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Residual Tumor

Residual Tumor: A term referring to the presence of cancerous cells that remain after initial treatment, such as surgery or chemotherapy.
These cells can continue to grow and spread, potentially leading to disease recurrence.
Effectively managing and understanding residual tumor is crucial for improving patient outcomes and developing more effective cancer treatments.
PubCompare.ai's AI-driven platform can help researchers optimize their residual tumor research protocols, enhancing reproducibility and identifying the most effective products and methodologies to advance this critical area of oncology.

Most cited protocols related to «Residual Tumor»

1
Simulation Study of Differential Expression
Cited 164 times
For each study, we simulated expression for 1,000 genes on 20 arrays divided between the two disease states. For simplicity, the expression measurements for each gene were drawn from a normal distribution with mean zero and variance one. We simulated expression heterogeneity with a dichotomous unmodeled factor independent of the disease state. The mean differences between disease states and states of the unmodeled factor were drawn from two independent normal distributions. For the real data example, we calculated the residuals from the regression of BRCA tumor type on expression for the Hedenfalk data [22 (link)]. Then, for each simulated study, we independently permuted each row of the expression data to create a matrix of residuals. To this matrix, we added signal, as in the case of the purely simulated data. The simulation studies were based on data generated using the R programming language [43 ]. All differential expression analyses were performed by a t-test based on standard linear regression. The genes were ranked for relative significance by the absolute values of their t-statistics.
Leek J.T, & Storey J.D. (2007). Capturing Heterogeneity in Gene Expression Studies by Surrogate Variable Analysis. PLoS Genetics, 3(9), e161.
Publication 2007
factor A Gene Expression Genes Genetic Heterogeneity Residual Tumor
2
Predicting Response to Neoadjuvant Chemotherapy in Breast Cancer
Cited 66 times
Differentially expressed probe sets in two responder groups: pCR or minimal residual cancer burden (RCB-I) defining excellent response, versus moderate or extensive residual cancer burden (RCB-II/III) defining partial response20 (link) were identified separately in ER+/HER2− and ER−/HER2− training cases using a robust unequal variance t-statistic under a bootstrap scheme. The 209 and 244 probe sets that were significant in at least 30% of the bootstrap replicates in the two cohorts were selected as candidates. Subsequently, a multivariate penalized optimization algorithm, gradient directed regularization, was then used with maximum penalization to select a minimal signature that maximized the area under the ROC curve (AUC) under complete cross-validation.28 The final response predictors used 39 and 55 probe sets for the ER+/HER2− and ER−/HER2− cohorts respectively. Risk scores calculated as the weighted sum of the standardized log2-transformed expression signal of the signature probe sets were dichotomized at zero for both cohorts to predict “responders” (positive scores) or “non-responders” (negative scores).
A similar procedure was followed to develop the predictor for resistance by comparing patients with extensive residual disease (RCB-III) after neoadjuvant chemotherapy treatment versus remaining patients. The final predictor of extensive residual disease used 73 and 54 probe sets for ER+/HER2−and ER−/HER2− subsets respectively (Supplemental Appendix).
Hatzis C., Pusztai L., Valero V., Booser D.J., Esserman L., Lluch A., Vidaurre T., Holmes F., Souchon E., Martin M., Cotrina J., Gomez H., Hubbard R., Chacón J.I., Ferrer-Lozano J., Dyer R., Buxton M., Gong Y., Wu Y., Ibrahim N., Andreopoulou E., Ueno N.T., Hunt K., Yang W., Nazario A., DeMichele A., O’Shaughnessy J., Hortobagyi G.N, & Symmans W.F. (2011). GENOMIC PREDICTOR OF RESPONSE AND SURVIVAL FOLLOWING TAXANE-ANTHRACYCLINE CHEMOTHERAPY FOR INVASIVE BREAST CANCER. JAMA, 305(18), 1873-1881.
