2014 Vol.26(5)
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2014, 26(5): 507-510.
doi: 10.3978/j.issn.1000-9604.2014.08.11
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Abstract:
2014, 26(5): 511-516.
doi: 10.3978/j.issn.1000-9604.2014.09.03
Abstract:
The WW domain-containing oxidoreductase (WWOX) is a tumor suppressor in a variety of cancers, including breast cancer. Reduced WWOX expression is associated with the basal-like subtype and a relatively poor disease-free survival rate among breast cancer patients. Though several WWOX partners have been identified, the functional mechanisms of WWOX’s role in cancers have not been fully addressed to date. In the current study, we found WWOX suppresses expression of KLF5—an oncogenic transcription factor—at protein level, and suppresses cancer cell proliferation in both bladder and breast cancer cell lines. Furthermore, we demonstrated that WWOX physically interacts with KLF5 via the former’s WW domains and the latter’s PY motifs. Interestingly, we found the expression of WWOX negatively correlates with KLF5 expression in a panel of breast cancer cell lines. Taken together, we conjecture that WWOX may suppress cancer cell proliferation partially by reducing the expression of KLF5.
The WW domain-containing oxidoreductase (WWOX) is a tumor suppressor in a variety of cancers, including breast cancer. Reduced WWOX expression is associated with the basal-like subtype and a relatively poor disease-free survival rate among breast cancer patients. Though several WWOX partners have been identified, the functional mechanisms of WWOX’s role in cancers have not been fully addressed to date. In the current study, we found WWOX suppresses expression of KLF5—an oncogenic transcription factor—at protein level, and suppresses cancer cell proliferation in both bladder and breast cancer cell lines. Furthermore, we demonstrated that WWOX physically interacts with KLF5 via the former’s WW domains and the latter’s PY motifs. Interestingly, we found the expression of WWOX negatively correlates with KLF5 expression in a panel of breast cancer cell lines. Taken together, we conjecture that WWOX may suppress cancer cell proliferation partially by reducing the expression of KLF5.
2014, 26(5): 517-524.
doi: 10.3978/j.issn.1000-9604.2014.08.17
Abstract:
PurposeTo determine the diagnostic performance of 3'-deoxy-3'-18F-fluorothymidine positron emission tomography/computed tomography (FLT PET/CT) and FLT PET for evaluating response to chemotherapy in patients with breast cancer. MethodsDatabases such as PubMed (MEDLINE included) and excerpta medica database (EMBASE), were searched for relevant original articles. The included studies were assessed for methodological quality with quality assessment of diagnosis accuracy studies (QUADAS) score tool. Histopathological analysis and/or clinical and/or radiological follow-up for at least 6 months were used as the reference standard. The data were extracted by two reviewers independently to analyze the sensitivity, specificity, summary receiver operating characteristic (SROC) curve, area under the curve (AUC), and heterogeneity. ResultsThe present study analyzed a total of 4 selected articles. The pool sensitivity was 0.773 [95% confidence interval (CI): 0.594-0.900]. The pooled specificity was 0.685 (95% CI: 0.479-0.849) on basis of FEM. The pooled LR+, LR-, and DOR were 2.874 (1.492-5.538), 0.293 (0.146-0.589), and 14.891 (3.238-68.475), respectively. The AUC was 0.8636 (±0.0655), and the Q* index was 0.7942 (±0.0636). ConclusionsOur results indicate that 18F-FLT PET/CT or PET is useful to predict chemotherapy response in breast cancer with reasonable sensitivity, specificity and DOR. However, future larger scale clinical trials will be needed to assess the regimen of 18F-FLT PET/CT or PET in monitoring the response to chemotherapy in breast cancer patients.
