human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: CEACAM1 , CEA/CEACAM5 , and CEACAM6 are cell adhesion molecules ( CAMs ) of the carcinoembryonic antigen ( CEA ) family that have been shown to be deregulated in lung cancer and in up to 50% of all human cancers . However , little is known about the functional impact of these molecules on undifferentiated cell growth and tumor progression . Here we demonstrate that cell surface expression of CEACAM1 on confluent A549 human lung adenocarcinoma cells plays a critical role in differentiated , contact-inhibited cell growth . Interestingly , CEACAM1-L , but not CEACAM1-S , negatively regulates proliferation via its ITIM domain , while in proliferating cells no CEACAM expression is detectable . Furthermore , we show for the first time that CEACAM6 acts as an inducer of cellular proliferation in A549 cells , likely by interfering with the contact-inhibiting signal triggered by CEACAM1-4L , leading to undifferentiated anchorage-independent cell growth . We also found that A549 cells expressed significant amounts of non-membrane anchored variants of CEACAM5 and CEACAM6 , representing a putative source for the increased CEACAM5/6 serum levels frequently found in lung cancer patients . Taken together , our data suggest that post-confluent contact inhibition is established and maintained by CEACAM1-4L , but disturbances of CEACAM1 signalling by CEACAM1-4S and other CEACAMs lead to undifferentiated cell growth and malignant transformation .
    OUTPUT:

agent
evading growth suppressors
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: CEACAM1 , CEA/CEACAM5 , and CEACAM6 are cell adhesion molecules ( CAMs ) of the carcinoembryonic antigen ( CEA ) family that have been shown to be deregulated in lung cancer and in up to 50% of all human cancers . However , little is known about the functional impact of these molecules on undifferentiated cell growth and tumor progression . Here we demonstrate that cell surface expression of CEACAM1 on confluent A549 human lung adenocarcinoma cells plays a critical role in differentiated , contact-inhibited cell growth . Interestingly , CEACAM1-L , but not CEACAM1-S , negatively regulates proliferation via its ITIM domain , while in proliferating cells no CEACAM expression is detectable . Furthermore , we show for the first time that CEACAM6 acts as an inducer of cellular proliferation in A549 cells , likely by interfering with the contact-inhibiting signal triggered by CEACAM1-4L , leading to undifferentiated anchorage-independent cell growth . We also found that A549 cells expressed significant amounts of non-membrane anchored variants of CEACAM5 and CEACAM6 , representing a putative source for the increased CEACAM5/6 serum levels frequently found in lung cancer patients . Taken together , our data suggest that post-confluent contact inhibition is established and maintained by CEACAM1-4L , but disturbances of CEACAM1 signalling by CEACAM1-4S and other CEACAMs lead to undifferentiated cell growth and malignant transformation .
    OUTPUT:
