Background/Aim: The utility of nanoparticle albumin-bound paclitaxel (nab-PTX) monotherapy in patients with relapsed small-cell lung cancer (SCLC) has not been fully evaluated. We aimed to investigate the efficacy and safety of nab-PTX monotherapy in relapsed SCLC patients, including heavily treated patients. Patients and Methods: We retrospectively analysed data from 17 patients with relapsed SCLC who were treated with weekly nab-PTX monotherapy at our hospital. We also reviewed past studies on nab-PTX monotherapy for relapsed SCLC. Results: The response rate, progression-free survival, and overall survival were 29. 4%,, respectively. The most common adverse event of grade ≥3 was leukopenia (17.6%), followed by neutropenia, neuropathy, fatigue, and infections. Our results were consistent with previous studies. Conclusion: The efficacy of nab-PTX monotherapy for heavily treated relapsed SCLC patients might be moderate. Further studies to improve outcomes are warranted.

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There are only a limited number of previous reports on clinical cases using tumour tracking with tomotherapy. Therefore, we present two cases of patients treated with tumour tracking with tomotherapy. First, a 74-year-old man with an inoperable lung cancer type T1bN0M0 underwent stereotactic body radiotherapy at a total dose of 48 Gy in four fractions. Second, a 68-year-old man with hepatocellular carcinoma with a portal venous tumour thrombosis and history of liver stereotactic body radiotherapy with fiducial marker implantation received radiotherapy at a total dose of 48 Gy in 20 fractions. The results of patient-specific quality assurance and tracking radiotherapy were sufficient to irradiate tumours. Tumour tracking with tomotherapy successfully delivered radiation in a total of 24 treatment fractions in both patients. Tumour tracking with tomotherapy is feasible in lung and liver cancer treatment. This study’s findings suggest the clinical use of tumour tracking with tomotherapy.

The osteosclerotic (oc/oc) mouse, a genetically distinct murine mutation that has a functional defect in its osteoclasts, also has rickets and shows an altered endochondral ossification in the epiphyseal growth plate. The disorder is morphologically characterized by an abnormal extension of hypertrophic cartilage at 10 days after birth, which is later (21 days after birth) incorporated into the metaphyseal woven bone without breakdown of the cartilage matrix following vascular invasion of chondrocyte lacunae. In situ hybridization revealed that the extending hypertrophic chondrocytes expressed type I and type II collagen mRNA, as well as that of type X collagen and that the osteoblasts in the metaphysis expressed type II and type X collagen mRNA, in addition to type I collagen mRNA. The topographic distribution of the signals suggests a possible co-expression of each collagen gene in the individual cells. Immunohistochemically, an overlapping deposition of type I, type II, and type X collagen was observed in both the extending cartilage and metaphyseal bony trabeculae. Such aberrant gene expression and synthesis of collagen indicate that pathologic ossification takes place in the epiphyseal/metaphyseal junction of oc/oc mouse femur in different way than in normal endochondral ossification. This abnormality is probably not due to a developmental disorder in the epiphyseal plate but to the failure in conversion of cartilage into bone, since the epiphyseal plate otherwise appeared normal, showing orderly stratified zones with a proper expression of cartilage-specific genes.

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