2014, 26(5): 525-531.
doi: 10.3978/j.issn.1000-9604.2014.09.02
Abstract:
ObjectiveColorectal cancer (CRC) is one of the most common types of human cancers. As a tumor suppressor, SMAD4 plays a key role in colorectal carcinogenesis and invasiveness. Copy number variations (CNVs) of the SMAD4 gene have been reported to be associated with cancer pathogenesis in array-based studies in different populations. Here we aimed to investigate the CNVs of the SMAD4 gene in a relatively large number of CRC patients from China. MethodsIn the present study, we collected 147 Chinese CRC tumors as well as self-paired normal control tissues. Quantitative PCR was carried out to examine the copy number as well as the mRNA expression of the SMAD4 gene. ResultsOur results showed that the copy number deletions of SMAD4 were frequent in a relatively high percentage of CRC samples (34.7%, 51 out of 147). There was a positive correlation between the copy number decrease of SMAD4 and tumor progression in CRCs. Furthermore, copy number loss of SMAD4 was correlated with decreased mRNA expression. ConclusionsThese findings suggested that the copy number deletions of SMAD4 were frequent in CRC patients from China and had the potential to serve as a diagnostic indicator, alone or in combination with other markers, for CRC.
2014, 26(5): 532-542.
doi: 10.3978/j.issn.1000-9604.2014.08.23
Abstract:
ObjectiveTo detect the activity of tumor cells and tumor blood flow before and after the radiotherapy of implanted pulmonary VX-2 carcinoma in rabbit models by using magnetic resonance diffusion-weighted imaging (MR-DWI) and magnetic resonance perfusion weighted imaging (MR-PWI), and to evaluate the effectiveness and safety of the radiotherapy based on the changes in the MR-DWI and MR-PWI parameters at different treatment stages. MethodsA total of 56 rabbit models with implanted pulmonary VX-2 carcinoma were established, and then equally divided into treatment group and control group. MR-DWI and MR-PWI were separately performed using a Philips Acheiva 1.5T MRI machine (Philips, Netherland). MRI image processing was performed using special perfusion software and the WORKSPACE advanced workstation for MRI. MR-DWI was applied for the observation of tumor signals and the measurement of apparent diffusion coefficient (ADC) values; whereas MR-PWI was used for the measurement of wash in rate (WIR), wash out rate (WOR), and maximum enhancement rate (MER). The radiation treatment was performed using Siemens PRIMUS linear accelerator. In the treatment group, the radiotherapy was performed 21 days later on a once weekly dosage of 1,000 cGy to yield a total dosage of 5,000 cGy. ResultsThe ADC parameters in the region of interest on DWI were as follows: on the treatment day for the implanted pulmonary VX-2 carcinoma, the t values at the center and the edge of the lesions were 1.352 and 1.461 in the treatment group and control group (P>0.05). During weeks 0-1 after treatment, the t values at the center and the edge of the lesions were 1.336 and 1.137 (P>0.05). During weeks 1-2, the t values were 1.731 and 1.736 (P<0.05). During weeks 2-3, the t values were 1.742 and 1.749 (P<0.05). During weeks 3-4, the t values were 2.050 and 2.127 (P<0.05). During weeks 4-5, the t values were 2.764 and 2.985 (P<0.05). The ADC values in the treatment group were significantly higher than in the control group. After the radiotherapy (5,000 cGy), the tumors remarkably shrank, along with low signal on DWI, decreased signal on ADC map, and remarkably increased ADC values. As shown on PWI, on the treatment day for the implanted pulmonary VX-2 carcinoma, the t values of the WIR, WOR, and MER at the center of the lesions were 1.05, 1.31, and 1.33 in the treatment group and control group (P>0.05); in addition, the t values of the WIR, WOR, and MER at the edge of the lesions were 1.35, 1.07, and 1.51 (P>0.05). During weeks 0-1 after treatment, the t values of the WIR, WOR, and MER at the center of the lesions were 1.821, 1.856, and 1.931 (P<0.05); in addition, the t values of the WIR, WOR, and MER at the edge of the lesions were 1.799, 2.016, and 2.137 (P<0.05). During weeks 1-1 after treatment, the t values of the WIR, WOR, and MER at the center of the lesions were 2.574, 2.156, and 2.059 (P<0.05) and the t values of the WIR, WOR, and MER at the edge of the lesions were 1.869, 2.058, and 2.057 (P<0.05). During weeks 2-3 after treatment, the t values of the WIR, WOR, and MER at the center of the lesions were 2.461, 2.098, and 2.739 (P<0.05) and the t values of the WIR, WOR, and MER at the edge of the lesions were 2.951, 2.625, and 2.154 (P<0.05). During weeks 3-4 after treatment, the t values of the WIR, WOR, and MER at the center of the lesions were 2.584, 2.107, and 2.869 (P<0.05) and the t values of the WIR, WOR, and MER at the edge of the lesions were 2.057, 2.637, and 2.951 (P<0.05). During weeks 4-5 after treatment, the t values of the WIR, WOR, and MER at the center of the lesions were 2.894, 2.827, and 3.285 (P<0.05) and the t values of the WIR, WOR, and MER at the edge of the lesions were 3.45, 3.246, and 3.614 (P<0.05). After the radiotherapy (500 cGy), the tumors shrank on the T1WI, WIR, WOR, and MER; meanwhile, the PWI parameter gradually decreased and reached its minimum value. ConclusionsMR-DWI and MR-PWI can accurately and directly reflect the inactivation of tumor cells and the tumor hemodynamics in rabbit models with implanted pulmonary VX-2 carcinoma, and thus provide theoretical evidences for judging the clinical effectiveness of radiotherapy for the squamous cell carcinoma of the lung.
