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.
    ###
    INPUT: The tumor suppressors Lats1 and Lats2 are mediators of the Hippo pathway that regulates tissue growth and proliferation . Their N-terminal non-kinase regions are distinct except for Lats conserved domains 1 and 2 ( LCD1 and LCD2 ) , which may be important for Lats1/2-specific functions . Lats1 knockout mice were generated by disrupting the N-terminal region containing LCD1 ( Lats1(ΔN/ΔN) ) . Some Lats1(ΔN/ΔN) mice were born safely and grew normally . However , mouse embryonic fibroblasts ( MEFs ) from Lats1(ΔN/ΔN) mice displayed mitotic defects , centrosomal overduplication , chromosomal misalignment , multipolar spindle formation , chromosomal bridging and cytokinesis failure . They also showed anchorage-independent growth and continued cell cycles and cell growth , bypassing cell-cell contact inhibition similar to tumor cells . Lats1(ΔN/ΔN) MEFs produced tumors in nude mice after subcutaneous injection , although the tumor growth rate was much slower than that of ordinary cancer cells . Yap , a key transcriptional coactivator of the Hippo pathway , was overexpressed and stably retained in Lats1(ΔN/ΔN) MEFs in a cell density independent manner , and Lats2 mRNA expression was downregulated . In conclusion , N-terminally truncated Lats1 induced Lats2 downregulation and Yap protein accumulation , leading to chromosomal instability and tumorigenesis .
    OUTPUT:

agent
evading growth suppressors;sustaining proliferative signaling;genomic instability and mutation
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.
    ###
    INPUT: The tumor suppressors Lats1 and Lats2 are mediators of the Hippo pathway that regulates tissue growth and proliferation . Their N-terminal non-kinase regions are distinct except for Lats conserved domains 1 and 2 ( LCD1 and LCD2 ) , which may be important for Lats1/2-specific functions . Lats1 knockout mice were generated by disrupting the N-terminal region containing LCD1 ( Lats1(ΔN/ΔN) ) . Some Lats1(ΔN/ΔN) mice were born safely and grew normally . However , mouse embryonic fibroblasts ( MEFs ) from Lats1(ΔN/ΔN) mice displayed mitotic defects , centrosomal overduplication , chromosomal misalignment , multipolar spindle formation , chromosomal bridging and cytokinesis failure . They also showed anchorage-independent growth and continued cell cycles and cell growth , bypassing cell-cell contact inhibition similar to tumor cells . Lats1(ΔN/ΔN) MEFs produced tumors in nude mice after subcutaneous injection , although the tumor growth rate was much slower than that of ordinary cancer cells . Yap , a key transcriptional coactivator of the Hippo pathway , was overexpressed and stably retained in Lats1(ΔN/ΔN) MEFs in a cell density independent manner , and Lats2 mRNA expression was downregulated . In conclusion , N-terminally truncated Lats1 induced Lats2 downregulation and Yap protein accumulation , leading to chromosomal instability and tumorigenesis .
    OUTPUT:
