CN103983763A - Reactivity of colon cancer artery to vasoconstrictive medium - Google Patents

Reactivity of colon cancer artery to vasoconstrictive medium Download PDF

Info

Publication number
CN103983763A
CN103983763A CN201410206440.2A CN201410206440A CN103983763A CN 103983763 A CN103983763 A CN 103983763A CN 201410206440 A CN201410206440 A CN 201410206440A CN 103983763 A CN103983763 A CN 103983763A
Authority
CN
China
Prior art keywords
artery
cancer
contraction
acceptor
colon cancer
Prior art date
Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
Pending
Application number
CN201410206440.2A
Other languages
Chinese (zh)
Inventor
李洁
林杰
王俊杰
徐雨佳
阳建军
王安发
陈碧
张永东
Current Assignee (The listed assignees may be inaccurate. Google has not performed a legal analysis and makes no representation or warranty as to the accuracy of the list.)
Chenzhou First People's Hospital
Original Assignee
李洁
林杰
王俊杰
Priority date (The priority date is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the date listed.)
Filing date
Publication date
Application filed by 李洁, 林杰, 王俊杰 filed Critical 李洁
Priority to CN201410206440.2A priority Critical patent/CN103983763A/en
Publication of CN103983763A publication Critical patent/CN103983763A/en
Pending legal-status Critical Current

Links

Classifications

    • G—PHYSICS
    • G01—MEASURING; TESTING
    • G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
    • G01N33/00—Investigating or analysing materials by specific methods not covered by groups G01N1/00 - G01N31/00
    • G01N33/48—Biological material, e.g. blood, urine; Haemocytometers
    • G01N33/50—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing
    • G01N33/5005—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving human or animal cells
    • G01N33/5008—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving human or animal cells for testing or evaluating the effect of chemical or biological compounds, e.g. drugs, cosmetics
    • G01N33/5014—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving human or animal cells for testing or evaluating the effect of chemical or biological compounds, e.g. drugs, cosmetics for testing toxicity
    • G01N33/5017—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving human or animal cells for testing or evaluating the effect of chemical or biological compounds, e.g. drugs, cosmetics for testing toxicity for testing neoplastic activity

Landscapes

  • Health & Medical Sciences (AREA)
  • Engineering & Computer Science (AREA)
  • Life Sciences & Earth Sciences (AREA)
  • Biomedical Technology (AREA)
  • Immunology (AREA)
  • Hematology (AREA)
  • Toxicology (AREA)
  • Chemical & Material Sciences (AREA)
  • Urology & Nephrology (AREA)
  • Molecular Biology (AREA)
  • Tropical Medicine & Parasitology (AREA)
  • Physics & Mathematics (AREA)
  • Cell Biology (AREA)
  • Biotechnology (AREA)
  • Bioinformatics & Cheminformatics (AREA)
  • Food Science & Technology (AREA)
  • Medicinal Chemistry (AREA)
  • Microbiology (AREA)
  • Analytical Chemistry (AREA)
  • Biochemistry (AREA)
  • General Health & Medical Sciences (AREA)
  • General Physics & Mathematics (AREA)
  • Pathology (AREA)
  • Investigating Or Analysing Biological Materials (AREA)

Abstract

The invention discloses the reactivity of a colon cancer artery to a vasoconstrictive medium. An alpha receptor and an ETA receptor are main vasoconstrictive receptors of a normal artery, and the vasoconstrictive action of the alpha receptor and the ETA receptor of the colon cancer artery is obviously weaker than that of a cancer peripheral artery. The maximal contraction and the half-maximal effect concentration of normal artery contraction caused by noradrenaline (NA) are respectively 97%+/-19% and 5.94+/-0.17, Emax and pEC50 of the NA contraction of the colon cancer artery are respectively 74%+/-5% and 5.54+/-0.21, and Emax and pEC50 of the contraction of the cancer peripheral artery are respectively 119%+/-11% and 5.84+/-0.09.

