Hemangioendothelioma of the spleen and liver in a 1-year-old child.

Concurrent occurrence of hemangioendothelioma in the spleen and liver of a 1-year-old child is a rare clinical case.She had a history of good health. Laboratory tests showed elevated inflammatory markers, but all other parameters were within normal range. In this article, we exhibit the typical clinical presentation and Pathology imaging features of this disease.CT imaging revealed a 9.8 cm×8.6 cm mass in the spleen, with areas of non-enhancing liquefactive necrosis. The mass exhibited heterogeneous enhancement during the arterial phase and progressive enhancement during the venous phase. Multiple nodules were observed in liver segments S2 and S4, the largest being approximately 3.7 cm×3.5 mm, with enhancement patterns similar to the splenic lesion. The patient underwent splenectomy, left hemihepatectomy, and cholecystectomy. Intraoperatively, the splenic mass exhibited some areas appearing spongy. Multiple nodules were observed in the left liver, presenting as gray-brown solid masses with a spongy texture. Pathology confirmed a diagnosis of hemangioendothelioma, supported by positive immunohistochemical staining for CD31, CD34, ERG, and FLI-1.

IGF-1 inhibits inflammation and accelerates angiogenesis via Ras/PI3K/IKK/NF-κB signaling pathways to promote wound healing.

Exogenous insulin-like growth factor-1 (IGF-1) has been reported to promote wound healing through regulation of vascular endothelial cells (VECs). Despite the existing studies of IGF-1 on VEC and its role in angiogenesis, the mechanisms regarding anti-inflammatory and angiogenetic effects of IGF-1 remain unclear. In this study, we investigated the wound-healing process and the related signaling pathway of IGF-1 using an inflammation model induced by IFN-γ. The results demonstrated that IGF-1 can increase cell proliferation, suppress inflammation in VECs, and promote angiogenesis. In vivo studies further confirmed that IGF-1 can reduce inflammation, enhance vascular regeneration, and improve re-epithelialization and collagen deposition in acute wounds. Importantly, the Ras/PI3K/IKK/NF-κB signaling pathways was identified as the mechanisms through which IGF-1 exerts its anti-inflammatory and pro-angiogenic effects. These findings contribute to the understanding of IGF-1's role in wound healing and may have implications for the development of new wound treatment approaches.

A case of Abernethy malformation type I combined with hepatoblastoma.

This article encountered an extremely rare case of a 2-year-old male with Abernethy malformation Type I combined with hepatoblastoma. Furthermore, the medical history was characterized by several other abnormalities: gross facial asymmetry and cardiac defects，thus, diagnosis of Goldenhar syndrome in the setting of Abernethy type I was made. In this article, we exhibit the typical clinical presentation and Pathology imaging features of this disease.

A meta-analysis of the value of serum TSH concentration in the diagnosis of differentiated thyroid cancer in patients with thyroid nodules.

