Aceon, Invader UGT1A1 Molecular Assay

Ascaridiosis is a very important parasitic disease of birds, it is caused by Ascaridia. This study was conducted to identify the Ascaridia species by microscopic and molecular assay in Baghdad city. One hundred and sixty fecal samples were collected from domestic pigeons during the period from 1/1/ 2019 to 31/3/ 2019. Results showed that the rate of infection for Ascaridia spp. 15.62% by microscopic examination. Significant difference was observed in infection rates between males and females pigeons. Fifty samples randomly selected and subjected to molecular diagnosis of Ascaridia spp.. Molecular examination results, the total infection rate showed 16%(8/50). The eight positive PCR products were sequenced and deposited in Gene bank data base, phylogenic analysis demonstrated that 4 sequences belongs to Ascaridia galli ( MK918635.1, MK918636.1, MK918847.1, MK919081.1), while 2 (MK919199.1, MK919200.1) belong to Ascaridia nymphii and 2 (MK919207.1, MK919264.1) belong to Ascaridia numidae. It is the first study in Iraq to diagnosis of Ascaridia nymphii and Ascaridia numidae in domesticed pigeons by using conventional PCR.

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HGG-48. ROS1 INHIBITOR ENTRECTINIB USE IN RELAPSE/REFRACTORY INFANTILE GLIOBLASTOMA WITH POSITIVE ROS1 FUSION - A CASE REPORT WITH PROMISING RESPONSE

Neuro-Oncology ◽

10.1093/neuonc/noaa222.328 ◽

2020 ◽

Vol 22 (Supplement_3) ◽

pp. iii352-iii352

Author(s):

Dennis Tak-Loi Ku ◽

Matthew Ming-Kong Shing ◽

Godfrey Chi-Fung Chan ◽

Eric Fu ◽

Ping-Wa Yau ◽

...

Keyword(s):

Targeted Therapy ◽

Facial Nerve ◽

Nerve Palsy ◽

Facial Nerve Palsy ◽

Tumour Progression ◽

Molecular Study ◽

Subtotal Resection ◽

Residual Tumour ◽

Molecular Assay ◽

Debulking Surgery

Abstract INTRODUCTION Infantile glioblastoma is rare with poor prognosis. Recent molecular study for infantile hemispheric high grade glioma found its association with ALK/ROS1/NTRK/MET pathway. This suggested the potential use of targeted therapy for refractory / relapse patients. CASE: A newborn presented with apnea, CT brain showed intracranial haemorrhage. MRI then showed a left parietal tumour with bleeding and mass effect. Craniotomy achieved subtotal resection. Chemotherapy VCR/CPM alternating with CDDP/VP-16 was given for one year. Patient was stable with static residual tumour during chemotherapy. However patient developed status epilepticus two weeks after off treatment. MRI showed significant tumour progression which required 2nd & 3rd debulking surgery. Molecular assay by nanostring panel showed BRAF-KIAA1549 fusion. MEK inhibitor Trametinib was tried for 3 months and stopped as disease progression. Further molecular assay by RNASeq showed presence of ROS1 fusion (ZCCHC8-ROS1) while absent of BRAF fusion. Patient underwent 4th debulking surgery as impending herniation while waiting for the targeted therapy. It was complicated with right hemiplegia and facial nerve palsy postoperatively. Finally, ROS1 inhibitor Entrectinib was started 2 weeks later. It was well tolerated without significant adverse reaction. Patient made dramatic neurological recovery including improved facial nerve palsy, able to walk unaided and self feed. MRI brain 1 and 3 months after Entrectinib showed interval reduction in residual tumour. Patient is currently progression-free for 6 months. CONCLUSION Early molecular study for infantile glioblastoma is useful to guide novel therapy. Molecular result may varies between different panels or change over time, to be interpreted with caution.

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