View clinical trials related to Adenocarcinoma.
Filter by:The purpose of this study was to evaluate the effect and safety of concurrent PD-1 antibody-based long-term radiotherapy followed by 2 cycles SOX with PD-1 in patients with locally advanced adenocarcinoma of esophagogastric junction.
Radical surgical resection is the only curative treatment option for pancreatic cancer, but borderline resectable tumors have a high probability of incomplete exeresis. Although neoadjuvant therapy can improve the chances of complete exeresis, not all patients respond as expected.
Short-term relapse and poor survival are prevalent in patients with pancreatic adenocarcinoma (PAAD) after surgeries. Despite the importance of adjuvant treatments for resected PAAD patients, there is currently no suitable biomarker to identify those individuals with high risk of recurrence and inform therapeutic decision making. In this study, we aim to examine whether postoperative circulating tumor DNA (ctDNA) could be used as a biomarker for early detection of minimal residual disease (MRD) and predicting relapse in resected PAAD through high-depth targeted next-generation sequencing.
a multifactorial model combining radiomics with frozen section analysis is a potential biomarker for assessing Spread Through Air Space during surgery, which can provide decision-making support to therapeutic planning for early-stage lung adenocarcinomas.
This is a single-arm, exploratory clinical study to evaluate the efficacy and safety of Preoperative short course radiotherapy with Envafolimab, Endostatin and SOX regimen in resectable locally advanced gastric/gastroesophageal junction adenocarcinoma.
This phase II trial studies whether tucatinib combined with trastuzumab and TAS-102 works to shrink tumors in patients with HER2 positive colorectal cancer that has spread to other parts of the body (metastatic) and has one of the following gene mutations detected in blood: PIK3CA, KRAS, NRAS, or BRAF V600. Tucatinib is in a class of medications called kinase inhibitors. It works by blocking the action of the abnormal protein that signals tumor cells to multiply. This helps stop or slow the spread of tumor cells. Trastuzumab is a form of targeted therapy because it attaches itself to specific molecules (receptors) on the surface of tumor cells, known as HER2 receptors. When trastuzumab attaches to HER2 receptors, the signals that tell the cells to grow are blocked and the tumor cell may be marked for destruction by the body's immune system. TAS-102 is a combination of 2 drugs; trifluridine and tipiracil. Trifluridine is in a class of medications called thymidine-based nucleoside analogues. It works by stopping the growth of tumor cells. Tipiracil is in a class of medications called thymidine phosphorylase inhibitors. It works by slowing the breakdown of trifluridine by the body. Giving tucatinib, trastuzumab, and TAS-102 together may work better than usual treatment for metastatic colorectal cancer.
This is a study of Camrelizumab combined with Apatinib versus Apatinib alone in the third-line treatment of metastatic gastric cancer. Paticipants will be radomized to receive treatment of Camrelizumab combined with Apatinib or Apatinib alone. The primary study hypothesis is that the adding Camrelizumab to Apatinib can prolong the progressive-free survival of the paticipants.
This is a multicentre open labelled phase III adjuvant trial of disease-free survival in patients with resected pancreatic ductal adenocarcinoma randomized to allocation of oxaliplatin- or gemcitabine-based chemotherapy by standard clinical criteria (control arm) or by a transcriptomic treatment specific stratification signature or TSS (test arm).
This phase I trial tests the safety, side effects studies chemotherapy followed by chemotherapy at the same time as radiation therapy (chemoradiation) before surgery (neoadjuvant) in treating patients with stage gastric (stomach) or gastroesophageal junction cancer . Chemotherapy drugs, such as docetaxel, oxaliplatin , leucovorin, fluorouracil, and capecitabine, work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Radiation therapy uses high energy x-rays to kill tumor cells and shrink tumors. Giving chemotherapy and chemoradiation before surgery may make the tumor smaller and may reduce the amount of normal tissue that needs to be removed.
Gastric cancer is the fifth most common malignancy in the world after cancers of the lung, breast, colorectum, and prostate. Gastric cancer is the third leading cause of cancer death and is responsible for 723,000 deaths yearly. Gastric carcinoma (GC) is a multifactorial disease which is difficult to diagnose in early-stage because of a time lag between the onset of growth and the appearance of clinical presentation. So, its prognosis is poor as evidenced by the 5-year survival rate. Klotho is anti-aging gene encoding a protein with multiple pleiotropic effect. Cancer and ageing share comparable principles. Klotho gene has been described as a tumor suppressor gene in numerous solid tumors and hematological malignancies. Klotho expression has been shown to be significantly down-regulated in malignant tissue compared to adjacent non-malignant tissue with good prognosis in cancers with high Klotho expression, including colorectal, pancreatic, gastric, esophageal, breast, hepatocellular, ovarian, and renal carcinomas. In contrast, a recent study documented that Klotho negative invasive duct carcinoma group exhibited good prognosis than the Klotho positive group regarding the disease- free survival after the surgical resection in breast cancer patient. Lipoprotein receptor- related protein 6 (LRP6) is a type I single transmembrane protein which is a member of the low-density lipoprotein receptor (LDLR) gene family of receptors that is highly conserved among species. In 2000, LRP6 was identified as a co-receptor for Wnt and Frizzled (FZD) to transduce Wnt/β-catenin signaling. Dysregulation of LRP6 is involved in cancer. LRP6 is highly expressed in several cancer cell lines and overexpression of LRP6 promotes cancer cell proliferation. LRP6 expression is frequently upregulated in breast cancer tissue, and respective overexpression or knockdown of LRP6 induces or inhibits breast tumorigenesis. LRP6 is highly expressed in tumors of liver cancer patients, and overexpression of LRP6 promotes liver cancer cell proliferation and tumor growth. In prostate cancer, high expression levels of LRP6 are detected which activate Wnt/β-catenin signaling and glycolysis through Akt signaling. The end result is increased prostate cancer cell proliferation. The mechanism of Klotho-mediated Wnt inhibition was as a result of Klotho binding to Wnt ligands, namely Wnt3A and Wnt5A; thereby impeding binding of these ligands to their cell surface receptor.