2014, 26(5): 543-549.
doi: 10.3978/j.issn.1000-9604.2014.10.03
Abstract:
ObjectiveTo compare clinical characteristics between familial nasopharyngeal carcinomas (NPCs) and sporadic NPCs in Guangdong province, China, a high-risk area. MethodsBetween 1991 and 2001, 993 NPC patients treated at the Cancer Center of Sun Yat-Sen University in Guangdong were randomly selected as probands. Information about NPC among the probands’ relatives and other information were obtained from a retrospective review of the patients’ medical records. The patients were divided into sporadic NPC, low-frequency familial NPC (one NPC patient in addition to the proband in three generations), and high-frequency familial NPC (2 or more additional NPC patients in three generations) groups. Pathological and clinical characteristics were compared among these groups. ResultsOf the 993 patients, 131 (13.2%) had a familial history of NPC. The average age at diagnosis was the lowest in the high-frequency familial NPC group (39 years; P=0.048). Although the overall survival (OS), distant metastasis-free survival (DMFS), and disease-free survival (DFS) rates did not differ between familial and sporadic NPCs, the locoregional recurrence-free survival (LRFS) rate increased in the order sporadic NPCs, low-frequency familial NPCs, and high-frequency familial NPCs (P=0.009), with 5-year rates of 70%, 83%, and 87%, respectively. Multivariate analysis showed that family history of NPC was an independent favorable prognostic factor for LRFS, with adjusted hazard ratio (aHR) of 0.548, 95% CI (0.342-0.878). The high LRFS for familial NPCs was mainly noted among young, advanced-stage patients who received continuous radiation treatment. ConclusionsGenetic factors may play an important role in the etiology of high-frequency familial NPC and underlie the early age of onset and sensitivity to radiotherapy.
2014, 26(5): 550-557.
doi: 10.3978/j.issn.1000-9604.2014.10.02
Abstract:
ObjectiveTo investigate the efficacy and safety of capecitabine maintenance therapy (MT) after initial capecitabine plus docetaxel (XT) chemotherapy in patients with metastatic triple-negative breast cancer (mTNBC). MethodsFifty-five mTNBC patients treated with XT chemotherapy between May 2007 and June 2013 were retrospectively analyzed. When initial disease control was achieved by the combination chemotherapy, capecitabine was continued for 32 patients (MT), while 23 patients remained without any treatment (non-MT). We compared progression-free survival (PFS) and safety of both groups. ResultsThe median PFS of 55 patients was 8.1 months, overall median PFS time of 32 patients in the capecitabine MT group and 23 in the non-MT group was 10.1 vs. 6.7 months (P=0.032), respectively. When compared PFS time of maintenance treatment, single-agent capecitabine prolonged PFS by 7.1 months, for non-MT patients, the PFS without any treatment was 3.1 months, and this between-group difference was statistically significant (P=0.003). Adverse events, including of hematologic toxicity, gastrointestinal toxicities, hand-foot syndrome and abnormal liver function were not significantly different between two groups. ConclusionsAfter initial disease control was achieved with the XT combination chemotherapy, capecitabine MT can significantly prolong PFS time with a favorable safety profile in mTNBC patients.
