Background: Neoadjuvant chemotherapy is a standard preoperative therapeutical procedure with locally advanced rectal adenocarcinoma. The aim of the study was to compare the tumour volume reduction before and after the oncological therapy in relation to the change in the CEA value and to the outcome of the histopathological evaluation of response to the treatment.
Patients And Methods: In the years 2004-2008, 274 rectal cancer patients were evaluated, of which 64 underwent neoadjuvant CRT with subsequent surgery and had also completed other inclusion criteria. The tumour volume before and after the CRT, percentage reduction in the tumour volume and the relation to the change in the CAE value and the histopathological evaluation were evaluated.
Results: The distance between the anus and the tumour was from 3 to 15 centimetres, the average value being 8.1 centimetres. In 5 cases the tumour was not histologically found in the resected specimen. Average value of the CEA value before the CRT was 18.12 ng/ml, range 0.7-98.1 ng/ml, after the CRT the average value was 7.00 ng/ml, range 0.5-18.7 ng/ml. The average tumour volume before CRT was 32.48, range 10.3-88.5, after the CRT the average volume was 20.13, range 4.7-55.1.
Conclusion: A relation between the change in the T value and the volume reduction before and after the CRT of statistical significance has been proven in this group of patients. This relation however has not been proved in the N value change. Only in one-third of the evaluated patients was there a positive change in both T and N classification. No relation between the CEA value and the tumour volume change has been proven.
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Int J Surg
January 2025
Department of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Background: The results of many large randomized clinical trials (RCTs) have transformed clinical practice in gastroesophageal reflux disease (GERD) and esophageal hiatal hernia (HH). However, research waste (i.e.
View Article and Find Full Text PDFClin Cancer Res
January 2025
Mater Research Institute - University of Queensland, Woolloongabba, Qld, Australia.
Purpose: Receptor CUB-domain containing- protein 1 (CDCP1) was evaluated as a target for detection and treatment of breast cancer.
Experimental Design: CDCP1 expression was assessed immunohistochemically in tumors from 423 patients (119 triple-negative breast cancer (TNBC); 75 HER2+; 229 ER+/HER2- including 228 primary tumors, 229 lymph node and 47 distant metastases). Cell cytotoxicity induced in vitro by a CDCP1-targeting antibody-drug conjugate (ADC), consisting of the human/mouse chimeric antibody ch10D7 and the microtubule disruptor monomethyl auristatin E (MMAE), was quantified, including in combination with HER2-targeting ADC T-DM1.
Cancer Epidemiol Biomarkers Prev
January 2025
Peking University Cancer Hospital, Beijing, China.
Background: Esophageal squamous cell carcinoma (ESCC) exhibits a long latency period and has a significant geographical disparity in incidence, which underscores the need for models predicting the long-term absolute risk adaptable to regional disease burden.
Methods: 31,883 participants in a large-scale population-based screening trial (Hua County, China) were enrolled to develop the model. Severe dysplasia and above (SDA) identified at screening or follow-up were defined as the outcome.
In our efforts to enhance sensitivity to PARP inhibitors, we identified clofarabine (CLF) as a potential therapy for drug-resistant ovarian cancer and nuclear trafficking of Cathepsin L (CTSL) as a treatment- responsive biomarker. Using PARP inhibitor-sensitive and -resistant OC cell lines, ex vivo cultures of patient-derived ovarian ascites (OVA), primary ovarian tumors, and xenografts (PDX), we found that CLF monotherapy induces nuclear CTSL (nCTSL) in CLF-responsive cells (CLF-r) and sensitizes them to PARP inhibitors olaparib and rucaparib. In CLF non-responsive cells (CLF-nr), a combination of CLF with olaparib is necessary for nCTSL trafficking and synergy.
View Article and Find Full Text PDFBackground: Targeting glutamine metabolism has emerged as a promising strategy in cancer therapy. However, several barriers, such as anti-tumor efficacy, drug toxicity, and safety, remain to be overcome to achieve clinical utility. Prior preclinical studies had generated encouraging data showing promises of cancer metabolism targeting drugs, although most were performed on immune-deficient murine models.
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