Publication 2011
ERBB2 protein, human Neoadjuvant Chemotherapy Patients Residual Cancer Residual Tumor
3
Predicting Sensitivity to Breast Cancer Therapy
Cited 57 times
We combined the individual predictions into a testing algorithm for predicted sensitivity to adjuvant treatment of HER2-negative breast cancer with taxane-anthracycline chemotherapy: 1) sensitivity to endocrine therapy assessed based on an independently validated 165-gene index of endocrine sensitivity (high or intermediate SET index)21 (link); 2) resistance to chemotherapy predicted either by early distant relapse events or by extensive residual disease after neoadjuvant chemotherapy; and 3) sensitivity (pathologic response) to chemotherapy (Figure 1). Additional methodological details are provided in the Supplemental Appendix.
Hatzis C., Pusztai L., Valero V., Booser D.J., Esserman L., Lluch A., Vidaurre T., Holmes F., Souchon E., Martin M., Cotrina J., Gomez H., Hubbard R., Chacón J.I., Ferrer-Lozano J., Dyer R., Buxton M., Gong Y., Wu Y., Ibrahim N., Andreopoulou E., Ueno N.T., Hunt K., Yang W., Nazario A., DeMichele A., O’Shaughnessy J., Hortobagyi G.N, & Symmans W.F. (2011). GENOMIC PREDICTOR OF RESPONSE AND SURVIVAL FOLLOWING TAXANE-ANTHRACYCLINE CHEMOTHERAPY FOR INVASIVE BREAST CANCER. JAMA, 305(18), 1873-1881.
Publication 2011
Anthracyclines erbb2 Gene Genes Hypersensitivity Malignant Neoplasm of Breast Neoadjuvant Chemotherapy Pharmaceutical Adjuvants Pharmacotherapy Relapse Residual Tumor System, Endocrine taxane Therapeutics
4
Computational Disorder Prediction and CDF Analysis
Cited 28 times

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Publication 2009
Amino Acids Base Pairing Biological Evolution Entropy Proteins Residual Tumor
5
Oral Cancer Gene Expression Profiling
Cited 25 times
Expression profile datasets from the Fred Hutchinson Cancer Research Center (FHCRC) and from the University of Texas M.D. Anderson Cancer Center (MDACC) were used. The FHCRC dataset, used for discovery, comprised the gene expression profiles of 167 tumor samples from OSCC patients and 45 normal oral mucosa samples from patients without oral cancer, all treated at the University of Washington Medical Center, the Harborview Medical Center, or the Veterans Affairs Puget Sound Health Care System during 2003 to 2007. The FHCRC dataset also contained information on patient demographics, medical and lifestyle history, vital status, cause of death, and tumor characteristics, including tumor site, stage, and HPV status. The specimen collection, storage protocols and assays for specimen processing, and generation and normalization of raw expression data were performed as previously described [8 (link)]. The MDACC dataset, used for validation, contained the gene expression profiles of 103 samples generated from residual tumor tissue, taken from the MDACC Head and Neck Tumor Bank. Demographic characteristics, tumor site, stage, vital status, and cause of death were abstracted from the medical record and the MDACC Tumor Registry. The gene expression and other data from these tissue samples were analyzed under protocol DR09-0664 and de-identified data were shared with the FHCRC under MT2010-6749. Among 103 samples from the MDACC dataset, 74 were cancer samples from OSCC patients, 24 were matched normal oral samples from OSCC patients, and 5 were normal oral samples from other cancer patients treated in the MDACC Head and Neck Center. The gene expression data obtained from the MDACC were extracted and normalized, also using the gcRMA algorithm but as implemented in Partek® Genomics Suite™ software. The microarray data can be found in the Gene Expression Omnibus database under the accession number GSE41613 and GSE42743
Lohavanichbutr P., Méndez E., Holsinger F.C., Rue T.C., Zhang Y., Houck J., Upton M.P., Futran N., Schwartz S.M., Wang P, & Chen C. (2013). A 13-gene signature prognostic of HPV-negative OSCC: discovery and external validation. Clinical cancer research : an official journal of the American Association for Cancer Research, 19(5), 1197-1203.