2014, 26(5): 558-563.
doi: 10.3978/j.issn.1000-9604.2014.10.05
Abstract:
ObjectiveTo evaluate the clinical effect of transurethral resection of bladder tumor (TUR-BT) combined with internal iliac artery chemotherapy and intravesical instillation therapy for muscle invasive bladder cancer (MIBC). MethodsFrom February 2007 to April 2014, 62 patients with MIBC were treated with TUR-BT combined with intravesical instillation therapy, with or without internal iliac artery chemotherapy, and the chemotherapy regimen is gemcitabine and cisplatin (GC). The bladder preservation and survival rate as well as cancer-specific survival (CSS) rate and overall survival (OS) rate of the two groups were compared. ResultsSixty-two patients were followed-up for 26-102 months with an average of 58.4±3.1 months. Recurrence-free survival (RFS) at 2-year for TUR + GC group and TUR group were 77.8% and 53.8%, respectively. Bladder preserved rate (BPR) at 3-year for TUR + GC group and TUR group were 94.4% and 80.8%. CSS rate at 2-year for TUR + GC group and TUR group were 94.4% and 84.6%. The disease-free survival (DFS) at 1-year for TUR + GC group and TUR group were 83.3% and 61.5%, and 77.8% and 53.8% for the 2nd year. OS at 2-year for TUR + GC group and TUR group were 88.9% and 92.3%. ConclusionsTUR-BT and intravesical instillation therapy combined with internal iliac artery chemotherapy for MIBC had a better outcome at RFS, BPR and DFS than the treatment without internal iliac artery chemotherapy, and no difference in OS and CSS.
2014, 26(5): 564-572.
doi: 10.3978/j.issn.1000-9604.2014.08.20
Abstract:
The activation of the PI3K/AKT/mTOR pathway plays a key role in ovarian cancer tumorigenesis, progression and chemotherapy resistance. This study aimed to explore the possible mechanism that PI-103, a dual inhibitor of phosphatidylinositide 3-kinase and mTOR, enhances the sensitivity of SKOV3/DDP ovarian cancer cell line to cisplatin chemotherapy. The results showed that PI-103 could significantly increase the sensitivity of SKVO3/DDP cells to cisplatin through inhibiting the activation of PI3K/Akt/mTOR signaling pathway and inducing cell cycle arrest and apoptosis.
The activation of the PI3K/AKT/mTOR pathway plays a key role in ovarian cancer tumorigenesis, progression and chemotherapy resistance. This study aimed to explore the possible mechanism that PI-103, a dual inhibitor of phosphatidylinositide 3-kinase and mTOR, enhances the sensitivity of SKOV3/DDP ovarian cancer cell line to cisplatin chemotherapy. The results showed that PI-103 could significantly increase the sensitivity of SKVO3/DDP cells to cisplatin through inhibiting the activation of PI3K/Akt/mTOR signaling pathway and inducing cell cycle arrest and apoptosis.
2014, 26(5): 573-578.
doi: 10.3978/j.issn.1000-9604.2014.08.21
Abstract:
Lung cancer is one of the most deadly human cancers and continues to be a major unsolved health problem worldwide. Here, we evaluate the function of Pbx1 in the proliferation of non-small-cell lung cancer (NSCLC). In contrast with its known proliferative function, we found that Pbx1 inhibits the proliferation of lung cancer cells. In particular, Pbx1-specific RNA interference resulted in increased proliferation in lung cancer cells. In addition, histone H3 phosphorylation was also increased following inhibition of Pbx1 expression. In contrast, Pbx1 overexpression repressed the proliferation of lung cancer cells and inhibited DNA synthesis. Collectively, our data indicate that Pbx1 inhibits proliferation in lung cancer cells, suggesting a complex role for Pbx1 in modulating the proliferation of cancer cells and making this protein a potential new target for lung cancer therapy.
