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Difference between revisions of "Libre Pathology talk:Study Group"
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Libre Pathology talk:Study Group (view source)
Revision as of 16:20, 14 May 2015
, 16:20, 14 May 2015no edit summary
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{{hidden|What are the three most common molecular alterations of Lung Adenocarcinoma|[[KRAS 23%, EGFR 15%, TP53 5%]]}} | {{hidden|What are the three most common molecular alterations of Lung Adenocarcinoma|[[KRAS 23%, EGFR 15%, TP53 5%]]}} | ||
{{hidden|What is the most common molecular alteration makes patients with EGFR mutations resistant to targetted therapies?|[[T790M]]}} | {{hidden|What is the two most common molecular alteration makes patients with EGFR mutations resistant to targetted therapies?|[[KRAS (primary) and T790M (primary and acquired)]]}} | ||
{{hidden|List two EGFR kinase inhibitors.|[[Gefitinib/Iressa, Erlotinib/Tarceva]]}} | {{hidden|List two EGFR kinase inhibitors.|[[Gefitinib/Iressa, Erlotinib/Tarceva]]}} | ||
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{{hidden|What are the three most common cancers associated with BRAF mutations?|[[Melanoma 70%, Papillary Thyroid Carcinoma 50%, Ovarian serious carcinoma 30%, Colon cancer 10%, Hint Papillary architecture]]}} | {{hidden|What are the three most common cancers associated with BRAF mutations?|[[Melanoma 70%, Papillary Thyroid Carcinoma 50%, Ovarian serious carcinoma 30%, Colon cancer 10%, Hint Papillary architecture]]}} | ||
{{hidden| | {{hidden|Beta catenin/CTNNB1 expression is found with which histological pattern of lung adenocarcinoma?|[[Low grade adenocarcinoma of fetal type, poor px, <40yo, and has glycogen rich glandular formations, may occur in FAP patients]]}} | ||
{{hidden|What is the most common ALK rearrangement found in NSCLC?|[[EML4-ALK (90% of the 13% of lung cancers found to due to ALK fusions)]]}} | |||
{{hidden|List some pros and cons of ALK FISH.|[[Pros: commercial FDA approved probes available, not too expensive, moderately easy to disseminate screening, clinically validated, and failed tests on poorly preserved tissues are not reported as negative. Cons: need fish lab expertise (including pathologist and PhD), can be tricky if genes are close]]}} | |||
{{hidden|List some pros and cons of ALK IHC.|[[Pros: fast, cheap, easy to disseminate screening, Cons: commercial antibodies sub-optimal, poorly preserved tissues (esp bx) may give false negative results due to loss of antigenicity, no internal control]]}} | |||
{{What is a positive count in the ALK-FISH?|[[Signal split >2 probe diameters]]}} | |||
===CAP Molecular Diagnosis of AML=== | |||
{{hidden|List 6 genes associated with Acute Myeloid Leukemia that have been identified by cloning translocation break points|[[RUNX1, RUNX1T1, PML, CBFB, ETV6, MLL]]}} | |||
{{hidden|List the 5 main categories of classification of Acute Myeloid Leukemia|[[1. AML with recurrent genetic abnormalities, 2. AML with myelodysplasia-related changes, 3. Therapy related myeloid neoplasms, 4. AML, NOS, 5. Myeloid sarcoma]]}} | |||
{{hidden|Give any three translocations identified in AML.|[[t(8,21), inv (16), t(15,17), t(9,11), t(6,9), inv(3), t(1,22), mutated NPM1, mutated CEBPA]]}} | |||
{{hidden|What entities are fall under the AML, NOS classification?|[[ AML with minimal differentiation, AML without maturation, AML with maturation, Acute myelomonocytic leukemia, Acute monoblastic/monocytic leukemia, Acute erythroid leukemias (pure erythroid, erythroleukemia, erythroid/myeloid), Acute Megakaryoblastic leukemia, Acute basophilic leukemia, Acte panmyelosis with myelofibrosis]]}} | |||