Description

The reactivity of colon cancer artery to contracting blood vessel medium
Technical field
The invention belongs to medicine technology field, relate to the reactivity of colon cancer artery to contracting blood vessel medium.
Background technology
Rapid growth is the maximum feature of tumor tissues, and blood supply is to ensure its growth, the key factor that infiltrates and shift [1], the vessel density of cancerous tissue is an important parameter of reflection malignant tumour biological behaviour, significant to growth of tumour cell, propagation, invasion and attack and transfer [2], be almost independently Prognostic Factors of solid tumor [3-5].Tumor vessel has notable difference with non-cancer patient vessel in cell composition, institutional framework and functional characteristics, lacks the periphery cell of complete blood vessel.The easypro contracting state of blood vessel is the greatest factor of impact domination Tissue Blood flow, is regulated and controled by angiokinesis acceptor and respective ligand.
Summary of the invention
The present invention is the reactivity of colon cancer artery to contracting blood vessel medium.For treatment malignant tumour provides theoretical foundation.
The variation of tumor vessel structure and the requirement of function may cause that tumor vessel changes vaso-active substance is reactive.The present invention verifies that tumour artery reduces the reactivity of vaso-excitor material, or the reactivity of vasodilator is increased, or the two haves both at the same time.The reactivity of the artery (cancer artery) that the present invention has verified supply colon cancer to several frequently seen vaso-excitor material, and compare with edge artery (cancer week artery) around of cancer piece and non-cancer patient's edge artery (normal artery), study cancer artery α-adrenoceptor, serotonin (5-HT) acceptor, Endothelin A (ET a) and Endothelin B (ET b) variation of function of receptors.
The present invention has studied the reactivity of colon cancer artery to contracting blood vessel medium.Method, get the artery (cancer artery) of colorectal cancer patients supply cancer piece, taking edge artery (cancer week artery) around of cancer piece and non-cancer patient's edge artery (normal artery) as contrasting, artery is cut into the arterial ring that is about 1mm, records the amount effect curve that 4 kinds of receptor stimulating agents shrink artery.Result: norepinephrine (NA) causes the maximum collapse (E that normal artery shrinks max) and half-maximal effect concentration (pEC 50) be respectively 97% ± 19% and 5.94 ± 0.17; The E that colon cancer artery NA shrinks maxand pEC 50be respectively 74% ± 5% and 5.54 ± 0.21, the E of cancer week artery contraction maxand pEC 50be respectively 119% ± 11% and 5.84 ± 0.09.The E that colon cancer artery NA shrinks maxcompared with cancer week artery and the E that shrinks with normal artery maxvalue significantly reduces (P < 0.01, P < 0.05).Endothelin B (ET b) receptor stimulating agent S6c do not cause contraction at arteria colica.The E that endothelin-1 (ET-1) shrinks normal artery maxand pEC 50be respectively 106% ± 7% and 8.85 ± 0.17, to the E of colon cancer artery and the artery contraction of cancer week maxraise, be respectively 130% ± 6% and 248% ± 34% (P < 0.01); ET-1 causes the pEC of cancer artery and the artery contraction of cancer week 50be respectively 8.09 ± 0.10 and 8.37 ± 0.04.5-HT only causes weak contraction at normal artery.Conclusion: α acceptor and ET aacceptor is the main contracting blood vessel acceptor of normal artery; α acceptor and the ET of colon cancer artery athe contracting blood vessel function of acceptor is obviously weaker than cancer week artery.
Brief description of the drawings
Fig. 1 is ET-1, S6c, concentration-contraction dose-effect curve map that NA and 5-HT cause at colorectal cancer patients cancer artery;
Fig. 2 is concentration-contraction dose-effect curve map that NA causes at colorectal cancer patients cancer artery, all arteries of cancer and non-cancer patient edge artery;