Lung cancer is one of the most deadly human cancers and continues to be a major unsolved health problem worldwide. Here, we evaluate the function of Pbx1 in the proliferation of non-small-cell lung cancer (NSCLC). In contrast with its known proliferative function, we found that Pbx1 inhibits the proliferation of lung cancer cells. In particular, Pbx1-specific RNA interference resulted in increased proliferation in lung cancer cells. In addition, histone H3 phosphorylation was also increased following inhibition of Pbx1 expression. In contrast, Pbx1 overexpression repressed the proliferation of lung cancer cells and inhibited DNA synthesis. Collectively, our data indicate that Pbx1 inhibits proliferation in lung cancer cells, suggesting a complex role for Pbx1 in modulating the proliferation of cancer cells and making this protein a potential new target for lung cancer therapy.
2014, 26(5): 579-587.
doi: 10.3978/j.issn.1000-9604.2014.10.06
Abstract:
BackgroundIntraductal administration of cytotoxic agents has been shown to inhibit the development of breast cancer in animal models. The object of this study was to demonstrate the safety of intraductal delivery cytotoxic agents in patients prior to mastectomy. This method is hopeful to be developed as a chemoprevention approach in patients with pre-malignant or non-invasive ductal lesions to prevent breast cancer which will be further developed. MethodsTwo drugs, pegylated liposomal doxorubicin (PLD) and carboplatin were administered at three dose levels (PLD: 10, 20, 50 mg and carboplatin 60, 120, 300 mg). There were five subjects in each group with 15 subjects treated with each drug once. Venous blood samples were obtained for pharmacokinetic analysis. The breast was removed surgically 2-5 days post administration and the treated ducts were marked to enable identification on pathological evaluation. ResultsIntraductal administration was generally well-tolerated with mild, transient breast discomfort. In the carboplatin arm, three women at the 300 mg dose experienced mild nausea and vomiting. In the PLD arm most women had mild erythema and swelling of the breast over the 72 hours following the drug administration. Patients receiving the 50 mg dose experienced local erythema until the time of surgery. Pharmacokinetic analysis showed that carboplatin rapidly entered systemic circulation with an early peak time (Tmax ~30 min) with a corresponding plasma ultrafiltrate area under the curve (AUC) consistent with the Calvert Formula using estimated glomerular filtration rate (GFR). Total plasma doxorubicin had delayed peak concentration times (Tmax >48 hours) with a linear dose response and peak concentrations substantially lower than expected from equivalent intravenous injection dosing. No doxorubicinol metabolite was detected in the plasma. ConclusionsThis study demonstrates that cytotoxic drugs can be safely administered into breast ducts with minimal toxicity.
2014, 26(5): 588-595.
doi: 10.3978/j.issn.1000-9604.2014.10.07
Abstract:
ObjectivePortal vein metastasis of hepatocellular carcinoma (HCC) results in a poor prognosis and seriously affects the survival rate of patients. The mechanism underlying the formation of portal vein tumor thrombus (PVTT) is complex and is not yet fully understood. This study was conducted to investigate the impact of portal vein blood on the proliferation, metastasis, invasion and apoptosis of PVTT cells and to explore its possible mechanisms, which was expected to lay a foundation for ascertaining the mechanism underlying the portal vein metastasis of HCC. MethodsPeripheral blood and portal vein blood were collected from patients with HCC, and the sera from these two sources were used to culture the PVTT-originated HCC cell line CSQT-2. The cells were collected after 24 h, and flow cytometry was performed to detect cell proliferation, cell cycle stages and apoptosis. Transwell migration and invasion assays were applied to detect the metastasis and invasion of the cells in each group. The changes in the expression of MMP-2 and MMP-9 in cells were detected via Western blotting. The contents of IL-12, IFN-γ, IL-1β, IL-2 and TNF-α in the two groups of sera were quantified using corresponding kits. ResultsCompared with the group of cells cultured with peripheral serum, the cells cultured with portal vein serum showed significantly lower apoptosis (P<0.01), significantly enhanced cell metastasis and invasion (P<0.01), whereas cell proliferation and the stages of the cell cycle did not differ significantly (P>0.05). A significantly increased expression level of MMP-2 has been observed in tumor cells treated portal vein serum. In addition, compared with peripheral serum, the content of IL-12 was significantly decreased in portal vein serum (P<0.05), while the contents of IFN-γ, IL-1β, IL-2, and TNF-α did not differ significantly (P>0.05). ConclusionsPortal vein serum from HCC patients could inhibit the apoptosis of PVTT-originated HCC cells and promote cell metastasis and invasion. This effect may be related to the lower level of IL-12 in portal vein serum.