Background: In recent years, most studies believe that high TSH level is positively correlated with the incidence of thyroid cancer, but it is still controversial. For this reason, the purpose of this study is to analyze the correlation between preoperative TSH level and thyroid malignant nodules using pathological diagnosis as the gold standard. To evaluate the role of serum TSH in predicting malignancy of thyroid nodules with uncertain cytology.As an important member of the hypothalamus-pituitary-thyroid axis in the endocrine system, TSH plays a crucial role in regulating the growth, differentiation, and function of thyroid cells (Zhang et al., 2023) [1]. Therefore, it has always been considered closely related to TC. Currently, most studies have compared the TSH levels of TC patients and individuals with benign thyroid disease or healthy controls. These findings from various studies indicated that TC patients often demonstrate elevated TSH levels, even when their TSH falls within the normal range. However, it is important to highlight that the current evidence primarily relies on cross-sectional studies, which mainly describe a phenomenon without establishing causal relationships. The involvement of TSH in the early onset or late progression of TC remains unknown, the interaction between TSH and other factors and how it affects TC is not well understood (Gubbi et al., 2020) [2].Symptoms of thyroid cancer are usually insidious, and early thyroid cancer often has no obvious clinical symptoms. Therefore, early detection and early treatment are particularly important, and how to improve the preoperative diagnosis rate of thyroid nodules is also a problem that clinicians pay close attention to. Objective: To evaluate the value of serum TSH concentration in the diagnosis of differentiated thyroid carcinoma in patients with thyroid nodules. Methods: Our study searched databases in both Chinese and English.China Academic Journals FULL-text Database (CNKI), China Online Journals, Chinese Scientific Journals database and Chinese Biomedical Literature Database (CBM) were searched by computer. The English literature was established by PubMed, Embase, Cochrane Library, Web of Science and other databases until June 2022 to search for relevant literatures on the diagnostic test of serum TSH concentration in patients with thyroid nodule. The literatures that met the criteria were screened, the data were extracted, and the literature quality was evaluated. The sensitivity, specificity, positive likelihood ratio, negative likelihood ratio and diagnostic odds ratio of the method for the diagnosis of differentiated thyroid carcinoma were calculated and summarized. The receiver operating characteristic (SROC) curve was drawn and the area under the curve was obtained. Results: A total of 23 diagnostic tests were included (5348 lesions). Meta-analysis showed that the combined sensitivity, specificity, positive likelihood ratio, negative likelihood ratio and diagnostic odds ratio of serum TSH concentration in the diagnosis of differentiated thyroid carcinoma were 0.64, 0.72, 2.511, 0.386 and 7.14, respectively. The area under SROC curve (AUC) was 0.79, and the Q index was 0.7283, indicating no statistically significant difference. Conclusion: Based on current evidence, detection of serum TSH concentration in thyroid nodule patients has high sensitivity and specificity for the diagnosis of differentiated thyroid cancer, which has good clinical application value. However, other auxiliary examinations are still needed to improve the diagnosis rate.

CircDLGAP4 overexpression ameliorates neuronal injury in Parkinson's disease by binding to EIF4A3 and increasing HMGA2 expression.

Parkinson's disease (PD) is a prevalent neurodegenerative disease, and its prevalence increases steadily with age. Circular RNAs (circRNAs) are involved in various neurodegenerative diseases. Here, we aimed to explore the role of circRNA DLG-associated protein 4 (circDLGAP4) in 1-methyl-4-phenylpyridinium ion (MPP+ )-induced neuronal injury in PD. SH-SY5Y cells were treated with MPP+ to establish PD cell models. The levels of circDLGAP4 and high mobility group AT-hook 2 (HMGA2) in SH-SY5Y cells were detected. SH-SY5Y cell viability and apoptosis were detected. The levels of inflammatory damage (IL-1ß, IL-6, TNF-α) and oxidative stress (reactive oxygen species, lactate dehydrogenase, superoxide dismutase, and malondialdehyde)-related factors were measured. The binding of eukaryotic initiation factor 4A3 (EIF4A3) to circDLGAP4 and HMGA2 was analyzed using RNA pull-down or RNA immunoprecipitation. The stability of HMGA2 was detected after actinomycin D treatment, and its effects on neuronal injury were tested. CircDLGAP4 expression was decreased in MPP+ -induced SH-SY5Y cells. CircDLGAP4 upregulation restored cell activity, decreased apoptosis, and reduced inflammatory damage and oxidative stress in PD cell models. CircDLGAP4 bound to EIF4A3 to increase HMGA2 expression and stability. Silencing HMGA2 attenuated the protective effect of circDLGAP4 overexpression. Overall, circDLGAP4 upregulated HMGA2 by recruiting EIF4A3, thus increasing the mRNA stability of HMGA2 and alleviating neuronal injury in PD.

MBD1 protects replication fork stability by recruiting PARP1 and controlling transcription-replication conflicts.

The replication-stress response is essential to ensure the faithful transmission of genetic information to daughter cells. Although several stress-resolution pathways have been identified to deal with replication stress, the precise regulatory mechanisms for replication fork stability are not fully understood. Our study identified Methyl-CpG Binding Domain 1 (MBD1) as essential for the maintaining genomic stability and protecting stalled replication forks in mammalian cells. Depletion of MBD1 increases DNA lesions and sensitivity to replication stress. Mechanistically, we found that loss of MBD1 leads to the dissociation of Poly(ADP-ribose) polymerase 1 (PARP1) from the replication fork, potentially accelerating fork progression and resulting in higher levels of transcription-replication conflicts (T-R conflicts). Using a proximity ligation assay combined with 5-ethynyl-2'-deoxyuridine, we revealed that the MBD1 and PARP1 proteins were recruited to stalled forks under hydroxyurea (HU) treatment. In addition, our study showed that the level of R-loops also increased in MBD1-delated cells. Without MBD1, stalled replication forks resulting from T-R conflicts were primarily degraded by the DNA2 nuclease. Our findings shed light on a new aspect of MBD1 in maintaining genome stability and providing insights into the mechanisms underlying replication stress response.