Publication 2013
Biological Assay Cancer of Mouth Gene Expression Genes, Neoplasm Head Head and Neck Neoplasms Malignant Neoplasms Microarray Analysis Mucosa, Mouth Neck Neoplasms Patients Residual Tumor Sound Specimen Collection Tissues Veterans

Most recents protocols related to «Residual Tumor»

1
Histopathological Assessment of HCC Response
For the patients in the neoadjuvant cohort, tissue specimens obtained from surgical resection were handled and sampled according to the guidelines for pathological diagnosis of HCC (23 (link)). Hematoxylin and eosin (H&E)-stained sections from these specimens were histologically assessed via experienced pathological experts, based on the immune-related pathologic response criteria (irPRC) (24 (link)). Pathologic complete response (pCR) was defined as the absence of any viable tumor in the tumor bed area. Patients with residual viable tumor (RVT) were stratified into three groups: major pathologic response (MPR, RVT% ≤ 10%), partial pathologic response (pPR, 10% < RVT% < 90%), and no pathologic response (pNR, RVT% ≥ 90%) (25 (link)). Neoadjuvant combination therapy failure was defined as reaching pPR or pNR.
Guo D.Z., Zhang S.Y., Dong S.Y., Yan J.Y., Wang Y.P., Cao Y., Rao S.X., Fan J., Yang X.R., Huang A, & Zhou J. (2023). Circulating immune index predicting the prognosis of patients with hepatocellular carcinoma treated with lenvatinib and immunotherapy. Frontiers in Oncology, 13, 1109742.
Full text: Click here
Publication 2023
Diagnosis Eosin Neoadjuvant Therapy Neoplasms Operative Surgical Procedures Patients Residual Tumor Response, Immune Tissues
2
Adjuvant Therapy for Residual Endometrial Cancer
1. Patients with residual tumors, whether measurable or non-measurable after surgery
2. Endometrioid adenocarcinoma combined with other histological types
3. Non-endometrial carcinoma, for example, serous carcinoma, clear cell carcinoma, undifferentiated carcinoma, neuroendocrine carcinoma, or uterine sarcoma (including carcinosarcoma)
4. An interval between the operation and the start of adjuvant therapy exceeding 8 weeks
5. Previous pelvic radiotherapy
6. Previous history of a second malignancy, unless potentially curative treatment has been completed with no evidence of malignancy for 5 years
7. History of myocardial infarction, stroke, unstable angina, decompensated heart failure, or deep vein thrombosis
8. Impaired renal or cardiac function.
9. Known intolerance to intervention therapy or any excipients
10. Known psychiatric or substance abuse disorders that would interfere with the participant's ability to cooperate with the requirements of the study.
Li Y., Zhu C., Xie H., Chen Y., Lv W., Xie X, & Wang X. (2023). Molecular profile-based recommendations for postoperative adjuvant therapy in early endometrial cancer with high-intermediate or intermediate risk: a Chinese randomized phase III trial (PROBEAT). Journal of Gynecologic Oncology, 34(2), e37.
Publication 2023
Adenocarcinoma, Clear Cell Adenocarcinoma, Endometrioid Angina, Unstable Carcinoma, Neuroendocrine Carcinosarcoma Cerebrovascular Accident Congestive Heart Failure Endometrial Carcinoma Heart Kidney Malignant Neoplasms Myocardial Infarction Neoplasms, Second Primary Patients Pelvis Pharmaceutical Adjuvants Residual Tumor Sarcoma Serous Cystadenocarcinoma Substance Abuse Therapeutics Undifferentiated Carcinoma Uterus Veins
3
Surgical Approaches for Cardiac Myxoma Resection
In 25 patients (25/28, 89.29%), RHMs were excised through median sternotomy under cardiopulmonary bypass using aortic and bicaval cannulation (cardiac arrest in 23, beating heart in 2). To prevent detachment of the mass and intra-operative embolization, we minimized movement and compression of the heart during the surgery. Right atriotomy was performed in all 25 patients; of these, 2 cases were RVM, and ventricular tumors were approached across the tricuspid valve in 1 patient and through an extra right ventriculotomy in the other patient. The basic principle of excision was the complete resection of the tumor and its attached sites. The attachment sites of RHM are listed in Table 1. All myxomas were excised completely. The defect of the atrial septum and right atrial free wall after myxoma resection was repaired with a bovine or autologous pericardial patch when needed. Transesophageal echocardiography was performed at the end of the procedure to assess the presence of a residual tumor or interatrial shunting after septal reconstruction.