2014, 26(5): 596-601.
doi: 10.3978/j.issn.1000-9604.2014.10.09
Abstract:
ObjectiveT-stage and N-stage have been proven to be the most important factors influencing survival in gastric cancer patients, and have been accepted for use in the Japanese Classification of Gastric Carcinoma (JCGC) and the Union International Cancer Control (UICC-TNM) staging systems. The purpose of this study was to compare the prognostic values of the different N classification systems in gastric cancer patients without serosal invasion. MethodsWe retrospectively compared the clinicopathological results of 1,115 patients with primary gastric cancer who underwent curative gastric resection. ResultsSerosal invasion was identified in 212 of 1,115 patients (19.0%), and it was associated with lymph node metastasis according to the JCGC13th (P<0.001) and TNM7th (P<0.001) systems. The 5-year survival rate for the serosal invasion-negative patients (78.2%) was significantly higher than that for the serosal invasion-positive patients (31.1%) (P<0.001). Multivariate Cox regression survival analysis showed that depth of invasion (P=0.013), 13th JCGC PN stage (P<0.001), and 7th TNM PN stage (P<0.001) were independent prognostic factors for serosal invasion-negative gastric cancer patients. ConclusionsThe prognosis of gastric cancer patients with serosal invasion is very poor. Both the 13th JCGC and 7th TNM N-staging systems were able to accurately estimate the prognosis of gastric cancer patients, but the 7th TNM system was simpler and easier to use.
2014, 26(5): 602-610.
doi: 10.3978/j.issn.1000-9604.2014.10.08
Abstract:
PurposeStanniocalcin (STC) has been recognized as a potential biomarker in a variety of cancers. The aim of this study was to examine STC1 and STC2 expression in tumor and serum samples from gastric cancer (GC) patients. MethodsA total of 83 GC patients treated with radical resection were enrolled in this study. Immunohistochemistry was used to detect STC protein expression in paired tumor and adjacent normal tissues. Serum STC levels were determined by enzyme-linked immunosorbent assay (ELISA). The receiver operating characteristics (ROC) curve was constructed to describe diagnostic specificity and sensitivity. ResultsBoth of STC1 and STC2 protein expression were upregulated in GC tissues compared with that in normal ones. Moreover, the high/moderate of STC1 protein was significantly associated with lymph metastasis, clinical stage and adverse 3-year progression-free survival (PFS). In addition, serum STC1 and STC2 expression in GC patients were much higher than that in patients with benign gastric disease, which decreased at postoperative 7-10 days. The sensitivity of serum STC protein also showed superiority over CEA and CA19-9. ConclusionsSTC upregulation plays an important role in GC development, and serum STC1 and STC2 might function as promising tumor markers for GC diagnosis and prognosis.
2014, 26(5): 611-621.
doi: 10.3978/j.issn.1000-9604.2014.09.04
Abstract:
Radiation is an important modality in cancer treatment, and eighty percent of cancer patients need radiotherapy at some point during their clinical management. However, radiation-induced damage to normal tissues restricts the therapeutic doses of radiation that can be delivered to tumours and thereby limits the effectiveness of the treatment. The use of radioprotectors represents an obvious strategy to obtain better tumour control using a higher dose in radiotherapy. However, most of the synthetic radioprotective compounds studied have shown inadequate clinical efficacy owing to their inherent toxicity and high cost. Hence, the development of radioprotective agents with lower toxicity and an extended window of protection has attracted a great deal of attention, and the identification of alternative agents that are less toxic and highly effective is an absolute necessity. Recent studies have shown that alpha-2-macroglobulin (α2M) possesses radioprotective effects. α2M is a tetrameric, disulfide-rich plasma glycoprotein that functions as a non-selective inhibitor of different types of non-specific proteases and as a carrier of cytokines, growth factors, and hormones. α2M induces protein factors whose interplay underlies radioprotection, which supports the idea that α2M is the central effector of natural radioprotection in the rat. Pretreatment with α2M has also induced a significant reduction of irradiation-induced DNA damage and the complete restoration of liver and body weight. Mihailović et al. concluded that the radioprotection provided by α2M was in part mediated through cytoprotection of new blood cells produced in the bone marrow; these authors also indicated that an important aspect of the radioprotective effect of amifostine was the result of the induction of the endogenous cytoprotective capability of α2M. The radioprotective effects of α2M are possibly due to antioxidant, anti-fibrosis, and anti-inflammatory functions, as well as the maintenance of homeostasis, and enhancement of the DNA repair and cell recovery processes. This review is the first to summarise the observations and elucidate the possible mechanisms responsible for the beneficial effects of α2M. The lacunae in the existing knowledge and directions for future research are also addressed.