A transcription-independent mechanism determines rapid periodic fluctuations of BRCA1 expression.

BRCA1 expression is highly regulated to prevent genomic instability and tumorigenesis. Dysregulation of BRCA1 expression correlates closely with sporadic basal-like breast cancer and ovarian cancer. The most significant characteristic of BRCA1 regulation is periodic expression fluctuation throughout the cell cycle, which is important for the orderly progression of different DNA repair pathways throughout the various cell cycle phases and for further genomic stability. However, the underlying mechanism driving this phenomenon is poorly understood. Here, we demonstrate that RBM10-mediated RNA alternative splicing coupled to nonsense-mediated mRNA decay (AS-NMD), rather than transcription, determines the periodic fluctuations in G1/S-phase BRCA1 expression. Furthermore, AS-NMD broadly regulates the expression of period genes, such as DNA replication-related genes, in an uneconomical but more rapid manner. In summary, we identified an unexpected posttranscriptional mechanism distinct from canonical processes that mediates the rapid regulation of BRCA1 as well as other period gene expression during the G1/S-phase transition and provided insights into potential targets for cancer therapy.

The efficacy of targeted therapy combined with radiotherapy and temozolomide-based chemotherapy in the treatment of glioma: A systemic review and meta-analysis of phase II/III randomized controlled trials.

Background: Glioma is the most common intracranial tumor, accounting for about half of the primary intracranial tumors, with the characteristics of hidden onset and high mortality. Even after surgery, radiotherapy and chemotherapy, the prognosis of glioma is not ideal. Targeted therapy has developed rapidly in the treatment of other malignant tumors, which is also an important direction in the research and development of new therapies for glioma. So far, targeting combined with radiotherapy and chemotherapy have been used as the treatment of glioma in many clinical trials, but the role of targeted combined radiotherapy and chemotherapy in the treatment of glioma is still controversial. The purpose of this study was to evaluate the efficacy of targeted therapy combined with radiotherapy and temozolomide (TMZ)-based chemotherapy in the treatment of glioma. Methods: Phase II or phase III clinical trials involving targeted therapy combined with radiotherapy and chemotherapy and temozolomide-based radiotherapy and chemotherapy for gliomas were searched using PubMed, Embase and Web of Science databases, and a comprehensive meta-analysis was conducted. The primary outcome was overall survival time (OS) and progression-free survival time (PFS), and the secondary outcome was adverse reaction. The time-to-event data is summarized as hazard ratio (HR), and the binary results are summarized as odds ratio (OR). Two researchers conducted literature screening, data extraction and quality evaluation according to inclusion and exclusion criteria. Stata16.0 software was used for analysis, random effect model was used for data merging, and forest map was used for display. Results: A total of 11 eligible literatures and 12 prospective randomized controlled clinical trials of 1284 cases were included in the meta-analysis. The results showed that compared with radiotherapy and chemotherapy alone, targeted drugs combined with temozolomide-based radiotherapy and chemotherapy could significantly improve OS in phase II trial, but there was no improvement in Phase III trial, and PFS of newly diagnosed glioma patients was improved (HR=0.82(0.71-0.94) 95%CI, p =0.005). The PFS of the third phase of the experiment also improved. Compared with radiotherapy and chemotherapy alone, there was no statistically significant increase in adverse events in targeted combined radiotherapy and chemotherapy group. Systematic review registration: https://www.crd.york.ac.uk/prospero, identifier CRD42022326012.

Circ_0008784 activates Wnt/ß-catenin pathway to affect the proliferation and apoptosis of triple-negative breast cancer cells.

