Application of Drug Testing Platforms in Circulating Tumor Cells and Validation of a Patient-Derived Xenograft Mouse Model in Patient with Primary Intracranial Ependymomas with Extraneural Metastases.

Primary intracranial ependymoma is a challenging tumor to treat despite the availability of multidisciplinary therapeutic modalities, including surgical resection, radiotherapy, and adjuvant chemotherapy. After the completion of initial treatment, when resistant tumor cells recur, salvage therapy needs to be carried out with a more precise strategy. Circulating tumor cells (CTCs) have specifically been detected and validated for patients with primary or recurrent diffused glioma.

Patient-Derived Tumor Chemosensitization of GKB202, an Mycelium-Derived Bioactive Compound.

Oral cancers, hepatocellular carcinoma, and colorectal cancers are the three most common cancers, leading to 18,000 cases of cancer-related mortality in Taiwan per year. To bridge the gap towards clinical translation, we developed a circulating tumor cell (CTC) organoid culture workflow that efficiently expands CTC from patients to test mycelium-derived bioactive compounds. Three ACM-derived bioactive compounds were evaluated for tumor chemosensitization characteristics.

Availability of prior mammograms affects incomplete report rates in mobile screening mammography.

Purpose: Mobile mammography can improve access to screening mammography in rural areas and underserved populations. We evaluated the frequency of incomplete reports in mobile mammography screening and the relationships between prior mammograms and recall rates.

Methods: The frequency of incomplete mammogram reports, the subgroups of those needing prior comparison mammograms, recalls for additional imaging, and availability of prior mammograms of a mobile screening mammography unit were compared with fixed site mammography from January 1, 2007 through December 31, 2009.

Lymphotoxin-β Interacts with Methylated EGFR to Mediate Acquired Resistance to Cetuximab in Head and Neck Cancer.

In head and neck squamous cell carcinoma (HNSCC), the incidence of mutation, which is the major cause of cetuximab resistance, is relatively rare compared with the other types of cancers, and the mechanism mediating acquired resistance is unclear compared with the driver gene mutation-mediated resistance. Here, we investigated the driver gene mutation-independent mechanism for cetuximab resistance in HNSCC. We used the -selected and -selected cetuximab-resistant sublines of HNSCC cell lines for investigating the mechanism of acquired resistance to cetuximab.