Ranga (Ranganathan)

40 statements · 4 topics

Liver Tumors (Hepatoblastoma/HCC) · guest expert

Featured statements

▶ Ep 16 · 1:03:19
Beta-catenin immunohistochemistry is frequently very weak positive or even negative in hepatocellular neoplasm NOS, which is a clue to diagnosis along with pleomorphic appearance and macrotrabecular arrangement.
clinical · Hepatoblastoma
▶ Ep 16 · 33:19
Once chemotherapy begins and the tumor gets replaced by pools of blood and fibrous tissue, there's nothing for the chemotherapy to kill, and the size doesn't decrease much further beyond a certain point.
clinical · Hepatoblastoma
▶ Ep 4 · 1:02:23
Conventional hepatoblastoma is genomically quiet with very low mutation burden and invariably has either a point mutation or small deletion in exon 3 of the CTNNB1 gene.
▶ Ep 4 · 1:03:51
Hepatocellular neoplasm NOS can be targeted with high-risk hepatoblastoma therapy to shrink tumors and make them amenable to surgery in most cases.

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Ranga's statements about Hepatoblastoma 8 statements

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Clinical & Research Update: Pediatric Liver Tumors - A Case-Based Discussion with Drs. Katherine Somers & Alex Bondoc

▶ Ep 16 · 30:05
quote the FIT trial, the AHP 1531 and the FIT trial actually mandated liver biopsy for diagnosis of the lesion before we start treatment. ↗
▶ Ep 16 · 30:05
guideline The FIT trial (AHEP 1531) mandated liver biopsy for diagnosis before starting treatment. ↗
▶ Ep 16 · 33:19
clinical Once chemotherapy begins and the tumor gets replaced by pools of blood and fibrous tissue, there's nothing for the chemotherapy to kill, and the size doesn't decrease much further beyond a certain point. ↗
▶ Ep 16 · 33:19
quote once chemotherapy begins and the tumor gets replaced by these pools of blood as well as fibrous tissue. There's nothing for the chemotherapy to kill. ↗
▶ Ep 16 · 1:02:23
clinical Conventional hepatoblastoma is genomically quiet with very low mutation burden and invariably has either a point mutation or small deletion in exon 3 of the CTNNB1 gene. ↗
▶ Ep 16 · 1:02:41
clinical Hepatocellular neoplasm NOS shows more genomic instability with chromosomal gains and losses, characterized by CTNNB1 deletion, often with large deletions or complete exon 3 skipping (exon 2 joined to exon 4). ↗
▶ Ep 16 · 1:03:19
clinical Beta-catenin immunohistochemistry is frequently very weak positive or even negative in hepatocellular neoplasm NOS, which is a clue to diagnosis along with pleomorphic appearance and macrotrabecular arrangement. ↗
▶ Ep 16 · 1:03:51
clinical Hepatocellular neoplasm NOS can be targeted with high-risk hepatoblastoma therapy to shrink tumors and make them amenable to surgery in most cases. ↗
Ranga's statements about Hepatocellular Carcinoma 8 statements

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Clinical & Research Update: Pediatric Liver Tumors - A Case-Based Discussion with Drs. Katherine Somers & Alex Bondoc

▶ Ep 4 · 30:05
guideline The FIT trial (AHEP 1531) mandated liver biopsy for diagnosis before starting treatment. ↗
▶ Ep 4 · 30:05
quote the FIT trial, the AHP 1531 and the FIT trial actually mandated liver biopsy for diagnosis of the lesion before we start treatment. ↗
▶ Ep 4 · 33:19
clinical Once chemotherapy begins and the tumor gets replaced by pools of blood and fibrous tissue, there's nothing for the chemotherapy to kill, and the size doesn't decrease much further beyond a certain point. ↗
▶ Ep 4 · 33:19
quote once chemotherapy begins and the tumor gets replaced by these pools of blood as well as fibrous tissue. There's nothing for the chemotherapy to kill. ↗
▶ Ep 4 · 1:02:23
clinical Conventional hepatoblastoma is genomically quiet with very low mutation burden and invariably has either a point mutation or small deletion in exon 3 of the CTNNB1 gene. ↗
▶ Ep 4 · 1:02:41
clinical Hepatocellular neoplasm NOS shows more genomic instability with chromosomal gains and losses, characterized by CTNNB1 deletion, often with large deletions or complete exon 3 skipping (exon 2 joined to exon 4). ↗
▶ Ep 4 · 1:03:19
clinical Beta-catenin immunohistochemistry is frequently very weak positive or even negative in hepatocellular neoplasm NOS, which is a clue to diagnosis along with pleomorphic appearance and macrotrabecular arrangement. ↗
▶ Ep 4 · 1:03:51
clinical Hepatocellular neoplasm NOS can be targeted with high-risk hepatoblastoma therapy to shrink tumors and make them amenable to surgery in most cases. ↗
Ranga's statements about Liver Tumors (Hepatoblastoma/HCC) 16 statements

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Clinical & Research Update: Pediatric Liver Tumors - A Case-Based Discussion with Drs. Katherine Somers & Alex Bondoc

