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Lung Cancer FISH Probes


ALK is recurrently rearranged in NSCLC, usually via ALK/EML4 fusion, but several other rearrangements have been detected. ALK translocations occur in 2-7% of NSCLC, where they're more prevalent in Asian populations than western, with a predilection for younger never-smokers.


EML4/ALK fusion produces an oncogenic tyrosine kinase found in 4-5% of NSCLC. The fusion is generated by a small inversion in the p arm of chromosome 2. EML4/ALK undergoes constitutive dimerization via interaction between the coiled coil domain in the EML4 portion of the chimera.


BCL2 family proteins are key regulators of apoptosis, and excess BCL2 likely contributes to tumor cell survival. BCL2 overexpression has been detected in multiple solid tumors, but is particularly prevalent in small-cell lung cancer (SCLC).


BRAF mutations are found in about 5% of lung adenocarcinomas. The two main types of mutations, V600E and non-V600E, have been shown to affect different patient groups, and are each associated with specific morphological and clinical features.


CCND1 is amplified and its protein frequently overexpressed in lung cancer tumors and pre-invasive bronchial lesions. CCND1's many oncogenic effects in include promoting tumor cell growth, migration, invasion, and EMT transition.


ROS1 rearrangements lead to constitutive activation and drive malignant transformation in NSCLC. Of the ROS1 fusions so far detected in NSCLC, CD74-ROS1 is the most frequent. A recent study showed that the fusion increases expression of TWIST1, a known EMT regulator in NSCLC.


Studies have shown that CDK4 is amplified in about 4% of lung cancers. The gene is involved in the RB1/CCND1/CDKN2A pathway that regulates G1-S transition, which is damaged in nearly all lung tumors.


Aberrant activity of the tyrosine kinase EGFR inhibits tumor cell apoptosis and contributes to tumor progression. EGFR may also interact with the integrin pathway and activate matrix metalloproteinases, stimulating cellular adhesion, cell motility/invasion, and promoting metastasis.


ERBB2 amplification occurs in 10-20% of NCSLC patients. The oncogene encodes a growth factor tyrosine kinase receptor that activates intracellular signal transduction pathways required for tumor cell proliferation.


High-level amplification of FGFR1 is frequent in squamous cell lung cancer of smokers, occurring in up to 10% of patients (compared to just 1% in other lung cancer subtypes). The abnormality is essential for tumor growth and survival, and, interestingly, occurs exclusively of the other mutation considered a biomarker for squamous cell lung cancer: SOX2 amplification.


HMGA2 encodes a member of the high motility group (HMG) protein family, which is widely expressed in undifferentiated mesenchymal tissues. The gene has been shown to contribute to lung cancer development via regulation of proliferation, metastasis, and EMT transition.


KIF5B-RET is a recently identified fusion generated by the chromosome inversion inv (10) (p11; q11). In lung cancer, the abnormality is more frequent in non-smokers and adenocarcinomas, and promotes tumor cell growth via STAT3 activation.


Amplification of the 4q12 chromosomal region, which contains both KIT and PDGFRA, is present in approximately 4% of NSCLC cases, and is more prevalent in ALK positive patients. KIT amplification has been shown to contribute TRK inhibitor resistance.


Between 15% and 25% of NSCLC patients harbor KRAS mutations, with more than 97% of these cases affecting KRAS exons 2 and 3. KRAS mutations are more prevalent in lung adenocarcinomas, white populations, and patients with a history of smoking.


Amplification of MET, which encodes the receptor for hepatocyte growth factor, leads to growth, invasion, and metastatic advantage in lung cancer cells. The tyrosine kinase has been found amplified in up to 4% of lung cancers.


NTRK1 rearrangements are found in in 1-3% of NSCLC patients. These translocations produce oncogenic fusions that induce constitutive activation of the NTRK kinase domain. Inhibition of NTRK signaling has generated dramatic responses in several tumor types, including lung.


PD-L1 encodes an immune receptor overexpressed by tumor cells as a means of avoiding T-cell detection. In NSCLC, this resistance mechanism is mediated by a pathway of preliminary genetic events specific to lung cancer; EGFR mutations, ALK rearrangements, and PTEN loss all induce PD-L1 overexpression in these tumors.


The chromosome 3q26 region containing PIK3CA is frequently amplified in lung cancer. Copy number gains occur at much higher frequencies than activating mutations, and appear to target squamous cell carcinoma, where they often appear as the sole genetic alteration.


The tumor suppressor PTEN negatively regulates the PI3K/mTOR/Akt oncogenic signaling pathway in lung cancer, and also helps maintain chromosomal integrity and DNA repair. PTEN gene alterations are found in approximately 2-7% of lung cancers.


RET rearrangements are rare but recurrent in NSCLC, occurring in 1-2% of cases. The gene has been found fused to several different genes in NSCLC. Nearly all of RET's fusion partners are found on chromosome 10, so appear to be generated primarily by intrachromosomal rearrangements.


ROS1 translocations are found in about 1% of NSCLC patients. Similar to ALK rearrangements, they are more prevalent in light or never-smokers. Rearrangements generate fusion proteins with the entire tyrosine kinase of ROS1, which becomes constitutively activated to drive cellular transformation.


The 15p15.33 locus on which TERT is found is frequently amplified in NSCLC. TERT's encoded protein regulates telomerase activity, which plays a direct role in early oncogenic transformation by stabilizing cancer cell telomere size, sustaining their unlimited growth.


VEGFR2 has been shown to contribute to tumor initiation, infiltration, and metastasis in NSCLC. As a major regulator of angiogenic development, it likely aids in the production of tumor vascular architecture.


WT1 and STAT3 synergistically stimulate the growth of NSCLC cells by up-regulating the cell cycle regulators Cyclin D1 and p-pRb. Overexpression of the gene may also potentially drive EMT via EMT-related targets, like Snail, Slug, and E-cadherin.


WWTR1 has been shown to upregulate cell proliferation and downregulate apoptosis in lung cancer cells. The oncogene accomplishes this via regulation of the cyclin A and CTGF proteins, which mediate cell cycle transition and cancer cell migration/invasion, respectively.