sábado, 18 de enero de 2020

Wilms Tumor and Other Childhood Kidney Tumors Treatment (PDQ®)–Health Professional Version - National Cancer Institute

Wilms Tumor and Other Childhood Kidney Tumors Treatment (PDQ®)–Health Professional Version - National Cancer Institute

National Cancer Institute

Wilms Tumor and Other Childhood Kidney Tumors Treatment (PDQ®)–Health Professional Version

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Renal Cell Carcinoma (RCC)

Incidence of RCC

Malignant epithelial tumors arising in the kidneys of children account for more than 5% of new pediatric renal tumors; therefore, they are more common than clear cell sarcoma of the kidney or rhabdoid tumors of the kidney. The annual incidence rate is approximately 4 cases per 1 million children, compared with an incidence of Wilms tumor of the kidney that is at least 29-fold higher.[1]
RCC, the most common primary malignancy of the kidney in adults, is rare in children younger than 15 years. In the older age group of adolescents (aged 15–19 years), approximately two-thirds of renal malignancies are RCC.[2] Children and adolescents with RCC (n = 515) present with more advanced disease than do those aged 21 to 30 years.[1]

Conditions Associated With RCC

Conditions associated with RCC include the following:
  • von Hippel-Lindau (VHL) disease. VHL disease is an autosomal dominant condition in which blood vessels in the retina and cerebellum grow excessively.[3] The gene for VHL disease is located on chromosome 3p26 and is a tumor-suppressor gene, which is either mutated or deleted in patients with the syndrome.
    Screening for the VHL gene is available.[4] To detect clear cell renal carcinoma in these individuals when the lesions are smaller than 3 cm and renal-sparing surgery can be performed, annual screening with abdominal ultrasonography or magnetic resonance imaging (MRI) is recommended, beginning at age 8 to 11 years.[5]
    (Refer to the Von Hippel-Lindau Disease section in the PDQ summary on Genetics of Kidney Cancer [Renal Cell Cancer] for more information.)
  • Tuberous sclerosis. In tuberous sclerosis, the renal lesions may actually be epithelioid angiomyolipoma (also called perivascular epithelioid cell tumor or PEComa), which is associated with aggressive or malignant behavior and expresses melanocyte and smooth muscle markers.[6,7]
  • Familial RCC. Familial RCC has been associated with an inherited chromosome translocation involving chromosome 3.[8] A high incidence of chromosome 3 abnormalities has also been demonstrated in nonfamilial renal tumors.
    Succinate dehydrogenase (SDHB, SDHC, and SDHD) is a Krebs cycle enzyme gene that has been associated with the development of familial RCC occurring with pheochromocytoma/paraganglioma. Germline mutations in a subunit of the gene have been reported in individuals with renal cancer and no history of pheochromocytoma.[9,10]
  • Renal medullary carcinoma. A rare subtype of RCC, renal medullary carcinoma may be associated with sickle cell hemoglobinopathy.[11] Renal medullary carcinomas are highly aggressive malignancies characterized clinically by a high stage at the time of detection, with widespread metastases and lack of response to chemotherapy and radiation therapy.[12,13][ Level of evidence: 3iiA] Survival is poor and ranges from 2 weeks to 15 months, with a mean survival of 4 months.[11,13-16]
  • Hereditary leiomyomatosis. Hereditary leiomyomatosis (of skin and uterus) and RCC is a distinct phenotype caused by dominant inheritance of a mutation in the FH gene. Screening for RCC starting as early as age 5 years has been recommended.[17,18]
  • Previous treatment for childhood cancer. Survivors of childhood cancer who were treated with radiation and/or chemotherapy are at more risk of developing renal cancers than are the general population. Highest risk has been observed among neuroblastoma survivors, with renal-directed radiation therapy of 5 Gy or more, and with platinum-based chemotherapy.[19] Renal cancers have also been reported after treatment for rhabdomyosarcoma, leiomyosarcoma, acute lymphoblastic leukemia, primitive neuroectodermal tumors (PNET), and Wilms tumor.[20-25] (Refer to the Subsequent Neoplasms section in the PDQ summary on Late Effects of Treatment for Childhood Cancer for more information.)

