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1. pediatric tumors  dr. sinhasan, mdzah
 Important cause of death in young children
 Malignancies Need to distinguish from benign lesions
 Heterotopia / Choristoma
 Hamartoma
 Early diagnosis is the aim
 Treatment is better tolerated
NEOPLASTIC LESIONS:
 Hemangioma
 Lymphangioma
 Sacrococcygeal Teratoma
BENIGN TUMORS
 Most common Benign Tumor of Childhood
1. Capillary
2. Cavernous
 ? Malformations.. ? Hamartoma
 Majority are superficial lesions
 Malignant Transformation is very Rare
Hemangioma
 Site - Skin , Subcutaneous tissue , Mucosa of oral
cavity / lips
 Morphology:: Bright red - Blue , Few mm - few cms.
 Strawberry Hemangioma Present since Birth.
Capillary Hemangioma
1. pediatric tumors  dr. sinhasan, mdzah
Capillary Hemangioma
 Site - Skin , Mucosa , Viscera (Liver)
 Morphology  Red-Blue , compressible , Spongy , well
defined lesions , 2 - 3 cms
 Cavernous Lymphangioma - Cystic Hygroma
Cavernous Hemangioma
Cavernous Hemangioma: spleen
Cavernous Hemangioma
Lymphangioma
Lymphangioma
 Contains the tissues derived from all ectoderm,
endoderm and mesoderm.
 Skin is most commonly seen: hence the name dermoid
cyst.
 Any tissues can be seen: cartilage, bone, tooth, hair,
sebaceous glands, brain tissues…..etc.
 Most commonly seen in the midline structures.
Congenital Teratoma:
1. pediatric tumors  dr. sinhasan, mdzah
Teratoma
MALIGNANT TUMORS
0 TO 4 YRS 5 TO 9 YRS 10 TO 14 YRS
Leukemia Leukemia HCC
Retinoblastoma Retinoblastoma Soft tissue
sarcoma
Neuroblastoma Neuroblastoma Osteogenic
sarcoma
Wilm’s tumor HCC Thyroid carcinoma
Hepatoblastoma Soft tissue
sarcoma
HD
CNS tumors CNS, ES, NHL
 Histologically malignant pediatric tumors are alike
 Primitive embryonal morphology
 Sheets of small cells, scant cytoplasm, dense round nucleus
 SBRCT
 Neuroblastoma, Lymphoma, RMS, ES, Wilm’s tumor
1. pediatric tumors  dr. sinhasan, mdzah
 Most common solid tumor of childhood next to CNS
tumors
 Most occur below 5 yrs of age
 Tendency to regress spontaneously
 Head to toe  Sympathetic chain
 75% arise within abdomen Adrenals
 Can arise in brain, Head & neck
 Range in size
 Advanced tumors may invade the renal vein
 Grey-White, Soft, Friable, Large areas of hemorrhage,
Cystic, Calcification
 Tendency to metastasize early and invade adjacent
structures
MORPHOLOGY- NEUROBLASTOMA
 SBRCT
 Some areas of differentiation seen
 Homer-Wright pseudorosettes
 Some ganglion like cells  Maturation
 Ganglioneuroblastoma
 Ganglioneuroma  Better differentiated
 Presence of Schwann cell stroma
MICROSCOPY- NEUROBLASTOMA
 Protuberant abdomen, fever, weight loss
 Hepatomegaly, metastasis, bone pain
 Elevated blood levels of catecholamines: VMA
 Staging of the tumors & age of patient decides the prognosis
 Del (1p36) & amplification of N-myc oncogene  Bad
prognosis
CLINICAL FEATURES
 Mc Malignant tumor of eye in childhood
 Multifocal or Bilateral
 Spontaneous regression is noted, secondary primary
tumors possible
 Familial & Sporadic
 Rb gene mutation
RETINOBLASTOMA
RETINOBLASTOMA
 1 in 20000 infants and children
 60% Familial; 40% Sporadic
 Autosomal dominant trait
 Gene is present on chromosome 13q14,
 Loss of both alleles leads to Retinoblastoma
(deletions)
 Arise from neuroepithelial cell
 SBRCT
 Some differentiated structures may be present
 Flexner- Wintersteiner rosettes
 Unlike pseudorosettes
 Dissemination by Optic nerve  CNS. Skull bones, LN.
