Clonal evolution and expansion associated with therapy resistance and relapse of colorectal cancer

Anupriya, S.; Chakraborty, Averi; Patnaik, Srinivas

doi:10.1016/j.mrrev.2022.108445

Cited by 9 publications

(4 citation statements)

References 111 publications

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“…Fourthly, intra-tumoural heterogeneity and clonal expansion after neoadjuvant treatment may result in resistance to further systemic treatment due to DNA repair mechanisms in the prevalent cell lines which reverse intended drug-induced damage. This concept was also suggested to account for the absence of survival benefit of HIPEC in the phase III trial (PRODIGE 7) which randomised neoadjuvant treated patients to receive CRS with HIPEC versus CRS alone [ 37 ]. From a pragmatic viewpoint on the other hand, neoadjuvant chemotherapy challenges tumour biology, which may not be fully reflected in existing synaptic reporting.…”

Section: Discussionmentioning

confidence: 99%

Neoadjuvant chemotherapy does not improve survival for patients with high volume colorectal peritoneal metastases undergoing cytoreductive surgery

Sarofim,

Wijayawardana,

Ahmadi

et al. 2024

World J Surg Onc

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Background Colorectal peritoneal metastases (CRPM) affects 15% of patients at initial colorectal cancer diagnosis. Neoadjuvant chemotherapy (NAC) prior to cytoreductive surgery (CRS) has been demonstrated to be a safe and feasible option, however there is limited data describing its efficacy in advanced peritoneal disease. This study evaluated the effect of NAC on survival in patients with high volume CRPM undergoing CRS with or without HIPEC. Methods A retrospective review of all patients who underwent CRS with or without HIPEC for CRPM from 2004 to 2019 at our institution was performed. The cohort was divided based on peritoneal carcinomatosis index (PCI) at surgery: Low Volume (PCI ≤ 16) and High Volume (PCI > 16). Results A total of 326 patients underwent CRS with HIPEC for CRPM. There were 39 patients (12%) with High Volume disease, and 15 of these (38%) received NAC. Patients with High Volume disease had significantly longer operating time, lower likelihood of complete macroscopic cytoreduction (CC-0 score), longer intensive care unit length of stay and longer hospital stay compared to Low Volume disease. In High Volume disease, the NAC group had a significantly shorter median survival of 14.4 months compared to 23.8 months in the non-NAC group (p = 0.046). Conclusion Patients with High Volume CRPM achieved good median survival following CRS with HIPEC, which challenges the current PCI threshold for offering CRS. The use of NAC in this cohort did not increase perioperative morbidity but was associated with significantly shorter median survival compared to upfront surgery.

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Section: Discussionmentioning

confidence: 99%

Neoadjuvant chemotherapy does not improve survival for patients with high volume colorectal peritoneal metastases undergoing cytoreductive surgery

Sarofim,

Wijayawardana,

Ahmadi

et al. 2024

World J Surg Onc

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“…In recent years, new therapeutics, such as targeted and immunotherapeutic drugs, have improved patients’ prognoses. However, due to tumor heterogeneity and the close relationship between patients’ individual differences and drug efficacy, some patients still do not benefit from existing treatments ( S et al, 2022 ). In addition, there is a gap between the current commonly used 2D culture tumor cell model and the cell characteristics of the original tumor, making it difficult to identify suitable drugs for personalized medication and new drug development ( Hay et al, 2014 ).…”

Section: Application Of Organoids In Crcmentioning

confidence: 99%

The application of organoids in colorectal diseases

Liu,

Wang,

Luan

et al. 2024

Front. Pharmacol.

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Intestinal organoids are a three-dimensional cell culture model derived from colon or pluripotent stem cells. Intestinal organoids constructed in vitro strongly mimic the colon epithelium in cell composition, tissue architecture, and specific functions, replicating the colon epithelium in an in vitro culture environment. As an emerging biomedical technology, organoid technology has unique advantages over traditional two-dimensional culture in preserving parental gene expression and mutation, cell function, and biological characteristics. It has shown great potential in the research and treatment of colorectal diseases. Organoid technology has been widely applied in research on colorectal topics, including intestinal tumors, inflammatory bowel disease, infectious diarrhea, and intestinal injury regeneration. This review focuses on the application of organoid technology in colorectal diseases, including the basic principles and preparation methods of organoids, and explores the pathogenesis of and personalized treatment plans for various colorectal diseases to provide a valuable reference for organoid technology development and application.

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“…In a study by Hayashi et al., inhibitors of Epidermal Growth Factor Receptors (EGFR) and anaplastic lymphoma kinase were developed targeting the altered phenotypes of the gene [109]. Various genetic mutations in therapy‐resistant cancer cells like BRAF , PTEN , MET , and TP53 have been observed in colorectal cancer, which are considered as clonal markers [110]. Studies to determine the reasons for these markers that lead to clonal evolution of the tumor are in PTEN , ROBO1, CDH1, PIK3CG, DMD , and LRP1B [111].…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Unraveling the dangerous duet between cancer cell plasticity and drug resistance

Chatterjee,

Pulipaka,

Subbalakshmi

et al. 2023

Comp Sys Onco

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Cancer cell plasticity is the ability of tumor cells to switch phenotypes and is one of the predominant requisites of cancer cells capable of undergoing metastasis. Cancer cell plasticity is also recognized as one of the major contributors to intratumoral heterogeneity, a critical factor underlying the progression of malignant tumors, which is known to modify tumor response and induce resistance against various modes of therapy, thus posing a barrier to efficient cancer management. Cancer cell plasticity is acquired by the subversion of cell signaling pathways like mitogen‐activated protein kinase pathway, phosphoinositide‐3‐kinase, signal transducer and activator of transcription 3, Wnt, Hedgehog and Notch as well as cellular programs such as epithelial to mesenchymal transition and phenotypic plasticity. This complex phenomenon has been studied in many cancer types like pancreatic cancer, colon cancer and breast cancer. This review will explore the current understanding we have in breast cancer on the intrinsic molecular mechanisms of cancer cell plasticity and the resistance to various types of cancer therapy that arise as a result of plasticity. We conclude by exploring the potential novel therapies that specifically target the pathways leading to plasticity and can be leveraged to treat patients living with the disease.

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Clonal evolution and expansion associated with therapy resistance and relapse of colorectal cancer

Cited by 9 publications

References 111 publications

Neoadjuvant chemotherapy does not improve survival for patients with high volume colorectal peritoneal metastases undergoing cytoreductive surgery

Neoadjuvant chemotherapy does not improve survival for patients with high volume colorectal peritoneal metastases undergoing cytoreductive surgery

The application of organoids in colorectal diseases

Unraveling the dangerous duet between cancer cell plasticity and drug resistance

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