Wilms Tumor Ppt New Guide

Wilms Tumor PPT New: A Modern Guide to Presentation, Diagnosis, and Treatment Updates

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Slide 3: Genetics & Associated Syndromes

• Sporadic vs. Syndromic: ~10% of cases are associated with congenital anomalies/syndromes.
• Key Genes:
  • WT1 (Chromosome 11p13): Tumor suppressor gene.
  • WT2 (Chromosome 11p15): Related to Beckwith-Wiedemann syndrome (IGF2 overexpression).
• Syndromes Table:
  • WAGR Syndrome: Wilms tumor, Aniridia, Genitourinary anomalies, intellectual disability (Range).
  • Beckwith-Wiedemann Syndrome: Hemihypertrophy, macroglossia, omphalocele. High risk of WT.
  • Denys-Drash Syndrome: WT, pseudohermaphroditism, renal failure (glomerular disease).
• Screening: High-risk patients (syndromic) require serial ultrasounds every 3–6 months until age 8.

Write-Up: Wilms Tumor – A New PowerPoint Presentation

Slide 5: Diagnostic Workup

• Imaging (gold standard):
  • Abdominal ultrasound: Solid intrarenal mass +/- hydronephrosis.
  • CT with contrast: Heterogeneous mass, "claw sign" (renal origin), vascular invasion (IVC/renal vein), lymphadenopathy.
  • Chest CT: Rule out lung metastases (most common site).
• Labs:
  • CBC, renal function, LFTs, urinalysis.
  • No specific tumor marker.
• Tissue diagnosis: Biopsy not routine – diagnosis made by imaging + nephrectomy (except if bilateral or unresectable).

Slide 8: Surgery – Precision Renal Surgery in 2025

• Transperitoneal approach – full exploration of contralateral kidney.
• Lymph node sampling mandatory – at least 7 nodes (hilar, para-aortic, perirenal).
• Avoid tumor spillage – upstages to Stage III.

Minimally invasive surgery (MIS): Laparoscopic nephrectomy for Stage I tumors (<500g, no IVC thrombus) is now acceptable in selected centers (new data 2024 shows equivalent outcomes). wilms tumor ppt new

Genetics and Pathogenesis

• Common genetic alterations:
  • WT1 (chromosome 11p13) — tumor suppressor; mutated in some familial and sporadic cases.
  • WT2/IGF2 region (11p15) — imprinting abnormalities linked to Beckwith–Wiedemann.
  • CTNNB1 (β-catenin) mutations in subset.
  • WTX (AMER1) on X chromosome.
• Pathogenesis: Abnormal persistence and proliferation of metanephric blastema and abortive differentiation lead to tumor formation. Histology may show triphasic pattern: blastemal, epithelial, stromal components.