Triple-negative breast cancer (TNBC), as a subtype of breast tumors with aggressive nature, threatens the health of females across the globe. It's urgent to explore novel therapeutic targets for the improvement of TNBC treatments. Bioinformatics was used to identify circular RNA (circRNA) differentially expressed in TNBC tissues. The circular structure and expression in TNBC cells was subjected to analysis of quantitative polymerase chain reaction (qPCR) and PCR-agarose gel electrophoresis. Functional experiments and qPCR assays were carried out to probe the biological functions of circ_0008784 and microRNA-506-3p (miR-506-3p). It was verified by the assays that circ_0008784 propels proliferation and inhibit apoptosis of TNBC cells; and miR-506-3p was found to suppress proliferation and facilitate apoptosis of TNBC cells. TOP/FOP-Flash reporter, luciferase reporter, RNA-binding protein immunoprecipitation (RIP), RNA pulldown and rescue assays were implemented for exploring the underlying mechanisms of circ_0008784. It was found that circ_0008784 regulates Wnt/ß-catenin signaling pathway, and augments TNBC cell progression via sponging miR-506-3p to modulate catenin beta 1 (CTNNB1). Circ_0008784 activates Wnt/ß-catenin pathway to affect the proliferation and apoptosis of TNBC cells. Elucidating the mechanism of circ_0008784 underlying TNBC is of great significance to TNBC treatment.

Suppression of DDX39B sensitizes ovarian cancer cells to DNA-damaging chemotherapeutic agents via destabilizing BRCA1 mRNA.

Multiple RNA processing events including transcription, mRNA splicing, and export are delicately coordinated by the TREX complex. As one of the essential subunits, DDX39B couples the splicing and export machineries by recruiting ALYREF onto mRNA. In this study, we further explore the functions of DDX39B in handling damaged DNA, and unexpectedly find that DDX39B facilitates DNA repair by homologous recombination through upregulating BRCA1. Specifically, DDX39B binds to and stabilizes BRCA1 mRNA. DDX39B ensures ssDNA formation and RAD51 accumulation at DSB sites by maintaining BRCA1 levels. Without DDX39B being present, ovarian cancer cells exhibit hypersensitivity to DNA-damaging chemotherapeutic agents like platinum or PARPi. Moreover, DDX39B-deficient mice show embryonic lethality or developmental retardation, highly reminiscent of those lacking BRCA1. High DDX39B expression is correlated with worse survival in ovarian cancer patients. Thus, DDX39B suppression represents a rational approach for enhancing the efficacy of chemotherapy in BRCA1-proficient ovarian cancers.

A study on the biological function of heat shock factor 1 proteins in breast cancer.

The present study aimed to investigate the effect of HSF1 proteins on cell proliferation, apoptosis and invasion of breast cancer. The Michigan Cancer Foundation-7 (MCF-7) HSF1-knocked down stable cell line (experimental group) and control cell line (control group) were obtained using a lentivirus assay, and the effects of HSF1 knockdown on the proliferation, tumor formation, apoptosis and invasion ability were analyzed, respectively. The effects of HSF1 on downstream signals were analyzed using western blotting. Western blotting results showed that lentivirus successfully established a HSF1 knockdown stable cell line of MCF-7. Compared with the control group, the growth rate of MCF-7 cells in the experimental group was significantly decreased (P<0.05). Flow cytometry showed that the proportion of apoptosis in the control group was significantly lower than that of the experimental group (P<0.05). Notably, the invasion ability of cells in the control group was significantly higher than that in the experimental group (P<0.05). Compared with cells in the control group, the levels of heat shock protein (HSP)70, HSP90, anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and macrophage migration inhibitory factor (MIF) in the experimental group were significantly downregulated, whereas the level of Bax was significantly increased (P<0.05). In conclusion, HSF1 protein, as a transcription factor, regulates the expression levels of HSP70, HSP90, MIF, Bcl-2 and Bax, thus controlling the proliferation, apoptosis and invasion of cells. These findings suggest HSF1 protein as a potential target for the treatment of breast cancer.

A study on the biological function of heat shock factor 1 proteins in breast cancer.

The present study aimed to investigate the effect of HSF1 proteins on cell proliferation, apoptosis and invasion of breast cancer. The Michigan Cancer Foundation-7 (MCF-7) HSF1-knocked down stable cell line (experimental group) and control cell line (control group) were obtained using a lentivirus assay, and the effects of HSF1 knockdown on the proliferation, tumor formation, apoptosis and invasion ability were analyzed, respectively. The effects of HSF1 on downstream signals were analyzed using western blotting. Western blotting results showed that lentivirus successfully established a HSF1 knockdown stable cell line of MCF-7. Compared with the control group, the growth rate of MCF-7 cells in the experimental group was significantly decreased (P<0.05). Flow cytometry showed that the proportion of apoptosis in the control group was significantly lower than that of the experimental group (P<0.05). Notably, the invasion ability of cells in the control group was significantly higher than that in the experimental group (P<0.05). Compared with cells in the control group, the levels of heat shock protein (HSP)70, HSP90, anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and macrophage migration inhibitory factor (MIF) in the experimental group were significantly downregulated, whereas the level of Bax was significantly increased (P<0.05). In conclusion, HSF1 protein, as a transcription factor, regulates the expression levels of HSP70, HSP90, MIF, Bcl-2 and Bax, thus controlling the proliferation, apoptosis and invasion of cells. These findings suggest HSF1 protein as a potential target for the treatment of breast cancer.