MORPHOLOGY
 Median age at presentation is 2 yrs
 Poor vision, strabismus, Leukocoria (Cat’s eye reflex)
 Rx: Enucleation
 Spontaneous regression, with or without Rx is also noted
 Secondary tumors like OS & Soft tissue sarcomas.
CLINICAL FEATURES
1. pediatric tumors  dr. sinhasan, mdzah
 Most common renal tumour in children
 10 / million, under 15 yrs,
 Common age – 2 to 5 yrs,
 5 to 10% bilateral – synchronous or metachronous
Wilms tumour
PATHOGENESIS AND GENETICS:
1. WAGR syndrome: Aniridia, Genital anomalies, Mental
retardation .
2. Denys- Drash syndrome: Gonadal dysgenesis (male
Psuedohermaproditism)
3. Beckwith-Wiedmann syndrome: Organomegaly,
Macroglossia, Hemihypertrophy, Omphalocele, Adrenal
cytomegaly.
Wilms tumour
 Tissue features showing an attempt to recapitulate
nephrogenesis
 Triphasic Tumor:: Blastemal, Stromal, Epithelial
components +
 Sheets of small blue cells without differentiation-
Blastemal
 Fibromyxoid stromal component, Smooth muscle, cartilage
 Abortive tubules & Glomeruli
MICROSCOPY
 2 to 5 yrs common
 Palpable abdominal mass
 Hematuria,
 Pain,
 Intestinal obstruction,
 Hypertension
 Pulmonary metastases
Wilms tumour – Clinical Course
PROGNOSIS
 Very Good,
 Nephrectomy + chemotherapy,
 2 yrs survival – 90%
 Prone for second primary tumours.
Wilms tumour – Clinical Course
1. pediatric tumors  dr. sinhasan, mdzah

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3. bleeding disorders dr. sinhasan- mdzah
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2. thrombosis, embolism, infarction dr. sinhasan- mdzah
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1. pediatric tumors dr. sinhasan, mdzah

  • 2.  Important cause of death in young children  Malignancies Need to distinguish from benign lesions  Heterotopia / Choristoma  Hamartoma  Early diagnosis is the aim  Treatment is better tolerated NEOPLASTIC LESIONS:
  • 3.  Hemangioma  Lymphangioma  Sacrococcygeal Teratoma BENIGN TUMORS
  • 4.  Most common Benign Tumor of Childhood 1. Capillary 2. Cavernous  ? Malformations.. ? Hamartoma  Majority are superficial lesions  Malignant Transformation is very Rare Hemangioma
  • 5.  Site - Skin , Subcutaneous tissue , Mucosa of oral cavity / lips  Morphology:: Bright red - Blue , Few mm - few cms.  Strawberry Hemangioma Present since Birth. Capillary Hemangioma
  • 8.  Site - Skin , Mucosa , Viscera (Liver)  Morphology  Red-Blue , compressible , Spongy , well defined lesions , 2 - 3 cms  Cavernous Lymphangioma - Cystic Hygroma Cavernous Hemangioma
  • 13.  Contains the tissues derived from all ectoderm, endoderm and mesoderm.  Skin is most commonly seen: hence the name dermoid cyst.  Any tissues can be seen: cartilage, bone, tooth, hair, sebaceous glands, brain tissues…..etc.  Most commonly seen in the midline structures. Congenital Teratoma:
  • 16. MALIGNANT TUMORS 0 TO 4 YRS 5 TO 9 YRS 10 TO 14 YRS Leukemia Leukemia HCC Retinoblastoma Retinoblastoma Soft tissue sarcoma Neuroblastoma Neuroblastoma Osteogenic sarcoma Wilm’s tumor HCC Thyroid carcinoma Hepatoblastoma Soft tissue sarcoma HD CNS tumors CNS, ES, NHL