Genetic Testing for Children and Adolescents With RCC

Indications for germline genetic testing of children and adolescents with RCC to check for a related syndrome are described in Table 8.
Table 8. Indications for Germline Genetic Analysis (Screening) of Children and Adolescents with Renal Cell Carcinoma (RCC)a
ENLARGE
Indication for TestingTumor HistologyGene TestRelated Syndrome
VHL = von Hippel-Lindau.
aAdapted from Linehan et al.[26]
Multifocal RCC or VHL lesionsClear cellVHL genevon Hippel-Lindau syndrome
Family history of clear cell RCC or multifocal RCC with absent VHL mutationClear cellChromosome 3 gene translocationsHereditary non-VHL clear cell RCC syndrome
Multifocal papillary RCC or family history of papillary RCCPapillaryMET geneHereditary papillary RCC syndrome
Multifocal RCC or cutaneous fibrofolliculoma or pulmonary cysts or spontaneous pneumothoraxChromophobe or oncocytic or clear cellGermline sequence BHD geneBirt-Hogg-Dubé syndrome
Personal or family history of early-onset uterine leiomyomata or cutaneous leiomyomataType 2 papillary or collecting duct carcinomaFH geneHereditary leiomyomata/RCC syndrome
Multifocal RCC or early-onset RCC or presence of paraganglioma/pheochromocytoma or family history of paraganglioma/pheochromocytomaClear cell or chromophobeSDHB gene, SDHC gene, SDHD geneHereditary paraganglioma/pheochromocytoma syndrome

Genomics of RCC

Translocation-positive carcinomas of the kidney are recognized as a distinct form of renal cell carcinoma (RCC) and may be the most common form of RCC in children, accounting for 40% to 50% of pediatric RCC.[27] In a Children's Oncology Group (COG) prospective clinical trial of 120 childhood and adolescent patients with RCC, nearly one-half of patients had translocation-positive RCC.[28,29] These carcinomas are characterized by translocations involving the TFE3 gene located on Xp11.2. The TFE3 gene may partner with one of the following genes:
  • ASPSCR in t(X;17)(p11.2;q25).
  • PRCC in t(X;1)(p11.2;q21).
  • SFPQ in t(X;1)(p11.2;p34).
  • NONO in inv(X;p11.2;q12).
  • CLTC in t(X;17)(p11;q23).
Another less-common translocation subtype, t(6;11)(p21;q12), involving a TFEB gene fusion, induces overexpression of TFEB. The translocations involving TFE3 and TFEB induce overexpression of these proteins, which can be identified by immunohistochemistry.[30]
Previous exposure to chemotherapy is the only known risk factor for the development of Xp11 translocation RCCs. In one study, the postchemotherapy interval ranged from 4 to 13 years. All reported patients received either a DNA topoisomerase II inhibitor and/or an alkylating agent.[31,32]
Controversy exists as to the biological behavior of translocation RCC in children and young adults. Whereas some series have suggested a good prognosis when RCC is treated with surgery alone despite presenting at a more advanced stage (III/IV) than translocation-associated RCC, a meta-analysis reported that these patients have poorer outcomes.[33-35] The outcomes for these patients are being studied in the ongoing COG AREN03B2 (NCT00898365) biology and classification study. Vascular endothelial growth factor receptor–targeted therapies and mammalian target of rapamycin (mTOR) inhibitors seem to be active in Xp11 translocation metastatic RCC.[36] Recurrences have been reported 20 to 30 years after initial resection of the translocation-associated RCC.[22]
Diagnosis of Xp11 translocation RCC needs to be confirmed by a molecular genetic approach, rather than using TFE3 immunohistochemistry alone, because reported cases have lacked the translocation. There is a rare subset of RCC cases that is positive for TFE3 and lack a TFE3 translocation, showing an ALK translocation instead. This subset of cases represents a newly recognized subgroup within RCC that is estimated to involve 15% to 20% of unclassified pediatric RCC. In the eight reported cases in children aged 6 to 16 years, the following was observed:[37-40]
  • ALK was fused to VCL in a t(2;10)(p23;q22) translocation (n = 3). The VCL translocation cases all occurred in children with sickle cell trait, whereas none of the TMP3 translocation cases did.
  • ALK was fused to TPM3 (n = 3).
  • ALK was fused to HOOK-1 on 1p32 (n = 1).
  • t(1;2) translocation fusing ALK and TMP3 (n = 1).

Histology of RCC

Pediatric RCC differs histologically from the adult counterparts. Although the two main morphological subgroups of papillary and clear cell can be identified, about 25% of RCCs show heterogeneous features that do not fit into either of these categories.[3] Childhood RCCs are more frequently of the papillary subtype (20%–50% of pediatric RCCs) and can sometimes occur in the setting of Wilms tumor, metanephric adenoma, and metanephric adenofibroma.[41]
RCC in children and young adults has a different genetic and morphologic spectrum than that seen in older adults.[3,32,41,42]