Radiation is an important modality in cancer treatment, and eighty percent of cancer patients need radiotherapy at some point during their clinical management. However, radiation-induced damage to normal tissues restricts the therapeutic doses of radiation that can be delivered to tumours and thereby limits the effectiveness of the treatment. The use of radioprotectors represents an obvious strategy to obtain better tumour control using a higher dose in radiotherapy. However, most of the synthetic radioprotective compounds studied have shown inadequate clinical efficacy owing to their inherent toxicity and high cost. Hence, the development of radioprotective agents with lower toxicity and an extended window of protection has attracted a great deal of attention, and the identification of alternative agents that are less toxic and highly effective is an absolute necessity. Recent studies have shown that alpha-2-macroglobulin (α2M) possesses radioprotective effects. α2M is a tetrameric, disulfide-rich plasma glycoprotein that functions as a non-selective inhibitor of different types of non-specific proteases and as a carrier of cytokines, growth factors, and hormones. α2M induces protein factors whose interplay underlies radioprotection, which supports the idea that α2M is the central effector of natural radioprotection in the rat. Pretreatment with α2M has also induced a significant reduction of irradiation-induced DNA damage and the complete restoration of liver and body weight. Mihailović et al. concluded that the radioprotection provided by α2M was in part mediated through cytoprotection of new blood cells produced in the bone marrow; these authors also indicated that an important aspect of the radioprotective effect of amifostine was the result of the induction of the endogenous cytoprotective capability of α2M. The radioprotective effects of α2M are possibly due to antioxidant, anti-fibrosis, and anti-inflammatory functions, as well as the maintenance of homeostasis, and enhancement of the DNA repair and cell recovery processes. This review is the first to summarise the observations and elucidate the possible mechanisms responsible for the beneficial effects of α2M. The lacunae in the existing knowledge and directions for future research are also addressed.
2014, 26(5): 622-626.
doi: 10.3978/j.issn.1000-9604.2014.09.01
Abstract:
Triptolide (TPL/TL) is a natural drug with novel anticancer effects. Preclinical studies indicated that TPL inhibits cell proliferation, induces cell apoptosis, inhibits tumor metastasis and enhances the effect of other therapeutic methods in various cancer cell lines. Multiple molecules and signaling pathways, such as caspases, heat-shock proteins, NF-κB, and deoxyribonucleic acid (DNA) repair-associated factors, are associated with the anti-cancer effect. TPL also improves chemoradiosensitivity in cancer therapy. Phase I trials indicate the potential clinical value of TPL use. However, further trials with larger sample sizes are needed to confirm these results.
Triptolide (TPL/TL) is a natural drug with novel anticancer effects. Preclinical studies indicated that TPL inhibits cell proliferation, induces cell apoptosis, inhibits tumor metastasis and enhances the effect of other therapeutic methods in various cancer cell lines. Multiple molecules and signaling pathways, such as caspases, heat-shock proteins, NF-κB, and deoxyribonucleic acid (DNA) repair-associated factors, are associated with the anti-cancer effect. TPL also improves chemoradiosensitivity in cancer therapy. Phase I trials indicate the potential clinical value of TPL use. However, further trials with larger sample sizes are needed to confirm these results.