  • 17.  Histologically malignant pediatric tumors are alike  Primitive embryonal morphology  Sheets of small cells, scant cytoplasm, dense round nucleus  SBRCT  Neuroblastoma, Lymphoma, RMS, ES, Wilm’s tumor
  • 19.  Most common solid tumor of childhood next to CNS tumors  Most occur below 5 yrs of age  Tendency to regress spontaneously  Head to toe  Sympathetic chain  75% arise within abdomen Adrenals  Can arise in brain, Head & neck
  • 20.  Range in size  Advanced tumors may invade the renal vein  Grey-White, Soft, Friable, Large areas of hemorrhage, Cystic, Calcification  Tendency to metastasize early and invade adjacent structures MORPHOLOGY- NEUROBLASTOMA
  • 21.  SBRCT  Some areas of differentiation seen  Homer-Wright pseudorosettes  Some ganglion like cells  Maturation  Ganglioneuroblastoma  Ganglioneuroma  Better differentiated  Presence of Schwann cell stroma MICROSCOPY- NEUROBLASTOMA
  • 22.  Protuberant abdomen, fever, weight loss  Hepatomegaly, metastasis, bone pain  Elevated blood levels of catecholamines: VMA  Staging of the tumors & age of patient decides the prognosis  Del (1p36) & amplification of N-myc oncogene  Bad prognosis CLINICAL FEATURES
  • 23.  Mc Malignant tumor of eye in childhood  Multifocal or Bilateral  Spontaneous regression is noted, secondary primary tumors possible  Familial & Sporadic  Rb gene mutation RETINOBLASTOMA
  • 24. RETINOBLASTOMA  1 in 20000 infants and children  60% Familial; 40% Sporadic  Autosomal dominant trait  Gene is present on chromosome 13q14,  Loss of both alleles leads to Retinoblastoma (deletions)
  • 25.  Arise from neuroepithelial cell  SBRCT  Some differentiated structures may be present  Flexner- Wintersteiner rosettes  Unlike pseudorosettes  Dissemination by Optic nerve  CNS. Skull bones, LN. MORPHOLOGY
  • 26.  Median age at presentation is 2 yrs  Poor vision, strabismus, Leukocoria (Cat’s eye reflex)  Rx: Enucleation  Spontaneous regression, with or without Rx is also noted  Secondary tumors like OS & Soft tissue sarcomas. CLINICAL FEATURES
  • 28.  Most common renal tumour in children  10 / million, under 15 yrs,  Common age – 2 to 5 yrs,  5 to 10% bilateral – synchronous or metachronous Wilms tumour
  • 29. PATHOGENESIS AND GENETICS: 1. WAGR syndrome: Aniridia, Genital anomalies, Mental retardation . 2. Denys- Drash syndrome: Gonadal dysgenesis (male Psuedohermaproditism) 3. Beckwith-Wiedmann syndrome: Organomegaly, Macroglossia, Hemihypertrophy, Omphalocele, Adrenal cytomegaly. Wilms tumour
  • 30.  Tissue features showing an attempt to recapitulate nephrogenesis  Triphasic Tumor:: Blastemal, Stromal, Epithelial components +  Sheets of small blue cells without differentiation- Blastemal  Fibromyxoid stromal component, Smooth muscle, cartilage  Abortive tubules & Glomeruli MICROSCOPY
  • 31.  2 to 5 yrs common  Palpable abdominal mass  Hematuria,  Pain,  Intestinal obstruction,  Hypertension  Pulmonary metastases Wilms tumour – Clinical Course
  • 32. PROGNOSIS  Very Good,  Nephrectomy + chemotherapy,  2 yrs survival – 90%  Prone for second primary tumours. Wilms tumour – Clinical Course