Fig. 3 is the concentration-contraction dose-effect curve map causing at colorectal cancer patients cancer artery, all arteries of cancer and non-cancer patient edge artery;
Fig. 4 is concentration-contraction dose-effect curve map that 5-HT causes at colorectal cancer patients cancer artery, all arteries of cancer and non-cancer patient edge artery.
Embodiment
Below the present invention is tested:
1 materials and methods:
1.1, material.The colorectal cancer patients (n=5,46～61 years old age, 4 male sex, 1 women) that preoperative biopsy or pathologic examination after operation are made a definite diagnosis, adopts radical operation, takes out cancer affected part position, separates the artery (cancer artery) of supply cancer piece; Around cancer, the edge artery of about 10cm is considered to the artery (cancer week artery) of non-cancer tissue, and operating room takes out; Non-cancer patient's edge artery is taken from traffic hazard patient (n=5,36～60 years old age, 4 male sex, 1 women), thinks normal artery.Take out after artery, put cold Krebs liquid (containing mmolL -1: NaCl119, NaHCO 315, KCl4.6, MgCl 21.2, NaH 2pO 41.2, CaCl 21.5 and glucose 5.5).
Norepinephrine (noradrenaline, NA), Propranolol, acetylcholine (ACh), serotonin (5-hydroxytryptamine, 5-HT), endothelin-1 (ET-1), Sarafotoxin6c (S6c) are Sigma company product, and by Lund, Sweden, university provides.Above reagent is dissolved in 0.1% bovine serum albumin(BSA), faces in order to Krebs liquid and dilutes.Concentration represents with the concentration of final medicine in bath.
1.2 methods:
1.2.1 the preparation of arterial ring: peel off blood vessel surrounding tissue under microscope, perfusion 10s, removes blood vessel endothelium in 0.1%Triton x-100 blood vessel, then rinses 10s with damping fluid, as the diastolic rate < 10% that ACh causes, think that endothelium removes.The blood vessel of handling well is cut into the long cylindrical section of 1mm, vascular circle external diameter 0.6～1.0mm, every part of sample is got 1～2 vascular circle.
1.2.2, antiotasis is traced: arterial ring is enclosed within on the metal needle of two L-types, one of them connects tonotransducer, and another connects micromatic setting (regulating load tension force), by 8 passage bridge amplifiers, antiotasis is shown in to computer screen [6,7].Mounted arterial ring is inserted to 37 DEG C that contain 1ml Krebs liquid thermostatic bath, continues to pass into containing 95%O 2and 5%CO 2mixed gas, pH keep 7.4.Before experiment, arterial ring tranquillization load 2.5mN, every 10min changes liquid once, stablizes 1.5h.With K +-Krebs liquid is (containing K+60mmolL -1) inspection arterial ring shrinkability, twice contraction is highly greater than 1mN and shrinkage amplitude differs < for experiment.K +-Krebs liquid consists of (mmolL -1: NaCl60, NaHCO 315, KCl63.5, MgCl 21.2, NaH 2pO 41.2, CaCl 21.5 and glucose 5.5).
Observing in vasoconstrictive functional experiment, use fresh blood pipe ring, investigate α function of receptors, first use Prop (10 -9molL -1) in bath, hatch blood vessel and block beta receptor half an hour, then concentration summation adds NA (10 -11～10 -4molL -1); Investigate 5-HT function of receptors, concentration summation adds 5-HT (10 -11～10 -4molL -1); Investigate ET b, ET afunction of receptors, first concentration summation adds S6c (10 -10～10 -6molL -1), the exciting ET of selectivity bacceptor, makes vessel retraction, and it is maximum that contraction reaches, and makes ET bacceptor internalization, ET bacceptor contraction disappears, and shrinkage curve is down to after baseline values stable at least 30min gradually, and cumulative concentration method adds ET-1 (10 -11～10 -6molL -1), can obtain respectively α acceptor, 5-HT acceptor, ET bacceptor, ET aacceptor dosage-blockage effect curve.