Of the remaining 3 patients, 2 underwent total endoscopic robotic RAM resection with da Vinci Surgical System (Intuitive Surgical, Sunnyvale, Calif, USA), and 1 underwent total thoracoscopic surgery for RAM resection. Both robotic and thoracoscopic surgeries are minimally invasive procedures for which the peripheral cardiopulmonary bypass was established via right internal jugular venous cannulation and femoral arterial and venous cannulations. In both these procedures, RAM was excised via right atriotomy on the beating heart without aortic occlusion. The principles for myxoma resection were the same as those for conventional surgeries with median sternotomy.
Liu Y., Li X., Liu Z., Jiang Y., Lu C., Ge S, & Zhang C. (2023). Clinical Characteristics and Surgical Outcomes of Right Heart Myxoma and Its Comparison with Left Heart Myxoma: A Single-Center Retrospective Study. Anatolian Journal of Cardiology, 27(3), 146-152.
Publication 2023
Aorta Arteries Atrial Septal Defects Atrium, Right Cannulation Cardiac Arrest Cardiac Tamponade Cardiopulmonary Bypass Cattle Dental Occlusion Echocardiography, Transesophageal Embolization, Therapeutic Endoscopy Femur Heart Heart Ventricle Jugular Vein Median Sternotomy Movement Myxoma Neoplasms Operative Surgical Procedures Patients Pericardium Reconstructive Surgical Procedures Residual Tumor Robotic Surgical Procedures Septum, Atrial Surgical Endoscopy Surgical Procedures, Thoracoscopic Valves, Tricuspid Veins
4
Gastric Adenocarcinoma Biomarker Expression
We performed this single-center, prospective pilot study at the University of Alberta in Edmonton, Alberta, Canada from January 2018 to January 2022. All human clinical participants consented according to the approved ethics protocol granted by the Health Research Ethics Board of Alberta (Study ID: HREBA.CC-17-0228_REN5). Treatment naïve Stage I-IV sporadic gastric adenocarcinoma patients aged greater than 18 years were included. A subset of patients enrolled was allocated to a second cohort on the basis of receiving curative intent neoadjuvant FLOT chemotherapy (Figure 1). Patients with a known inherited oncogenic germline mutation or hereditary syndrome (i.e., Familial Adenomatous Polyposis) were excluded.
Specimens were retrieved via endoscopic biopsy at the time of diagnosis, screening laparoscopy or at the time of surgical resection at the Walter C Mackenzie Health Sciences Centre or Royal Alexandra Hospital. Normal biopsies were obtained from gastric mucosa greater than 5 cm away from the cancerous lesion or associated gastritis. The initial study protocol retrieved two tissue biopsies for permanent pathology, however, following interim review four biopsies were retrieved thereafter. The presence of cancer in specimens was confirmed by a gastrointestinal pathologist. In the absence of cancer, clinical formalin-fixed paraffin-embedded pathology blocks were retrieved when available. In clinical samples with treatment effect, residual cancer cells were detected using anti-pan cytokeratin (Abcam, clone C-11, ab7753) IHC staining followed by the manual assembly of tissue microarray (TMA) blocks with 4mm cores of regions containing residual tumour.
Our primary outcome for all patients was the difference in expression of selected biomarkers between normal and cancer tissue. In the subgroup of patients receiving neoadjuvant chemotherapy, our primary outcome was the difference in expression between tumour treatment response and incomplete treatment response. We also evaluated the difference in expression of biomarkers in paired samples before and after chemotherapy treatment.
Treatment response was retrieved from clinical pathology reports. The Tumour Regression Score was graded according to the College of American Pathologists and National Comprehensive Cancer Network protocol on a 4-point scale (0 = Complete response, 1 = near complete response, 2 = partial response, 3 = poor or no response)[40 (link)]. In accordance with prior studies, treatment response was expressed as a binary variable consisting of response and incomplete response categories[12 (link)]. Responsive tumours included complete and near-complete responses, whereas incomplete responses included partial, and poor no response. Patients who progressed to metastasis while receiving neoadjuvant treatment were classified as an incomplete response.
Skubleny D., Lin A., Garg S., McLean R., McCall M., Ghosh S., Spratlin J.L., Schiller D, & Rayat G. (2023). Increased CD4/CD8 Lymphocyte ratio predicts favourable neoadjuvant treatment response in gastric cancer: A prospective pilot study. World Journal of Gastrointestinal Oncology, 15(2), 303-317.
