News - CRKL amplification

2ms

Novel molecular subtypes of intracranial germ cell tumours expand therapeutic opportunities. (PubMed, Neuro Oncol)

Novel genomic aberrations and molecular subtypes were identified in IGCTs. These findings provide molecular basis for the potential introduction of new treatment strategies in this setting.

2 months ago

Journal

KRAS (KRAS proto-oncogene GTPase) • CRKL (CRK Like Proto-Oncogene, Adaptor Protein)

KRAS mutation • KRAS amplification • MTOR mutation • CRKL amplification

4ms

Characterization of two transcriptomic subtypes of marker-null large cell carcinoma of the lung suggests different origin and potential new therapeutic perspectives. (PubMed, Virchows Arch)

In conclusion, our study split the histological marker-null LCC into two different transcriptomic entities, with POU2F3, FOXI1, and AIM2 genes as differential expression markers that might be probed by immunohistochemistry for the differential diagnosis between Pure-LCC and ADLike-LCC. Finally, the identification of several signatures linked to replication stress in Pure-LCC and inflammasome complex in ADLike-LCC could be useful for designing new potential therapeutic approaches for these subtypes.

4 months ago

Journal

TP53 (Tumor protein P53) • RB1 (RB Transcriptional Corepressor 1) • KEAP1 (Kelch Like ECH Associated Protein 1) • CRKL (CRK Like Proto-Oncogene, Adaptor Protein) • POU2F3 (POU Class 2 Homeobox 3)

TP53 mutation • CRKL amplification

over1year

Genetic alterations of GI-NECs involving three main signaling pathways. (PubMed, Cancer Med)

Genetic alterations were very common in NECs and rare in NETs, and frequently involved three main signaling pathways. NEC patients harboring these genetic alterations may benefit from targeted therapy and PD-1/PD-L1 immunotherapy.

over 1 year ago

Journal • Tumor mutational burden • BRCA Biomarker • PD(L)-1 Biomarker • IO biomarker

TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • MSI (Microsatellite instability) • RB1 (RB Transcriptional Corepressor 1) • mTOR (Mechanistic target of rapamycin kinase) • CCNE1 (Cyclin E1) • MCL1 (Myeloid cell leukemia 1) • SMAD4 (SMAD family member 4) • ERBB4 (erb-b2 receptor tyrosine kinase 4) • SDHB (Succinate Dehydrogenase Complex Iron Sulfur Subunit B) • CRKL (CRK Like Proto-Oncogene, Adaptor Protein) • TGFB1 (Transforming Growth Factor Beta 1) • DDR2 (Discoidin domain receptor 2)

TP53 mutation • CCNE1 amplification • MTOR mutation • CRKL amplification

2years

Anatomic position determines oncogenic specificity in melanoma. (PubMed, Nature)

Abrogation of this CRKL-driven programme eliminated the anatomic specificity of acral melanoma. These data suggest that the anatomic position of the cell of origin endows it with a unique transcriptional state that makes it susceptible to only certain oncogenic insults.

2 years ago

Journal

BRAF (B-raf proto-oncogene) • CRKL (CRK Like Proto-Oncogene, Adaptor Protein)

BRAF mutation • CRKL amplification

2years

The genomic landscape of primary and secondary angiosarcomas, a rare heterogenous group of soft tissue sarcomas (AACR 2022)

We showed a clear distinction in genomic profiles of AS subgroups with specific pathogenic alterations. Especially secondary AS may benefit from treatment with ICI based on frequent MYC amplifications, DDR mutations, and high TMB. These data show clear evidence for the development of future treatment strategies with targeted therapy and ICI for this rare heterogeneous group of STS.

2 years ago

Late-breaking abstract • Tumor mutational burden

BRAF (B-raf proto-oncogene) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase) • FLT4 (Fms-related tyrosine kinase 4) • CRKL (CRK Like Proto-Oncogene, Adaptor Protein) • ERCC4 (ERCC Excision Repair 4, Endonuclease Catalytic Subunit)

TP53 mutation • TMB-H • BRAF mutation • MYC amplification • CRKL amplification

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