2014, 26(5): 627-631.
doi: 10.3978/j.issn.1000-9604.2014.10.04
Abstract:
Primary small cell carcinoma (SCC) is a group of aggressive neoplasms that mainly arise from the lung and digestive tract. Endometrial small cell carcinoma (ESCC) is extremely rare. To our knowledge, less than 90 cases have been reported, and most of these reports were dedicated to describing the clinicopathologic or immunochemical features of ESCC. Herein, we present a new case of ESCC involving a 51-year-old woman and mainly focus on the magnetic resonance imaging (MRI) and positron emission tomography/computed tomography (PET/CT) findings. MRI showed that the uterus was significantly enlarged (11.6 cm × 11.1 cm × 14.4 cm), and a giant irregular mass (7.5 cm × 8.4 cm × 8.5 cm) was observed in the uterine cavity. The lesion demonstrated an extremely low apparent diffusion coefficient (ADC) value [(0.553±0.088)×10–3 mm2/s] and a high FDG uptake value (22.7). Multiple metastatic lymph nodes (LNs) were identified at different positions, with diameters ranging from 0.3 to 2.8 cm and a maximum standardized uptake value (SUVmax) ranging from 6.9 to 19.3.
Primary small cell carcinoma (SCC) is a group of aggressive neoplasms that mainly arise from the lung and digestive tract. Endometrial small cell carcinoma (ESCC) is extremely rare. To our knowledge, less than 90 cases have been reported, and most of these reports were dedicated to describing the clinicopathologic or immunochemical features of ESCC. Herein, we present a new case of ESCC involving a 51-year-old woman and mainly focus on the magnetic resonance imaging (MRI) and positron emission tomography/computed tomography (PET/CT) findings. MRI showed that the uterus was significantly enlarged (11.6 cm × 11.1 cm × 14.4 cm), and a giant irregular mass (7.5 cm × 8.4 cm × 8.5 cm) was observed in the uterine cavity. The lesion demonstrated an extremely low apparent diffusion coefficient (ADC) value [(0.553±0.088)×10–3 mm2/s] and a high FDG uptake value (22.7). Multiple metastatic lymph nodes (LNs) were identified at different positions, with diameters ranging from 0.3 to 2.8 cm and a maximum standardized uptake value (SUVmax) ranging from 6.9 to 19.3.
2014, 26(5): 632-638.
doi: 10.3978/j.issn.1000-9604.2014.10.01
Abstract:
Paraneoplastic dermatoses are known to be certain dermatosis related with tumor. The common paraneoplastic dermatoses are acanthosis nigricans, acquired ichthyosis, dermatomyositis, erythroderma, and so on. Here we report two cases of paraneoplastic dermatoses associated with gastric cancer. One case was a 57-year-old man with dermatomyositis and proved to be associated with gastric cancer through stomachoscopy. The other was a 66-year-old man with erythroderma and proved to be associated with gastric cancer through stomachoscopy. Both cases were treated with radical total gastrectomy with lymphadenectomy (D2) and esophagojejunostomy of Roux-en-Y. The skin symptom of both cases had improved a lot but still existed after operation. Paraneoplastic dermatoses can be seen as the early manifestation of visceral carcinomas. As a result, gastric cancers should be excluded in the patients with paraneoplastic dermatoses.
Paraneoplastic dermatoses are known to be certain dermatosis related with tumor. The common paraneoplastic dermatoses are acanthosis nigricans, acquired ichthyosis, dermatomyositis, erythroderma, and so on. Here we report two cases of paraneoplastic dermatoses associated with gastric cancer. One case was a 57-year-old man with dermatomyositis and proved to be associated with gastric cancer through stomachoscopy. The other was a 66-year-old man with erythroderma and proved to be associated with gastric cancer through stomachoscopy. Both cases were treated with radical total gastrectomy with lymphadenectomy (D2) and esophagojejunostomy of Roux-en-Y. The skin symptom of both cases had improved a lot but still existed after operation. Paraneoplastic dermatoses can be seen as the early manifestation of visceral carcinomas. As a result, gastric cancers should be excluded in the patients with paraneoplastic dermatoses.
