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1                                              HLRCC is associated with clinically significant uterine
2                                              HLRCC is caused by germline inactivating pathogenic vari
3                                              HLRCC patients are at risk for the development of an agg
4                                              HLRCC-associated tumors harbor biallelic FH inactivation
5 150 mg once daily) in patients with advanced HLRCC-associated or sporadic papillary renal-cell carcin
6  therapy is known for patients with advanced HLRCC-associated papillary renal-cell carcinoma, and mos
7                                     Although HLRCC tumors metastasize rapidly, FH-deficient mice deve
8 rate that inactivating mutations of FH in an HLRCC-derived cell line result in glucose-mediated gener
9 basic mechanism of tumorigenesis in HPGL and HLRCC is likely to be pseudo-hypoxic drive, just as it i
10 ider that the study of rare diseases such as HLRCC, combining analyses of human tumours and cell line
11 ipts previously described as altered between HLRCC and NS ULMs, 51 co-altered at the protein level an
12 ditary leiomyomatosis and renal cell cancer (HLRCC) and increase the risk of developing uterine leiom
13 ditary leiomyomatosis and renal cell cancer (HLRCC) is an autosomal dominant disorder characterized b
14 ditary leiomyomatosis and renal cell cancer (HLRCC) is an inherited cancer syndrome linked to biallel
15 ditary leiomyomatosis and renal-cell cancer (HLRCC) is an inherited disorder characterized by germlin
16 ditary leiomyomatosis and renal cell cancer (HLRCC), and recently, FH mutations have been detected in
17 ditary leiomyomatosis and renal cell cancer (HLRCC), characterised by benign smooth muscle cutaneous
18 ditary leiomyomatosis and renal cell cancer (HLRCC), implicated FH, a gene on chromosome 1q43 encodin
19 viduals to leiomyomas and renal cell cancer (HLRCC), whereas mutations in SDH cause paragangliomas an
20 ditary leiomyomatosis and renal cell cancer (HLRCC).
21 ditary leiomyomatosis and renal-cell cancer (HLRCC).
22  hereditary leiomyomatosis and renal cancer (HLRCC) syndrome, and have shown that these cancers may h
23 ary leiomyomatosis and renal cell carcinoma (HLRCC) is an aggressive cancer characterized by bialleli
24 ary leiomyomatosis and renal cell carcinoma (HLRCC) is an autosomal dominant condition characterized
25 ary leiomyomatosis and renal cell carcinoma (HLRCC) is characterized by germline mutations of the FH
26 ary leiomyomatosis and renal cell carcinoma (HLRCC), a cancer syndrome characterized by a highly aggr
27 ary leiomyomatosis and renal cell carcinoma (HLRCC), a disease in which mutation of the tricarboxylic
28 ary leiomyomatosis and renal cell carcinoma (HLRCC), a type of kidney cancer that harbors fumarate hy
29                       Consistently, clinical HLRCC tissues showed increased expression levels of both
30  chemoproteomic analysis of a kidney-derived HLRCC cell line.
31 s supports it as the susceptibility gene for HLRCC, its role in families in North America has not bee
32  in uterine leiomyoma tissues collected from HLRCC patients and underscore conserved molecular altera
33 tegrated proteogenomic analysis of ULMs from HLRCC (n = 16; FH-mutation confirmed) and non-syndromic
34 tly higher protein:transcript correlation in HLRCC (R = 0.35) vs. NS ULMs (R = 0.242, MWU p = 0.0015)
35  understanding of their metabolic effects in HLRCC may lead to the development of effective therapeut
36 at the protein level and several elevated in HLRCC ULMs are involved in regulating cellular metabolis
37 f which sixty were significantly elevated in HLRCC vs. NS ULMs (LogFC = 1.86, MWU p < 0.0001).
38 emonstrated that accumulation of fumarate in HLRCC tumors inactivated the core factors responsible fo
39 succino)cysteine peptides were identified in HLRCC ULMs, of which sixty were significantly elevated i
40 at the obligate glycolytic switch present in HLRCC is critical to HIF stabilization via ROS generatio
41 iated oxidative stress response signaling in HLRCC ULMs.
42                                     Thus, in HLRCC cells, proteasome inhibition disrupts glucose and
43 understanding mechanisms of tumorigenesis in HLRCC and the development of targeted treatments for pat
44  by genetic reintroduction of active FH into HLRCC cell lines.
45 tients who showed clinical manifestations of HLRCC but were negative for known pathogenic FH gene var
46 we found that it modulates the metabolism of HLRCC cells.
47 e-containing proteins in different models of HLRCC.
48 ient who also showed a clinical phenotype of HLRCC.
49                                 Treatment of HLRCC cells with dimethyl fumarate or PKM2 activators al
50 roviding a new potential target for treating HLRCC patients.
51 95% confidence interval [CI], 57 to 83) with HLRCC-associated papillary renal-cell carcinoma; the med
52 ows that mutations in FH are associated with HLRCC in North America.
53 enal tumors and FH mutations associated with HLRCC.
54                             Individuals with HLRCC are at risk to develop cutaneous and uterine leiom
55 b showed antitumor activity in patients with HLRCC-associated or sporadic papillary renal-cell carcin
56                  A total of 43 patients with HLRCC-associated papillary renal-cell carcinoma and 40 p
57 spiratory chain in tumors from patients with HLRCC.