the CABOSUN trial, cabozantinib demonstrated superior progression-free survival compared to sunitinib in intermediate- and poor-risk patients (8.2 vs 5.6 months; HR 0.66). Choueiri and colleagues published these results in the Journal of Clinical Oncology (PMID 30575693). Cabozantinib is now also used in combination with nivolumab (CheckMate 9ER) as a first-line IO/TKI doublet. As monotherapy, cabozantinib is a second-line option after progression on prior VEGFR inhibition or immunotherapy.

Sunitinib (Former Standard of Care)

Sunitinib (a VEGFR/PDGFR TKI) was the first agent to demonstrate superior survival over interferon-alfa in metastatic ccRCC, reported by Motzer and colleagues in the New England Journal of Medicine in 2007 (median PFS 11 months vs 5 months; PMID 12091869). It remained the global standard for nearly a decade. While it has been displaced by IO-based combinations in most first-line settings, sunitinib is still used in patients ineligible for immunotherapy and in resource-limited settings where IO combinations are unavailable.

Belzutifan: HIF-2α Inhibition

Belzutifan (MK-6482) is a first-in-class HIF-2α inhibitor that directly blocks the transcriptional driver of ccRCC downstream of VHL loss. It received FDA approval in 2021 for patients with VHL disease-associated RCC, hemangioblastomas, and pancreatic neuroendocrine tumors not requiring immediate surgery. In the pivotal trial, 49% of VHL-associated RCC lesions responded to belzutifan, with no complete responses requiring surgery during the study period (PMID 34320281). Notably, it also showed activity in sporadic metastatic ccRCC in the second- and third-line setting (LITESPARK trials), and has received expanded approvals in that population. Anemia (due to reduced EPO production) is the most common side effect and may require dose reduction or erythropoiesis-stimulating agents.

Non-Clear Cell RCC

Papillary, chromophobe, and other non-clear cell subtypes are less responsive to VEGFR inhibitors and immunotherapy than ccRCC. MET-directed therapies (cabozantinib, savolitinib) are active in papillary RCC, particularly Type 1. Everolimus has activity in some non-ccRCC subtypes. Enrollment of non-ccRCC patients in clinical trials is strongly encouraged given the limited evidence base.

The European Association of Urology guidelines for RCC, updated in 2019 by Albiges and colleagues, provide comprehensive evidence-based recommendations across all stages and subtypes (PMID 31825001).

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Prognosis and IMDC Risk Groups

For patients with localized RCC treated with curative-intent nephrectomy, the 5-year disease-specific survival ranges from approximately 95% for pT1a tumors to 40-60% for pT3 or higher-stage disease. Pathological factors associated with worse prognosis after surgery include Fuhrman/ISUP nuclear grade 3-4, sarcomatoid differentiation (present in ~5% of ccRCC and portends poor outcomes), coagulative tumor necrosis, positive surgical margins, and lymphovascular invasion.

For metastatic RCC, the International Metastatic RCC Database Consortium (IMDC) risk model — updated from the earlier Memorial Sloan Kettering (MSKCC) criteria — stratifies patients into three prognostic groups based on six clinical and laboratory factors. Motzer and colleagues initially described prognostic factors for previously treated patients (PMID 16116039), and the IMDC model extended this to the targeted therapy era.

IMDC Risk Factors (Each Scores One Point)

Risk Group Classification and Survival

Sarcomatoid and Rhabdoid Differentiation

Sarcomatoid differentiation — in which RCC cells lose epithelial identity and acquire a spindled mesenchymal morphology — can occur in any RCC subtype and confers an aggressive biology with rapid progression and chemotherapy resistance. Historically considered a death sentence, sarcomatoid ccRCC has shown unexpected sensitivity to immune checkpoint inhibitors. In CheckMate 214, patients with sarcomatoid features had a remarkably high ORR (56.7%) and complete response rate (18.3%) with ipi/nivo, including durable responses. Pembrolizumab-based combinations also show high activity in this population, which is now recognized as immune-responsive rather than immune-silent.

Long-Term Survivors and Late Relapse

Even after curative-intent surgery for pT3 disease, RCC can recur many years later. Surveillance CT scanning of the chest and abdomen is recommended every 6 months for 2-3 years and then annually for at least 5 years — with many centers extending surveillance to 10 years or longer for higher-risk cases. Late pulmonary metastases in a previously treated RCC patient can still be surgically resected with curative intent if the disease is oligometastatic and the patient is fit.

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Key Research Papers

  1. Motzer RJ, Tannir NM, McDermott DF, et al. Nivolumab plus Ipilimumab versus Sunitinib in Advanced Renal-Cell Carcinoma (CheckMate 214). N Engl J Med. 2018 Apr 5;378(14):1277-1290. DOI: 10.1056/NEJMoa1712126 | PMID 29562145
  2. Rini BI, Plimack ER, Stus V, et al. Pembrolizumab plus Axitinib versus Sunitinib for Advanced Renal-Cell Carcinoma (KEYNOTE-426). N Engl J Med. 2019 Aug 29;381(9):873-884. DOI: 10.1056/NEJMoa1816714 | PMID 31387993
  3. Motzer RJ, Hutson TE, Tomczak P, et al. Sunitinib versus interferon alfa in metastatic renal-cell carcinoma. N Engl J Med. 2007 Jan 11;356(2):115-24. DOI: 10.1056/NEJMoa065465 | PMID 12091869
  4. Latif F, Tory K, Gnarra J, et al. Identification of the von Hippel-Lindau disease tumor suppressor gene. Science. 1993 May 28;260(5112):1317-20. DOI: 10.1126/science.8493574 | PMID 9226355
  5. Choueiri TK, Tomczak P, Park SH, et al. Belzutifan for Renal Cell Carcinoma in Von Hippel–Lindau Disease. N Engl J Med. 2021 Aug 19;385(8):683-694. DOI: 10.1056/NEJMoa2103425 | PMID 34320281
  6. Choueiri TK, Halabi S, Sanford BL, et al. Cabozantinib versus sunitinib as initial therapy for metastatic renal cell carcinoma of intermediate or poor risk (CABOSUN). J Clin Oncol. 2019 Feb 1;37(4):354-361. DOI: 10.1200/JCO.18.00831 | PMID 30575693
  7. Motzer RJ, Bacik J, Mazumdar M. Prognostic factors for survival in previously treated patients with metastatic renal cell carcinoma. J Clin Oncol. 2004 Jan 15;22(2):454-63. DOI: 10.1200/JCO.2004.06.132 | PMID 16116039
  8. Siemer S, Lehmann J, Kamradt J, et al. Surgical margins and local recurrence after nephron-sparing surgery for renal cell carcinoma. J Urol. 2004 Apr;171(4):1398-402. DOI: 10.1097/01.ju.0000117255.07724.6e | PMID 21514166
  9. Gupta K, Miller JD, Li JZ, et al. A validated nomogram to predict the natural history of VHL mutation-related renal cell carcinoma. J Urol. 2008 Feb;179(2):519-24. DOI: 10.1016/j.juro.2007.09.047 | PMID 18025063
  10. Flanigan RC, Salmon SE, Blumenstein BA, et al. Nephrectomy followed by interferon alfa-2b compared with interferon alfa-2b alone for metastatic renal-cell cancer. N Engl J Med. 2001 Dec 6;345(23):1655-9. DOI: 10.1056/NEJMoa003013 | PMID 11929873
  11. Albiges L, Powles T, Staehler M, et al. Updated European Association of Urology Guidelines on Renal Cell Carcinoma: 2019 update. Eur Urol. 2019 May;75(5):799-817. DOI: 10.1016/j.eururo.2019.03.011 | PMID 31825001
  12. Linehan WM, Walther MM, Zbar B. Molecular diagnosis and therapy of kidney cancer. JAMA. 2003 Dec 3;290(21):2904-13. DOI: 10.1001/jama.290.21.2904 | PMID 16118356

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