Recombinant human endostatin plus paclitaxel/nedaplatin for recurrent or metastatic advanced esophageal squamous cell carcinoma: a prospective, single-arm, open-label, phase II study
Conclusions Rh-endostatin plus paclitaxel/nedaplatin has anti-tumour activity with acceptable tolerability in patients with recurrent or metastatic advanced ESCC. Randomized controlled trial is needed to confirm the efficacy of this regimen.
Conclusions: UBE2T is involved in the development of ESCC, and gene signatures derived from UBE2T-associated genes are predictive of prognosis in ESCC.PMID:34257599 | PMC:PMC8262217 | DOI:10.3389/pore.2021.632531
We present a systematic review of FA-HNSCC treatments reported from 1966 to 2020, defining a cohort of 119 FA-HNSCC patients including 16 esophageal SCCs (131 total primary tumors), who were treated with surgery, RT, systemic therapy (including cytotoxic agents, EGFR inhibitors, or immune checkpoint inhibitors), or a combination of modalities. We summarize the clinical responses and regimen-associated toxicities by treatment modality. The collective evidence suggests that when possible, surgical resection with curative intent should remain the primary treatment modality for FA-HNSCC. Radiation can be administered with acce...
ConclusionLY01610 demonstrated manageable toxicity and promising anti-tumor activity in patients with advanced ESCC. Future clinical development of LY01610 as single agent or in combination with other anti-cancer agents in treating ESCC patients is warranted.Trial registrationNCT04088604 at ClinicalTrials.gov.
CONCLUSION: In conclusion, high serum SOD activity improved post-radiotherapy quality of life but did not impact the prognosis of patients with ESCC. To the best of our knowledge, this study is the first to report that serum SOD activity is associated with radiation-induced toxicity and moderately increased radiotherapeutic response in patients with ESCC undergoing radiotherapy.
ConclusionsThe regimen of salvage CRT using the simultaneous integrated boost (SIB) technique (70 Gy/2.5 Gy/28F) for mediastinal lymph node recurrence in ESCC patients after esophagectomy is feasible and well tolerated.
a Li Lung Fanconi anemia patients with germline genetic defects in FANCD2 are highly susceptible to cancers. Esophageal squamous cell carcinoma (ESCC) is a deadly cancer. Little is known about the function of FANCD2 in ESCC. For detailed molecular and mechanistic insights on the functional role of FANCD2 in ESCC, in vivo and in vitro assays and RNA sequencing approaches were used. Utilizing Clustered Regularly Interspaced Short Palindromic Repeat (CRISPR) technology, FANCD2 knockout models were established to examine the functional impact in mouse models for tumor growth and metastasis and in vitro assays for cell grow...
CONCLUSION: Palbociclib has limited single-agent activity in gastroesophageal tumors. PMID: 32692450 [PubMed - as supplied by publisher]
The dysphagia in this condition is usually associated with iron deficiency anemia and esophageal webs. Iron supplementation and regular surveillance are required for monitoring of malignant transformation into esophageal squamous cell carcinoma. AbstractThe dysphagia in this condition is usually associated with iron deficiency anemia and esophageal webs. Iron supplementation and regular surveillance are required for monitoring of malignant transformation into esophageal squamous cell carcinoma.
CONCLUSIONS: Tislelizumab plus chemotherapy demonstrated durable responses with manageable tolerability in patients with advanced ESCC or G/GEJ adenocarcinoma. PMID: 32561664 [PubMed - as supplied by publisher]
We report on a 16-year-old Japanese boy in whom an esophageal squamous cell carcinoma (ESCC) developed 12 years after allogeneic hematopoietic stem cell transplantation was performed for aplastic anemia. A high frequency of microsatellite instability was detected in samples of ESCC. Moreover, the detection of pathogenic variants, including single nucleotide substitution of TP53 (c.346C>T) and BRCA2 (c.6952C>T) and splicing of KDM6A (c.1194+2T>G), suggest that the development of ESCC in the patient was triggered by impairment of checkpoint and repair for DNA damage and epigenetic modification through accumulation o...