Publication 2023
Adenocarcinoma Adenomatous Polyposis Coli Anesthesia, Conduction Biological Markers Biopsy Cells Clone Cells Cytokeratin Diagnosis Endoscopy Formalin Gastritis Germ-Line Mutation Germ Line Homo sapiens Laparoscopy Malignant Neoplasms Microarray Analysis Mucosa, Gastric Neoadjuvant Chemotherapy Neoadjuvant Therapy Neoplasm Metastasis Neoplasms Neoplastic Cell Transformation Paraffin Pathologists Patients Pharmacotherapy Residual Cancer Residual Tumor Specimen Handling Stomach Syndrome Tissues
5
Phase Ib/II Study of Immunotherapy
The primary endpoint of the Phase Ib study was dose-limiting toxicity (DLT), with the intention that a Phase II study would be conducted if DLT occurred in fewer than two-sixths of the treated patients, whereas the study would be terminated if DLT occurred in two or more patients. DLT was defined as any of the following adverse events occurring within 21 d of initial drug administration: Grade 4 neutropenia > 7 d; ≥ Grade 3 neutropenia with fever (T ≥ 38.5 °C) lasting > 24 h; Grade 4 thrombocytopenia or Grade 3 thrombocytopenia with bleeding; Grade 4 anemia; ≥ Grade 3 clinically significant nonhematologic toxicity; ≥ Grade 2 immune-related cardiotoxicity, immune-related pneumonia, immune-related ophthalmopathy; and ≥ Grade 3 other immune-related toxicity.
The primary endpoint of the Phase II study was the major pathological response (MPR) rate, with secondary endpoints consisting of the R0 resection rate, pCR rate, safety, disease-free survival (DFS), event-free survival (EFS), and OS. The Becker standard was used to evaluate pathological regression of the primary tumor after surgery. No residual tumor cells were defined as type 1a, less than 10% were defined as type 1b, 10–50% were defined as type 2, and the remainder were defined as type 3. Pathological remission assessed at Grades 1a and 1b was considered to be MPR (including pCR), while pCR was defined as the absence of residual tumor cells (including primary tumors and lymph nodes).
Li Y., Zhou A., Liu S., He M., Chen K., Tian Z., Li Y., Qin J., Wang Z., Chen H., Tian H., Yu Y., Qu W., Xue L., He S., Wang S., Bie F., Bai G., Zhou B., Yang Z., Huang H., Fang Y., Li B., Dai X., Gao S, & He J. (2023). Comparing a PD-L1 inhibitor plus chemotherapy to chemotherapy alone in neoadjuvant therapy for locally advanced ESCC: a randomized Phase II clinical trial: A randomized clinical trial of neoadjuvant therapy for ESCC. BMC Medicine, 21, 86.
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Publication 2023
Anemia Cardiotoxicity Cells Eye Disorders Febrile Neutropenia Leukopenia Neoplasms Nodes, Lymph Operative Surgical Procedures Patients Pneumonia Residual Tumor Safety Thrombocytopenia Thrombocytopenia 3

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More about "Residual Tumor"

Residual tumor, also known as minimal residual disease (MRD) or leftover cancer cells, refers to the presence of cancerous cells that remain after initial treatment, such as surgery or chemotherapy.
These cells can continue to grow and spread, potentially leading to disease recurrence, making effective management and understanding of residual tumor crucial for improving patient outcomes and developing more effective cancer treatments.
Researchers often utilize statistical software like SPSS Statistics, SAS version 9.4, and R version 3.6.1 to analyze data related to residual tumor, while tools like GraphPad Prism 7 can be used for data visualization and presentation.
The use of contrast agents like Lipiodol Ultra-Fluide and Zombie Aqua dye can also aid in the detection and monitoring of residual tumor cells.
PubCompare.ai's AI-driven platform can help optimize research protocols for residual tumor, enhancing reproducibility and identifying the most effective products and methodologies to advance this critical area of oncology.
By leveraging advanced comparison tools, researchers can easily locate the best protocols from literature, pre-prints, and patents, while AI-powered insights can help improve the quality and efficacy of their work.