MYC (V-myc avian myelocytomatosis viral oncogene homolog)

These findings highlight STC2 as a key regulator of CRC progression, which regulates c-Myc-driven glycolysis through the PI3K/AKT/mTOR pathway. Targeting STC2 or its downstream metabolic effectors may provide new therapeutic strategies for CRC management.

The patient demonstrated only a transient response to initial therapy with R-CHOP plus bortezomib, following which she had rapid disease progression, resulting in an overall survival of 10 months. It also provides important insights into the biology of DLBCL-to-PBL evolution. These findings highlight the need for more precise molecular diagnostic tools and novel approaches to improve outcomes for patients with such highly aggressive lymphoma.

EBV-positive DLBCL is a rare group of highly aggressive lymphomas with predominantly ABC subtypes, with a high overall morbidity and mortality. The expression of EBER and the ECOG score were associated with DLBCL prognosis.

We recently completed a clinical trial in dogs with DLBCL using a combination of canine anti-CD20 antibody and low dose doxorubicin followed by one of three small molecule immune-modulating agents (KPT-9274, TAK-981 or RV1001). To facilitate point-of-care PBMC gene expression testing that could be used to distinguish those dogs likely to require more intensive treatment regimens in advance of relapse, we developed qPCR assays for TBHD, NPNT and ISG20. Together these data provide proof of principle that biomarker interrogation in PBMCs can help predict early relapse and poor responders to inform clinical management of DLBCL.

Proximity ligation assays indicate that both cMYC and MYCN are in close proximity to CDCA2 in vivo. Furthermore, we have shown that CDC2A is a bona fide MYC target gene in cancer cells, revealing a reciprocal regulatory loop that could be exploited for therapeutic purposes.

Despite broadly altered histone methylation, genetically or pharmacologically normalizing MYC completely restored neuronal differentiation. These data indicated that a primary metabolic disturbance activated MYC to favor self-renewal and suppress neuronal lineage commitment.

Crucially, MYC silencing restored the expression of core circadian clock genes. Our findings unveil a promising RNAi-based strategy that concurrently targets MYC-driven tumorigenesis, corrects circadian dysfunction, and reinstates antitumor immunity, presenting a multifaceted therapeutic approach for NSCLC.

Among them, 35 patients received BTKi (zanubrutinib, orelabrutinib, acalabrutinib) combined with R-CHOP (BTKi + R-CHOP group) , and 60 received R-CHOP regimen alone (R-CHOP group) . Grade ≥ 3 adverse events primarily included neutropenia (28.6% ) and pulmonary infection (14.3% ) ; no fatal bleeding or cardiovascular events occurred. BTKi combined with R-CHOP significantly improved response rates and survival in patients with DE-DLBCL, with manageable safety.

Although benign, APRVP carries a 16-46% risk of recurrence or further development of new lesions, recommending long-term surveillance. Future research priorities include identifying predictive biomarkers and establishing evidence-based management protocols for this increasingly recognized complication of breast cancer treatment.

The diagnosis of SSLd appears to have good reproducibility among pathologists and positive diagnostic trends that are observed in recent years. MLH1 is the only IHC marker with robust clinical utility to identify SSLd that do not meet the morphologic criteria for overt dysplasia but should be used only in selected cases due to its low prevalence.

This study presents the first integrated molecular and functional analyses of patient tumors and matched organoid and xenograft models in cervical SCNEC. These models offer robust resources for mechanistic studies and may enable precision therapeutic strategies for this rare malignancy.

The review is structured in two sections, the first introducing the IBDs and the homeostatic mechanisms that preserve integrity and prevent colorectal neoplasia. The second section compares failure modes in sporadic and colitic settings and describes the differences in the resulting neoplasms.