6 research outputs found

    Image_2_ALK-rearranged and EGFR wild-type lung adenocarcinoma transformed to small cell lung cancer: a case report.jpeg

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    BackgroundCases of ALK-rearranged EGFR wild-type lung adenocarcinoma (LUAD) transforming into small cell lung cancer (SCLC) are rarely reported, and diagnosis is often delayed. The emergence of this transformation phenomenon is often regarded as a consequence of acquired resistance mechanisms.Case presentationA 47-year-old male diagnosed with poorly differentiated adenocarcinoma of the right middle lung (pT2N2M0, stage IIIA) achieved a 46-month progression-free survival (PFS) following surgery and adjuvant chemotherapy. During routine follow-up, tumor recurrence and metastasis was detected. Genetic testing revealed ALK rearrangement and wild-type EGFR, prompting treatment with ALK-TKIs. In May 2023, abdominal CT scans showed significant progression of liver metastases and abnormal elevation of the tumor marker NSE. Immunohistochemical results from percutaneous liver biopsy indicated metastatic SCLC.ResultsAfter resistance to ALK-TKIs and transformation to SCLC, the patient received chemotherapy combined with immunotherapy for SCLC, but the patient’s disease progressed rapidly. Currently, the patient is being treated with albumin-bound paclitaxel in combination with oral erlotinib and remains stable.ConclusionHistological transformation emerges as a compelling mechanism of resistance to ALK-TKIs, necessitating the utmost urgency for repeat biopsies in patients displaying disease progression after resistance. These biopsies are pivotal in enabling the tailor-made adaptation of treatment regimens to effectively counteract the assorted mechanisms of acquired resistance, thus optimizing patient outcomes in the battle against ALK-driven malignancies.</p

    Image_3_ALK-rearranged and EGFR wild-type lung adenocarcinoma transformed to small cell lung cancer: a case report.jpeg

    No full text
    BackgroundCases of ALK-rearranged EGFR wild-type lung adenocarcinoma (LUAD) transforming into small cell lung cancer (SCLC) are rarely reported, and diagnosis is often delayed. The emergence of this transformation phenomenon is often regarded as a consequence of acquired resistance mechanisms.Case presentationA 47-year-old male diagnosed with poorly differentiated adenocarcinoma of the right middle lung (pT2N2M0, stage IIIA) achieved a 46-month progression-free survival (PFS) following surgery and adjuvant chemotherapy. During routine follow-up, tumor recurrence and metastasis was detected. Genetic testing revealed ALK rearrangement and wild-type EGFR, prompting treatment with ALK-TKIs. In May 2023, abdominal CT scans showed significant progression of liver metastases and abnormal elevation of the tumor marker NSE. Immunohistochemical results from percutaneous liver biopsy indicated metastatic SCLC.ResultsAfter resistance to ALK-TKIs and transformation to SCLC, the patient received chemotherapy combined with immunotherapy for SCLC, but the patient’s disease progressed rapidly. Currently, the patient is being treated with albumin-bound paclitaxel in combination with oral erlotinib and remains stable.ConclusionHistological transformation emerges as a compelling mechanism of resistance to ALK-TKIs, necessitating the utmost urgency for repeat biopsies in patients displaying disease progression after resistance. These biopsies are pivotal in enabling the tailor-made adaptation of treatment regimens to effectively counteract the assorted mechanisms of acquired resistance, thus optimizing patient outcomes in the battle against ALK-driven malignancies.</p

    Image_1_ALK-rearranged and EGFR wild-type lung adenocarcinoma transformed to small cell lung cancer: a case report.jpeg

    No full text
    BackgroundCases of ALK-rearranged EGFR wild-type lung adenocarcinoma (LUAD) transforming into small cell lung cancer (SCLC) are rarely reported, and diagnosis is often delayed. The emergence of this transformation phenomenon is often regarded as a consequence of acquired resistance mechanisms.Case presentationA 47-year-old male diagnosed with poorly differentiated adenocarcinoma of the right middle lung (pT2N2M0, stage IIIA) achieved a 46-month progression-free survival (PFS) following surgery and adjuvant chemotherapy. During routine follow-up, tumor recurrence and metastasis was detected. Genetic testing revealed ALK rearrangement and wild-type EGFR, prompting treatment with ALK-TKIs. In May 2023, abdominal CT scans showed significant progression of liver metastases and abnormal elevation of the tumor marker NSE. Immunohistochemical results from percutaneous liver biopsy indicated metastatic SCLC.ResultsAfter resistance to ALK-TKIs and transformation to SCLC, the patient received chemotherapy combined with immunotherapy for SCLC, but the patient’s disease progressed rapidly. Currently, the patient is being treated with albumin-bound paclitaxel in combination with oral erlotinib and remains stable.ConclusionHistological transformation emerges as a compelling mechanism of resistance to ALK-TKIs, necessitating the utmost urgency for repeat biopsies in patients displaying disease progression after resistance. These biopsies are pivotal in enabling the tailor-made adaptation of treatment regimens to effectively counteract the assorted mechanisms of acquired resistance, thus optimizing patient outcomes in the battle against ALK-driven malignancies.</p

    Table_1_ALK-rearranged and EGFR wild-type lung adenocarcinoma transformed to small cell lung cancer: a case report.docx

    No full text
    BackgroundCases of ALK-rearranged EGFR wild-type lung adenocarcinoma (LUAD) transforming into small cell lung cancer (SCLC) are rarely reported, and diagnosis is often delayed. The emergence of this transformation phenomenon is often regarded as a consequence of acquired resistance mechanisms.Case presentationA 47-year-old male diagnosed with poorly differentiated adenocarcinoma of the right middle lung (pT2N2M0, stage IIIA) achieved a 46-month progression-free survival (PFS) following surgery and adjuvant chemotherapy. During routine follow-up, tumor recurrence and metastasis was detected. Genetic testing revealed ALK rearrangement and wild-type EGFR, prompting treatment with ALK-TKIs. In May 2023, abdominal CT scans showed significant progression of liver metastases and abnormal elevation of the tumor marker NSE. Immunohistochemical results from percutaneous liver biopsy indicated metastatic SCLC.ResultsAfter resistance to ALK-TKIs and transformation to SCLC, the patient received chemotherapy combined with immunotherapy for SCLC, but the patient’s disease progressed rapidly. Currently, the patient is being treated with albumin-bound paclitaxel in combination with oral erlotinib and remains stable.ConclusionHistological transformation emerges as a compelling mechanism of resistance to ALK-TKIs, necessitating the utmost urgency for repeat biopsies in patients displaying disease progression after resistance. These biopsies are pivotal in enabling the tailor-made adaptation of treatment regimens to effectively counteract the assorted mechanisms of acquired resistance, thus optimizing patient outcomes in the battle against ALK-driven malignancies.</p

    Facile Synthesis of Ni(OH)<sub>2</sub>/Carbon Nanofiber Composites for Improving NiZn Battery Cycling Life

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    Carbon nanofibers (CNFs) were successfully functionalized by the hydrothermal treatment of wet CNFs containing concentrated HNO<sub>3</sub>. The method of synthesis was facile and eco-friendly. With the use of oxidized CNFs as substance, Ni­(OH)<sub>2</sub>/oxidized CNFs hybrid materials were prepared by taking a two-step solution phase reaction. The XRD pattern and TEM image suggested a well crystalline Ni­(OH)<sub>2</sub> nanoplate with β-phase structure growth on the surface of CNFs. Electrochemistry test results displayed high specific capacitances and long cycle life of the composites. With the use of Ni­(OH)<sub>2</sub>/CNFs as cathode and Zn foil as anode, assembled NiZn pouch cells could achieve ∼1.75 V discharge voltage plateau, with a specific capacity ranging from 184 mAh·g<sup>–1</sup> at a discharging current density of 5 mA·cm<sup>–2</sup> to 91 mAh·g<sup>–1</sup> at a discharging current density of 50 mA·cm<sup>–2</sup>. Its cycle stability was up to 1200 cycles with a capacity retention of >96% at attaining an energy density of 150 Wh·kg<sup>–1</sup>. Compared with a 6 mol·L<sup>–1</sup> KOH solution electrolyte battery, the sodium polyacrylate gel electrolyte battery displayed better cycle performance. The function of the gel electrolyte was discussed. The facile method could be extended to the oxidization of the other carbon materials and synthesis of the others carbon composites

    Additional file 1 of Patients with metastatic renal cell carcinoma who receive immune-targeted therapy may derive survival benefit from nephrectomy

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    Additional file 1: Table 1. Category and dosage of target medicine and PD-1 inhibitors. Table 2. Two groups of PD-1 inhibitors combined with targeted therapy. Table 3. Distribution of oligometastasis in the two groups
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