Osteosarcoma is a primary malignant bone tumor. Effective chemotherapy regimens for refractory disease are scarce, accounting for no improvement in survival. Immune-based cell therapies have emerged as novel alternatives. However, advancements with these therapies have been seen mostly when immune cells are armed to target specific tumor Ags. Recent studies identified cluster of differentiation 70 (CD70) as a promising target to osteosarcoma particularly because CD70 is highly expressed in osteosarcoma lung metastases (Pahl et al. 2015. Cancer Cell Int. 15: 31), and its overexpression by tumors has been correlated with immune evasion and tumor proliferation (Yang et al. 2007. Blood 110: 2537–2544). However, the limited knowledge of the overall CD70 expression within normal tissues and the potential for off-target effect pose several challenges (Flieswasser et al. 2022. J. Exp. Clin. Cancer Res. 41: 12). Nonetheless, CD70-based clinical trials are currently ongoing and are preliminarily showing promising results for patients with osteosarcoma. The present review sheds light on the recent literature on CD70 as it relates to osteosarcoma and highlights the benefits and challenges of targeting this pathway.

Pediatric patients with cancer experience significant distress from both treatment and cancer-related pain. Careful selection of an analgesic regimen should be based upon individual patient factors, including the level of pain, response to therapy, and physiologic profile. Refractory pain is a therapeutic dilemma frequently encountered in the pediatric cancer setting. Systemic lidocaine infusions have been described as both safe and efficacious, as prior studies show patients reporting decreased pain scores and improved quality of life after lidocaine treatment. Given the favorable side effect profile of lidocaine, it has the potential to be considered for analgesia in the setting of refractory pain. This review discusses the use of systemic lidocaine infusions for analgesia in pediatric oncology patients with cancer-related pain.

In the vast majority of human populations, the gene encoding CASPASE-12 (CASP12) has a premature termination codon that precludes the production of protein. However, approximately 20% of persons of recent African descent have a single nucleotide polymorphism (#rs497116; A->G) that turns the stop codon into one encoding Arg. The subsequent functional allele is a risk factor for sepsis as it uniquely downregulates inflammatory cytokines in African-Americans (AA). To determine if CASP12 could be protective for systemic lupus erythematosus (SLE) in AA, we genotyped AA SLE patients and controls. There was a weak association between CASP12 genotype with the absence of anti-dsDNA autoantibodies in SLE patients. No effect was seen upon serum interleukin-1 beta levels, nor was any other protective effect noted for the CASP12 genotype, whether upon association with SLE, or any of the 11 American College of Rheumatology classification criteria. CASP12 genotype thus does not influence the phenotype of SLE in AA.

Stenotrophomonas maltophilia is a bacterial pathogen that can be fatal in hospitalized and immunocompromised patients with mortality as high as 69%. Risk factors for infection include those apparent in many pediatric cancer patients. Treatment is challenging as S. maltophilia is resistant to several antibiotics. Furthermore, the presentation of soft tissue infection in neutropenic patients may be atypical. We present three immunocompromised pediatric patients with S. maltophilia infections. All three cases were fatal. We hope our experience at MD Anderson can guide providers to diagnose and properly treat Stenotrophomonas infection, as timely treatment may improve morbidity and mortality.