Lentivirus-mediated RNA interference inhibits the tumorigenicity of cluster of differentiation 44+ tumor cells in hypopharyngeal cancer.

The present study aimed to investigate whether the inhibition of cluster of differentiation (CD)44 expression reduces the tumorigenicity of CD44+ cancer stem cells in hypopharyngeal cancer. To assess this, effective recombinant CD44 short hairpin RNA-expressing lentiviruses were produced. Lentivirus-mediated RNA interference (RNAi) was then used to knockdown CD44 gene expression in the hypopharyngeal cancer FaDu cell line. The viability of FaDu cells in the two control groups and the RNAi group (RNAi-CD44 lentiviral vector) was detected using an MTT assay in vitro. Cells from each group were injected into non-obese diabetic/severe combined immunodeficiency mice and their tumorigenicity determined in vivo. Following lentivirus-mediated RNAi, an MTT assay indicated that cells from the RNAi group exhibited lower viability than the control group. The in vivo tumorigenicity study further revealed a significant difference in tumorigenic rates between the RNAi group and the control group (Fisher's exact test, P<0.05). In addition, tumors in the RNAi group of animals had a longer incubation period than those in the control groups, and the mean tumor volume was also significantly smaller (t=3.47, P<0.05). Pathological study confirmed that all tumors were poorly differentiated squamous cell carcinomas with cellular heterogeneity. The viability of the hypopharyngeal cancer FaDu cells in vitro and their tumorigenicity in vivo were markedly inhibited once CD44 was knocked down. The results of the present study therefore suggest that CD44 may confer tumorigenic characteristics upon CD44+ cancer stem cells in hypopharyngeal cancer.

Downregulation of Heparanase Expression Results in Suppression of Invasion, Migration, and Adhesion Abilities of Hepatocellular Carcinoma Cells.

OBJECTIVE: Heparanase (HPSE) is high-expressed in most malignant tumors including hepatocellular carcinoma (HCC) and promotes cancer cell invasion and migration. The aim of the study is to explore whether HPSE enhances adhesion in metastasis of HCC cells. METHODS: HPSE expressions in human HCC cells were measured with real-time RT-PCR and Western blot analysis. Four recombinant miRNA vectors pcDNATM6.2-GW/EmGFP-miR-HPSE (pmiR-HPSE) were transfected into HCCLM3 cell. HPSE expression in transfected cell was measured. The cell invasion, migration, and adhesion abilities were detected, respectively. RESULTS: Both HPSE mRNA and protein relative expression levels were higher in HepG2, BEL-7402, and HCCLM3 cells than those in normal hepatocyte (P < 0.05). HPSE showed highest expression level in HCCLM3 cell (P < 0.05). Transfection efficiencies of four miRNA vectors were 75%-85%. The recombinant vectors significantly decreased HPSE expression in transfected HCCLM3 cells (P < 0.01), and pmiR-HPSE-1 showed best interference effect (P < 0.05). pmiR-HPSE-1 significantly decreased the penetrated and migrating cells numbers and adherence rate of HCCLM3 cells (P < 0.05). CONCLUSION: HPSE is a potentiator of cell adhesion in metastasis of HCC.

Mid-term results of frontovertical partial laryngectomy for early glottic carcinoma with anterior commissure involvement.

CONCLUSION: Frontovertical partial laryngectomy is useful for treatment of T1 and T2 glottic squamous cell carcinoma with anterior commissure involvement. OBJECTIVE: To evaluate the efficiency of frontovertical partial laryngectomy for T1 and T2 glottic carcinoma with anterior commissure involvement. METHODS: This was a retrospective review of 58 cases of glottic squamous cell carcinoma with anterior commissure involvement (T1, n = 28; T2, n = 30) that were treated by frontovertical partial laryngectomy between August 2000 and August 2010. RESULTS: Postoperative pathology reports confirmed negative tumor margins in every case. All patients were followed postoperatively, with a median follow-up interval of 55 months. Three patients had local recurrence; there were no patients who had cervical or distant metastases. The 3-year local control rate was 94% according to life tables curves. There were no reports of laryngostenosis or dysphagia in any patients, and mean Voice Handicap Index (VHI) questionnaire scores were 32.9.

