scholarly journals Low skeletal muscle density is associated with poor survival in patients who receive chemotherapy for metastatic gastric cancer

2015 ◽  
Vol 35 (3) ◽  
pp. 1727-1731 ◽  
Author(s):  
NAOMI HAYASHI ◽  
YUICHI ANDO ◽  
BISHAL GYAWALI ◽  
TOMOYA SHIMOKATA ◽  
OSAMU MAEDA ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Skeletal Muscle ◽  
Metastatic Gastric Cancer ◽  
Poor Survival ◽  
Muscle Density

scholarly journals Baseline Sarcopenia and Skeletal Muscle Loss During Chemotherapy Affect Survival Outcomes in Metastatic Gastric Cancer

2018 ◽  
Vol 38 (10) ◽  
pp. 5859-5866 ◽  
Author(s):  
KEIJI SUGIYAMA ◽  
YUKIYA NARITA ◽  
SEIICHIRO MITANI ◽  
KAZUNORI HONDA ◽  
TOSHIKI MASUISHI ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Skeletal Muscle ◽  
Metastatic Gastric Cancer ◽  
Survival Outcomes ◽  
Muscle Loss ◽  
Skeletal Muscle Loss

Pretreatment skeletal muscle depletion as an adverse prognostic factor in metastatic gastric cancer.

2014 ◽  
Vol 32 (3_suppl) ◽  
pp. 161-161
Author(s):  
Hiroko Hasegawa ◽  
Kazumasa Fujitani ◽  
Yusuke Yamaoka ◽  
Motohiro Hirao ◽  
Shoichi Nakazuru ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Skeletal Muscle ◽  
Prognostic Factor ◽  
Cancer Patients ◽  
Performance Status ◽  
Metastatic Gastric Cancer ◽  
First Line ◽  
Skeletal Muscle Index ◽  
Pre Treatment ◽  
The Impact

161 Background: Body composition has emerged as an important prognostic factor in cancer patients. Especially, skeletal mass depletion has been associated with poor performance status, toxicity of chemotherapy and shortened survival in cancer patients. However, the impact of pre-treatment skeletal muscle index on survival or toxicity in metastatic gastric cancer patients remains uncertain. Methods: In this retrospective study, we reviewed 98 metastatic gastric cancer (mGC) patients who received S-1 based combination chemotherapy as first-line treatment from April 2006 to March 2013. Pre-treatment skeletal muscle mass was quantified by CT cross sectional area at the third lumbar vertebrae and evaluated as lumbar skeletal muscle index (SMI) (cm2/m2) after normalization for stature (m2). Patients were categorized into 2 groups depending on initial SMI: 35 patients with SMI ≤ 40 and 63 patients with SMI > 40. Results: Median overall survival was significantly shorter in the SMI ≤ 40 group than in the SMI >40 group (439 days versus 565 days; p= 0.03). Progression free survival was also better in the SMI> 40 group without statistical significance (175 days versus 151 days; p= 0.17). Toxicity (grade 3 or 4) was more common in the SMI ≤ 40 group than in the SMI >40 group. (41.1% versus 11.1%; p=0.001). In multivariate analysis, performance status of 2 (HR 4.711, 95%CI 1.065 to 20.832, p=0.04), presence of primary tumor (HR 2.322, 95%CI 1.007 to 5.357, p=0.04) and pre-treatment SMI (HR 2.525, 95%CI 1.145 to 5.568, p=0.02) were independent prognostic factors for OS. Conclusions: The present study suggests that skeletal muscle depletion at the initiation of first-line chemotherapy might be an independent prognostic factor for mGC patients.

scholarly journals Retroperitoneal Fibrosis With Skeletal Muscle Invasion as an Early Manifestation of Metastatic Gastric Cancer

2021 ◽  
Vol 8 (4) ◽  
pp. e00553
Author(s):  
Naman S. Shetty ◽  
Avery Calhoun ◽  
Dharma Sunjaya ◽  
Ashley Greer ◽  
Field F. Willingham
Keyword(s):  
Gastric Cancer ◽  
Skeletal Muscle ◽  
Retroperitoneal Fibrosis ◽  
Metastatic Gastric Cancer ◽  
Muscle Invasion ◽  
Early Manifestation

scholarly journals Severe loss of visceral fat and skeletal muscle after chemotherapy predicts poor prognosis in metastatic gastric cancer patients without gastrectomy

2020 ◽  
Vol 11 (11) ◽  
pp. 3310-3317 ◽  
Author(s):  
Wanjing Feng ◽  
Mingzhu Huang ◽  
Xiaoying Zhao ◽  
Siyuan Chen ◽  
Chenchen Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Skeletal Muscle ◽  
Cancer Patients ◽  
Visceral Fat ◽  
Poor Prognosis ◽  
Metastatic Gastric Cancer ◽  
Severe Loss ◽  
Gastric Cancer Patients

scholarly journals Trifluridine/tipiracil versus placebo for third or later lines of treatment in metastatic gastric cancer: an exploratory subgroup analysis from the TAGS study

ESMO Open ◽  
2021 ◽  
Vol 6 (4) ◽  
pp. 100200
Author(s):  
J. Tabernero ◽  
K. Shitara ◽  
A. Zaanan ◽  
T. Doi ◽  
S. Lorenzen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Subgroup Analysis ◽  
Metastatic Gastric Cancer

scholarly journals Lymph node metastasis-derived gastric cancer cells educate bone marrow-derived mesenchymal stem cells via YAP signaling activation by exosomal Wnt5a

Oncogene ◽  
2021 ◽  
Vol 40 (12) ◽  
pp. 2296-2308
Author(s):  
Mei Wang ◽  
Xinxin Zhao ◽  
Rong Qiu ◽  
Zheng Gong ◽  
Feng Huang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Metastatic Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Node Metastasis ◽  
Signaling Activation

AbstractLymph node metastasis (LNM), a common metastatic gastric-cancer (GC) route, is closely related to poor prognosis in GC patients. Bone marrow-derived mesenchymal stem cells (BM-MSCs) preferentially engraft at metastatic lesions. Whether BM-MSCs are specifically reprogrammed by LNM-derived GC cells (LNM-GCs) and incorporated into metastatic LN microenvironment to prompt GC malignant progression remains unknown. Herein, we found that LNM-GCs specifically educated BM-MSCs via secretory exosomes. Exosomal Wnt5a was identified as key protein mediating LNM-GCs education of BM-MSCs, which was verified by analysis of serum exosomes collected from GC patients with LNM. Wnt5a-enriched exosomes induced YAP dephosphorylation in BM-MSCs, whereas Wnt5a-deficient exosomes exerted the opposite effect. Inhibition of YAP signaling by verteporfin blocked LNM-GC exosome- and serum exosome-mediated reprogramming in BM-MSCs. Analysis of MSC-like cells obtained from metastatic LN tissues of GC patients (GLN-MSCs) confirmed that BM-MSCs incorporated into metastatic LN microenvironment, and that YAP activation participated in maintaining their tumor-promoting phenotype and function. Collectively, our results show that LNM-GCs specifically educated BM-MSCs via exosomal Wnt5a-elicited activation of YAP signaling. This study provides new insights into the mechanisms of LNM in GC and BM-MSC reprogramming, and will provide potential therapeutic targets and detection indicators for GC patients with LNM.

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