To accelerate our endeavors to overcome cancer, Chinese Journal of Cancer has launched a program of publishing 150 most important questions in cancer research and clinical oncology. In this article, 10 more questions are presented as follows. Question 15: Can tumor-induced erythrogenesis provide qualified red blood cells for carrying oxygen to distant organs? Question 16: Can we overcome tumor resistance to platinum-containing antineoplastic drugs by activating the sensitivity factors in the tumor? Question 17: How can a cancer cell stay dormant for years? Question 18: Why do cancer cells use distinct transcriptomic and proteomic programs to reach the same metastatic phenotype? Question 19: Why do some cancers regress spontaneously? Question 20: What are the regulatory mechanisms occurring in donor cells that determine selective sorting of biological content into vesicles and their biological consequences in recipient cells? Are the genetic transfer and exchange of biological messages between cells transient? Is the phenotypic manipulation of recipient cells temporary or prolonged and persistent? If extracellular vesicles possess immune-modulatory potential, how could they be exploited for immune interventions and cancer immunotherapy? Presumably the cargo of extracellular vesicles reflects the cells of their origin and can be used for cancer diagnosis, how could the uniform/stringent capture criteria be met universally for applying EVs in point-of-care diagnostics for cancer patients? Question 21: Can we use self-sampling technologies to monitor the tumor genetic alterations for more precise targeted therapy? Can we cure a heterogeneous tumor by sequentially targeting the driver molecules? Question 22: Can we postpone the onset of non-infection-related cancers? Question 23: How many types of cells can jointly form the tumor vasculature to provide blood supply for tumor progression? Question 24: How tumor cells transmit their epigenetic features to daughter cells and maintain the malignant phenotype? Question 18: Why do cancer cells use distinct transcriptomic and proteomic programs to reach the same metastatic phenotype? Background and implications Transcriptomic and proteomic profiles of metastases versus primary tumors have been compared by several investigators. Profoundly distinct profiles have been revealed in most cases, with trends for similarity between pairs of metastases and primary tumors from individual patients. However, rare tight-matches were revealed even across different metastases originating from an individual tumor. Next-generation sequencing confirmed the complexity of such a scenario. These findings suggest distinct, albeit self-supporting, control modules for metastatic spreading. Determining the underlying molecular mechanisms may be very helpful for a better understanding of the metastatic process. It may also help avoiding misleading classifications of metastatic factors. Ultimately, it may allow for a better design of therapeutic strategies for metastatic tumors.

The 150 most important questions in cancer research and clinical oncology series: questions 15-24 : Edited by Chinese Journal of Cancer

Alberti, Saverio
Conceptualization
;
2017-01-01

Abstract

To accelerate our endeavors to overcome cancer, Chinese Journal of Cancer has launched a program of publishing 150 most important questions in cancer research and clinical oncology. In this article, 10 more questions are presented as follows. Question 15: Can tumor-induced erythrogenesis provide qualified red blood cells for carrying oxygen to distant organs? Question 16: Can we overcome tumor resistance to platinum-containing antineoplastic drugs by activating the sensitivity factors in the tumor? Question 17: How can a cancer cell stay dormant for years? Question 18: Why do cancer cells use distinct transcriptomic and proteomic programs to reach the same metastatic phenotype? Question 19: Why do some cancers regress spontaneously? Question 20: What are the regulatory mechanisms occurring in donor cells that determine selective sorting of biological content into vesicles and their biological consequences in recipient cells? Are the genetic transfer and exchange of biological messages between cells transient? Is the phenotypic manipulation of recipient cells temporary or prolonged and persistent? If extracellular vesicles possess immune-modulatory potential, how could they be exploited for immune interventions and cancer immunotherapy? Presumably the cargo of extracellular vesicles reflects the cells of their origin and can be used for cancer diagnosis, how could the uniform/stringent capture criteria be met universally for applying EVs in point-of-care diagnostics for cancer patients? Question 21: Can we use self-sampling technologies to monitor the tumor genetic alterations for more precise targeted therapy? Can we cure a heterogeneous tumor by sequentially targeting the driver molecules? Question 22: Can we postpone the onset of non-infection-related cancers? Question 23: How many types of cells can jointly form the tumor vasculature to provide blood supply for tumor progression? Question 24: How tumor cells transmit their epigenetic features to daughter cells and maintain the malignant phenotype? Question 18: Why do cancer cells use distinct transcriptomic and proteomic programs to reach the same metastatic phenotype? Background and implications Transcriptomic and proteomic profiles of metastases versus primary tumors have been compared by several investigators. Profoundly distinct profiles have been revealed in most cases, with trends for similarity between pairs of metastases and primary tumors from individual patients. However, rare tight-matches were revealed even across different metastases originating from an individual tumor. Next-generation sequencing confirmed the complexity of such a scenario. These findings suggest distinct, albeit self-supporting, control modules for metastatic spreading. Determining the underlying molecular mechanisms may be very helpful for a better understanding of the metastatic process. It may also help avoiding misleading classifications of metastatic factors. Ultimately, it may allow for a better design of therapeutic strategies for metastatic tumors.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/3136100
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