[The spiral ganglion degeneration and the expression of EFR3A in the cochlea of the deaf mice induced by co-administration of kanamycin and furosemide].

OBJECTIVE: To investigate the spiral ganglion degeneration and the expression of EFR3A in the cochlea of the deaf mice induced by co-administration of kanamycin and furosemide. METHODS: Eight weeks old C57BL/6J mice were administered with a single dose of kanamycin followed by furosemide, then fluorescent immunohistochemistry staining and transmission electron microscopy were applied to observe the SGNs' degeneration process and extent characteristics at 1, 5, 15, 30 and 60 days following treatment. We detected the expression of EFR3A during the degeneration of SGNs via fluorescent immunohistochemistry and western blotting. RESULTS: Co-administration of kanamycin and furosemide quickly induced cochlear hair cell death in mice, and then caused progressive degeneration of SGNs. Our results showed that the abnormal morphology of SGNs occurredat day 5 following administration, and the number of SGNs began to decrease at day 15. Compared to the control group, it was found the remarkable increase of the EFR3A protein at the fifth day after co-administration, then decreased to the nearly normal at 15 days following treatment, and no further significant changes thereafter. CONCLUSION: The changes of the EFR3A protein expression in the spiral ganglion of the cochlea in mice are coincidence with the time of the SGNs degeneration to happen, which imply that EFR3A may play an important role in the occurrence of the SGNs' degeneration in the cochlea in mice following hair cells loss.

CD44 as a molecular marker to screen cancer stem cells in hypopharyngeal cancer.

CONCLUSIONS: The CD44(+) cells have a stronger proliferative capacity and higher tumorigenic potential than the CD44(-) cells, which suggests that the cancer stem cells of hypopharyngeal cancer may exist in the CD44(+) tumor cell population. Therefore, we propose that CD44 is an important biological marker to screen cancer stem cells of hypopharyngeal cancer. OBJECTIVES: To study the significance of CD44 as a molecular marker for screening cancer stem cells in hypopharyngeal cancer. METHODS: The CD44 expression levels in the hypopharyngeal cancer cell line FaDu were analyzed using flow cytometry. To investigate the biological significance of the CD44(+) population, we sorted the CD44(+) and CD44(-) cell populations by using magnetic-associated cell sorting (MACS) technology. After the separation, the purity of the CD44(+) cells was determined using flow cytometry. The MTT method was used to detect the different proliferation capabilities of the CD44(+) and CD44(-) cells in vitro. The tumorigenicity of the CD44(+) and CD44(-) cells was determined by injecting CD44(+) or CD44(-) cells (1 × 10(6) and 1 × 10(5)) into the body of NOD/SCID mice. RESULTS: Some (21.1 ± 1.56)% of the hypopharyngeal cancer cell line FaDu cells expressed CD44. The CD44(+) population was efficiently sorted by MACS, and after separation, the purity of the CD44(+) cells was (99.4 ± 0.29)%. The MTT assay indicated that the sorted CD44(+) cells had a stronger proliferative capacity than the CD44(-) cells. The tumorigenicity study showed that all the mice injected with 1 × 10(6) CD44(+) cells developed tumors (8/8), half the mice injected with 1 × 10(6) CD44(-) cells developed tumors (4/8), 1 of the 8 mice injected with 1 × 10(5) CD44(+) cells developed tumors (12.5%), but none of the mice injected with 1 × 10(5) CD44(-) cells developed any tumors (0/8). At the same concentration, the difference in tumorigenic rates between the CD44(+) and CD44(-) groups was statistically significant (Fisher's exact test, p < 0.05). Furthermore, the CD44(+) group had a shorter incubation period than the CD44(-) group. In addition, the average tumor volume of the CD44(+) group was (2017.81 ± 538.50) mm(3); however, the average tumor volume of the CD44(-) group was (1153.25 ± 503.18) mm(3). The difference was statistically significant (t = 2.67, p < 0.05).