PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19067746-3	2009	In this study, the effect of different treatment regimens for MM on serum DKK-1 was evaluated and correlated with the response to treatment in 101 myeloma patients receiving bortezomib, thalidomide, lenalidomide, adriamycin and dexamethasone (AD) or high-dose chemotherapy (HDCT) followed by autologous stem cell transplantation (ASCT).	Thalidomide	186-197	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	74-79	
18687985-6	2009	Studies suggest that DKK1 activation in osteoblasts is the underlying cause of glucocorticoid- and estrogen deficiency-mediated osteoporosis, and at least partially underlies the teratogenic effects of thalidomide on limb development.	Thalidomide	202-213	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	21-25	
19067746-7	2009	Thalidomide led to a non-significant decrease in DKK-1 (1705 pg/mL vs. 1269 pg/mL, P = 0.081).	Thalidomide	0-11	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	49-54	
17255354-5	2007	Despite its role as a tumor suppressor and mediator of apoptosis in other cell types including osteoblasts, our data suggest that DKK1, a stress-responsive gene in MM, does not mediate apoptotic signaling, is not activated by TP53, and its forced overexpression could not inhibit cell growth or sensitize MM cells to apoptosis following treatment with thalidomide or lenalidomide.	Thalidomide	352-363	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	130-134	
17283219-0	2007	Thalidomide induces limb deformities by perturbing the Bmp/Dkk1/Wnt signaling pathway.	Thalidomide	0-11	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	59-63	
17283219-6	2007	Thalidomide-induced cell death was dramatically reduced in HEFs and in embryonic limb buds by the use of inhibitors against Bmps, Dkk1, and Gsk3beta, a beta-catenin antagonist acting downstream of Dkk1 in the Wnt pathway.	Thalidomide	0-11	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	130-134	
17283219-6	2007	Thalidomide-induced cell death was dramatically reduced in HEFs and in embryonic limb buds by the use of inhibitors against Bmps, Dkk1, and Gsk3beta, a beta-catenin antagonist acting downstream of Dkk1 in the Wnt pathway.	Thalidomide	0-11	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	197-201	
17283219-7	2007	Most interestingly, blocking of Dkk1 or Gsk3beta dramatically counteracts thalidomide-induced limb truncations and microphthalmia.	Thalidomide	74-85	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	32-36	
17283219-8	2007	From this, we conclude that perturbing of Bmp/Dkk1/Wnt signaling is central to the teratogenic effects of thalidomide.	Thalidomide	106-117	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	46-50