PMC6529614_01
Hepatic metastases and incision implantation metastasis before apatinib treatment. Metastatic lesions when the patient first attended our hospital on March 2015 (A1, A2, A3); During the treatment of icotinib, the metastatic mass became bigger (C1, C2, June 2016), compared to two months earlier (B1, B2, April 2016). Red arrows indicate the hepatic metastasis and incision implantation metastasis.
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Abdominal computed tomography (CT) showed progression of hepatic metastases (Figure 1A1-A3). Besides, hepatic and incision implantation metastasis lesions were also enlarged (Figure 1B1, B2, C1, C2). The response after two cycles was stable disease (SD) but went PD after four cycles (Figure 2A1, B1).
Hepatic metastasis and incision implantation metastasis change during apatinib treatment. Hepatic metastatic mass and incision implantation metastasis lesion before the treatment of apatinib (A1, B1, October 2016) and after two months of apatinib treatment (A2, B2); From March 2017 to August 2018, the metastatic lesions showed no obvious change (A3-A6, B3-B6). Red arrows indicate the hepatic metastasis and incision implantation metastasis.
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Abdominal computed tomography (CT) showed progression of hepatic metastases (Figure 1A1-A3). Besides, hepatic and incision implantation metastasis lesions were also enlarged (Figure 1B1, B2, C1, C2). The response after two cycles was stable disease (SD) but went PD after four cycles (Figure 2A1, B1). After two months of apatinib treatment, the first therapeutic evaluation was stable disease (SD) (Figure 2 A2, B2).
Timeline of treatment and trend in level of CA 125 and CA 15-3 during treatment. Green color indicates time without treatment.. Abbreviations: TC, paclitaxel/carboplatin; GP, gemcitabine/cisplatin; DC/CIK, dendritic cell/cytokine induced killer biological cell immunotherapy; DTX, docetaxel; TP, liposome paclitaxel/lobaplatin; PP, pemetrexed/nedaplatin; IF, irinotecan/capecitabine; SD, stable disease; PD, progressive disease.
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Abdominal computed tomography (CT) showed progression of hepatic metastases (Figure 1A1-A3). The CA19-9 level and the CA15-3 level showed a downward trend after the first rise (Figure 3). At the same time, the CA125 level decreased significantly from 563.2 U/mL to 131.6U/mL, and the CA15-3 level also declined sharply from 245.9 U/mL to 64.12U/mL. After eight months treatment (In June 2017), the level of CA125 and CA15-3 went up again (Figure 3), but the therapeutic evaluation on tumor volume exhibited SD. From August 9, 2017, to August 8, 2018, the CT scan showed no obvious changes (Figure 2 A4-A6, B4-B6), the CA125 level was maintained between 158.1 U/mL and 229.2 U/mL, the CA15-3 level was maintained between 88.0 U/mL and 107.9 U/mL (Figure 3).
Positron emission tomography-computed tomography scan showed that the disease had progressed, metastatic lesions in liver, lung and the pelvic peritoneal had progressed and multiple lymph node metastases (include left lower neck, left superior clavicle, left internal breast area, anterior costal diaphragm angle, abdominal cavity and retroperitoneum) (A-F).
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In October 2018, the PET-CT showed disease progression (Figure 4).