CBL (Cbl proto-oncogene)

CN-LOH was confirmed by single nucleotide polymorphism array. This patient presented with an aggressive clinical course and required an allogeneic stem cell transplant.

To the best of our knowledge, this is the first example of genetically confirmed TGCT in the nasal cavity. Our study broadens the anatomical spectrum of TGCT and highlights the inclusion of TGCT in the differential diagnosis of nasal cavity lesions.

Our findings identify CBL as a functional tumor suppressor in NSCLC that exerts its anti-cancer effects via ubiquitin-mediated degradation of KDR. The CBL-KDR axis signifies a new regulatory route with significant therapeutic potential for NSCLC therapy.

MSC-derived exosomal CBLB has therapeutic potential in ameliorating the progression of IP probably by ubiquitinating MAPK14, which could lead to novel clinical interventions for treating this condition.

CBL-mediated AQP1 ubiquitination aggravates KYDS by promoting lipid metabolism dysregulation, offering promising insights for targeted therapeutic interventions.

c.2213A > G mutation on the CBLB gene causes a new type of inherited thrombocytopenia, and the potential pathogenesis involves an imbalance in cellular immunity and excessive ferroptosis of megakaryocytes.

In vitro and in vivo studies showed that siRNA against cblb caused an effective inhibition of tumor progression in subcutaneous B16-F10 and LLC models, in which a significant increase of effector T cells in peripheral blood mononuclear cells and an increase of effector T cells and a significant decrease of Treg cells in the tumor were clearly observed. This polymersome-mediated down-regulation of the cblb gene in T cells provides a promising approach for activating T cells and enhancing their anti-tumor capacity.

CBL syndrome can present with severe EBV infection early in life. RCD masquerading as severe panuveitis is also a possible feature of CBL syndrome. RCD should be kept in mind in patients with this syndrome who present with idiopathic intraocular inflammation and are refractory to IMT. Carbonic anhydrase inhibitors (CAI) should be tried early to treat CME.

c-CBL alleviated asthma and suppressed Th2 differentiation by facilitating LCK ubiquitination, interrupting c-JUN activation and CD28 expression in vivo and in vitro. c-CBL/LCK/c-JUN/ETS1/CD28 axis was partially involved in childhood asthma, and may provide novel insights for clinical treatment for asthma.

She was treated with modified Ph-negative EWALL induction (Vincristine, Idarubicin, dexamethasone) and achieved a complete remission. However, she subsequently experienced an early relapse and was refractory to targeted therapy with blinatumomab. After treatment with inotuzumab ozogamicin, she achieved a second complete remission...It demonstrates that patients with ostensibly favourable prognostic factors may experience poor response rates to traditional chemotherapy as well as targeted salvage agents. It also illustrates the challenges of treating B-ALL in the elderly population.

At the molecular level, METTL14 could improve the stability and expression of CBLN4 mRNA via m6A methylation. Our findings indicated that m6A methylase METTL14-mediated upregulation of CBLN4 mRNA stability could repress Aβ1-42-triggered SK-N-SH cell injury, providing a promising therapeutic target for AD treatment.

PD-1/LAG-3 co-blockade inhibited CBL-B expression, while the use of a bispecific drug in clinical development also repressed C-CBL expression, which reverted T-cell dysfunctionality in lung cancer patients resistant to PD-L1/PD-1 blockade. The combination of CBL-B-specific small molecule inhibitors with anti-PD-1/anti-LAG-3 immunotherapies demonstrated notable therapeutic efficacy in models of lung cancer refractory to immunotherapies, overcoming PD-1/LAG-3 mediated resistance.