▶ Ep 17 · 30:05
guideline The FIT trial (AHEP 1531) mandated liver biopsy for diagnosis before starting treatment. ↗
▶ Ep 17 · 30:05
quote the FIT trial, the AHP 1531 and the FIT trial actually mandated liver biopsy for diagnosis of the lesion before we start treatment. ↗
▶ Ep 17 · 30:05
guideline The FIT trial (AHEP 1531) mandated liver biopsy for diagnosis before starting treatment. ↗
▶ Ep 17 · 30:05
quote the FIT trial, the AHP 1531 and the FIT trial actually mandated liver biopsy for diagnosis of the lesion before we start treatment. ↗
▶ Ep 17 · 33:19
clinical Once chemotherapy begins and the tumor gets replaced by pools of blood and fibrous tissue, there's nothing for the chemotherapy to kill, and the size doesn't decrease much further beyond a certain point. ↗
▶ Ep 17 · 33:19
clinical Once chemotherapy begins and the tumor gets replaced by pools of blood and fibrous tissue, there's nothing for the chemotherapy to kill, and the size doesn't decrease much further beyond a certain point. ↗
▶ Ep 17 · 33:19
quote once chemotherapy begins and the tumor gets replaced by these pools of blood as well as fibrous tissue. There's nothing for the chemotherapy to kill. ↗
▶ Ep 17 · 33:19
quote once chemotherapy begins and the tumor gets replaced by these pools of blood as well as fibrous tissue. There's nothing for the chemotherapy to kill. ↗
▶ Ep 17 · 1:02:23
clinical Conventional hepatoblastoma is genomically quiet with very low mutation burden and invariably has either a point mutation or small deletion in exon 3 of the CTNNB1 gene. ↗
▶ Ep 17 · 1:02:23
clinical Conventional hepatoblastoma is genomically quiet with very low mutation burden and invariably has either a point mutation or small deletion in exon 3 of the CTNNB1 gene. ↗
▶ Ep 17 · 1:02:41
clinical Hepatocellular neoplasm NOS shows more genomic instability with chromosomal gains and losses, characterized by CTNNB1 deletion, often with large deletions or complete exon 3 skipping (exon 2 joined to exon 4). ↗
▶ Ep 17 · 1:02:41
clinical Hepatocellular neoplasm NOS shows more genomic instability with chromosomal gains and losses, characterized by CTNNB1 deletion, often with large deletions or complete exon 3 skipping (exon 2 joined to exon 4). ↗
▶ Ep 17 · 1:03:19
clinical Beta-catenin immunohistochemistry is frequently very weak positive or even negative in hepatocellular neoplasm NOS, which is a clue to diagnosis along with pleomorphic appearance and macrotrabecular arrangement. ↗
▶ Ep 17 · 1:03:19
clinical Beta-catenin immunohistochemistry is frequently very weak positive or even negative in hepatocellular neoplasm NOS, which is a clue to diagnosis along with pleomorphic appearance and macrotrabecular arrangement. ↗
▶ Ep 17 · 1:03:51
clinical Hepatocellular neoplasm NOS can be targeted with high-risk hepatoblastoma therapy to shrink tumors and make them amenable to surgery in most cases. ↗
▶ Ep 17 · 1:03:51
clinical Hepatocellular neoplasm NOS can be targeted with high-risk hepatoblastoma therapy to shrink tumors and make them amenable to surgery in most cases. ↗
Ranga's statements about Pediatric Oncology 8 statements

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Clinical & Research Update: Pediatric Liver Tumors - A Case-Based Discussion with Drs. Katherine Somers & Alex Bondoc

▶ Ep 666 · 30:05
quote the FIT trial, the AHP 1531 and the FIT trial actually mandated liver biopsy for diagnosis of the lesion before we start treatment. ↗
▶ Ep 666 · 30:05
guideline The FIT trial (AHEP 1531) mandated liver biopsy for diagnosis before starting treatment. ↗
▶ Ep 666 · 33:19
clinical Once chemotherapy begins and the tumor gets replaced by pools of blood and fibrous tissue, there's nothing for the chemotherapy to kill, and the size doesn't decrease much further beyond a certain point. ↗
▶ Ep 666 · 33:19
quote once chemotherapy begins and the tumor gets replaced by these pools of blood as well as fibrous tissue. There's nothing for the chemotherapy to kill. ↗
▶ Ep 666 · 1:02:23
clinical Conventional hepatoblastoma is genomically quiet with very low mutation burden and invariably has either a point mutation or small deletion in exon 3 of the CTNNB1 gene. ↗
▶ Ep 666 · 1:02:41
clinical Hepatocellular neoplasm NOS shows more genomic instability with chromosomal gains and losses, characterized by CTNNB1 deletion, often with large deletions or complete exon 3 skipping (exon 2 joined to exon 4). ↗
▶ Ep 666 · 1:03:19
clinical Beta-catenin immunohistochemistry is frequently very weak positive or even negative in hepatocellular neoplasm NOS, which is a clue to diagnosis along with pleomorphic appearance and macrotrabecular arrangement. ↗
▶ Ep 666 · 1:03:51
clinical Hepatocellular neoplasm NOS can be targeted with high-risk hepatoblastoma therapy to shrink tumors and make them amenable to surgery in most cases. ↗