Prognosis and Prognostic Factors for RCC

Prognostic factors for RCC include the following:
  • Stage of disease.
  • Lymph node involvement.
The primary prognostic factor for RCC is stage of disease. In 304 children and adolescents with RCC identified in the National Cancer Data Base, the median age was 13 years; 39% of patients presented with localized stage I disease, 16% with stage II disease, 33% with stage III disease, and 12% with stage IV disease. The 5-year overall survival (OS) rates were 100% for patients with stage I and stage II disease, 71% for stage III disease, and 8% for stage IV disease.[43] Age and sex had no significant impact on survival. Survival was negatively impacted by increasing tumor size (P < .001), positive nodal status (P = .001), and higher pathologic stage (P < .001).[43] The data attained in this article from the National Cancer Data Base are limited, as some patient details are not available and follow up is incomplete. Tumor size of 4 cm or smaller may or may not impact survival and local lymph node involvement may not be as significant in children.
An important difference between the outcomes in children and adults with RCC is the prognostic significance of local lymph node involvement. Adults presenting with RCC and involved lymph nodes have a 5-year OS rate of approximately 20%, but the literature suggests that 72% of children with RCC and local lymph node involvement at diagnosis (without distant metastases) survive their disease.[27] In another series of 49 patients from a population-based cancer registry, the findings were similar. In this series, 33% of the patients had papillary subtype, 22% had translocation type, 6% had clear-cell subtype, and 16% were unclassified. The survival rates at 5 years were 96% for patients with localized disease, 75% for patients with positive regional lymph nodes, and 33% for patients with distant metastatic RCC.[44]

Clinical Features and Diagnostic Evaluation of RCC

RCC may present with the following:
  • Abdominal mass.
  • Abdominal pain.
  • Hematuria.
Refer to the Clinical Features of Wilms Tumor and Diagnostic and Staging Evaluation for Wilms Tumor sections of this summary for more information about the clinical features and diagnostic evaluation of childhood kidney tumors. In a COG prospective clinical trial of 40 patients with small (7 cm) primary tumors whose lymph nodes were adequately sampled, 19 had positive nodes.[28] Outcome results of this trial are pending. (Refer to the Stage Information for Renal Cell Cancer section in the PDQ summary on adult Renal Cell Cancer Treatment summary for more information about the staging evaluation.)

Treatment of RCC

Survival of patients with RCC is affected by stage of disease at presentation and the completeness of resection at radical nephrectomy. OS rates for all patients with RCC range from 64% to 87%. The 5-year survival rates for pediatric RCC are 90% or higher for stage I, higher than 80% for stage II, 70% for stage III, and lower than 15% for stage IV.[27] Retrospective analyses and the small number of patients involved place limitations on the level of evidence in the area of treatment.
Standard treatment options for RCC include the following:
  1. Radical nephrectomy with lymph node dissection.
  2. Renal-sparing surgery with lymph node dissection.

Radical nephrectomy with lymph node dissection

The primary treatment for RCC includes total surgical removal of the kidney and associated lymph nodes.[27]

Renal-sparing surgery with lymph node dissection

Renal-sparing surgery may be considered for carefully selected patients with low-volume localized disease. In two small series, patients who had partial nephrectomies seemed to have outcomes equivalent to those who had radical nephrectomies.[32,45]

Other approaches

As with adult RCC, there is no standard treatment for unresectable metastatic disease in children. The response to radiation is poor, and chemotherapy is not effective. Immunotherapy with such agents as interferon-alpha and interleukin-2 may have some effect on cancer control.[46,47] Spontaneous regression of pulmonary metastasis rarely occurs with resection of the primary tumor.
Several targeted therapies (e.g., sorafenib, sunitinib, bevacizumab, temsirolimus, pazopanib, axitinib, and everolimus) have been approved for use in adults with RCC; however, these agents have not been tested in pediatric patients with RCC. Case reports of pediatric and adolescent patients with TFE3 translocation–positive RCC suggest responsiveness to multiple tyrosine kinase inhibitors.[29,48,49] Disease regression and improvement in symptoms have been reported with the use of cabozantinib in pediatric patients with translocation-positive RCC expressing MET.[50] Any RCC that is positive for TFE3 and lacks a translocation should be tested for ALK expression and translocation. Recognition of this subtype may lead to consideration of ALK inhibitor therapy.[37]
(Refer to the PDQ summary on adult Renal Cell Cancer Treatment for more information about the use of targeted therapies.)

Treatment Options Under Clinical Evaluation for RCC

Information about National Cancer Institute (NCI)–supported clinical trials can be found on the NCI website. For information about clinical trials sponsored by other organizations, refer to the ClinicalTrials.gov website.
The following is an example of a national and/or institutional clinical trial that is currently being conducted:
  • AREN1721 (NCT03595124) (Axitinib and Nivolumab in Treating Participants With Unresectable or Metastatic TFE/Translocation RCC [tRCC]): TFE/tRCC is a distinct, typically translocation-associated RCC with characteristic morphology and immunohistochemical expression of TFE3 or TFEB. Nearly 50% of pediatric RCCs are tRCC, and it accounts for 1% to 5% of RCCs overall, typically in the adolescent and young adult population. This is the first prospective therapeutic study of patients with tRCC. Patients aged 12 months and older who have histologically confirmed unresectable TFE/tRCC or metastatic TFE/tRCC diagnosed using WHO-defined criteria are eligible. Patients may be newly diagnosed or have received previous cancer therapy and must have measurable disease. Patients will be randomly assigned at the time of enrollment to one of three therapeutic arms: axitinib, nivolumab, or a combination of axitinib and nivolumab.

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.
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