1.3, statistical method: data with represent, contractile response causes that with variable concentrations activator blockage effect is with respect to 63.5mmolL -1the blockage effect percentage that potassium causes is expressed, and response feature is expressed as E max(maximum collapse percent) and pEC 50(the negative logarithm of required receptor agonism agent concentration while producing half maximum collapse).Statistical study and mapping are used Prism4.0 software.Conspicuousness is investigated in ANOVA two-way and Student t inspection, has been considered to conspicuousness in the time of P < 0.05.
2 results:
The contractile response of 2.1 arteries to K+: 63.5mmolL -1k +can make artery produce significantly and shrink, the contraction that different arteries produces is without significant difference, and cancer arterial ring is to 63.5mmolL -1k +convergent force be 2.54 ± 0.83mN (n=32), the convergent force of all arteries of cancer is 2.74 ± 0.96mN (n=32), the convergent force of normal arterial ring is 2.92 ± 0.78mN (n=32), 3 groups of convergent force more equal P > 0.05 mutually.
2.2 cancer arteries are observed the concentration shrinkage curve of 4 kinds of activators to cancer arterial ring to the cumulative concentration method of the reactive difference of vaso-excitor material, and result shows, shrinks cancer artery, E ET-1 and NA energy concentration dependent maxbe respectively 60mmolL -1k +130% ± 6% and 74% ± 5%, the pEC that shrink 50be respectively 8.09 ± 0.10 and 5.54 ± 0.21.5-HT can make cancer artery produce faint contraction, and S6c does not cause contraction, ET-1 as shown in Figure 1, S6c, concentration-contraction amount effect curve that NA and 5-HT cause at colorectal cancer patients cancer artery.Numeric representation is n=5 (n=patient's number).
2.3 cancer arteries, all arteries of cancer and the reactivity of non-cancer artery to NA: under Propranolol existence condition, investigate concentration-blockage effect curve of NA induction artery, result shows that NA can shrink non-cancer patient's edge artery, its E in concentration dependent ground maxand pEC 50be respectively 97% in non-cancer patient's edge artery, E maxand pEC 50be respectively 74% ± 5% (p < 0.05) and 5.54 ± 0.21; The all arteries of cancer are the edge artery apparently higher than non-cancer patient to concentration-blockage effect curve of NA, its E maxand pEC 50be respectively 119% ± 11% (p < 0.05) and 5.84 ± 0.09, n=5 as shown in Figure 2, NA is at colorectal cancer patients cancer artery, cancer week artery and concentration-contraction amount effect curve of causing of non-cancer patient edge artery.Numeric representation is n=5 (n=patient's number).With the comparison of non-cancer patient's artery *p < 0.05, with the artery comparison of cancer week ++p < 0.01.Table 1 is NA, S6c, and ET-1,5-HT is at the R of colon cancer cancer artery, cancer circumferential edges artery and non-cancer patient edge artery concentration-contraction amount effect curve maxand pEC 50value.
Table 1
E maxfor maximal contractile response, pEC 50for causing the negative logarithm of the required agonist concentration of half maximal contractile response.Numeric representation is n=5 (n=patient's number).Negative logarithm with the moving concentration of cancer circumferential edges.Numeric representation is x ± s, n=5 (n=patient's number).With the comparison of cancer circumferential edges artery *p < 0.01, with non-cancer patient's edge artery comparison △p < 0.05
2.4 cancer arteries, all arteries of cancer and the reactivity of non-cancer artery to S6c and ET-1: the demonstration of Fig. 3 A result, S6c is to all arteries of normal artery, cancer artery and cancer all without agonism, and concentration-shrinkage curve is straight line.Fig. 3 B result is presented under S6c existence condition, concentration-shrinkage curve that ET-1 induction artery shrinks.ET-1 can shrink non-cancer patient's edge artery in concentration dependent ground, and concentration-shrinkage curve that the cancer artery of ET-1 induction shrinks is lower than non-cancer patient's edge arterial curve, numerical tabular in figure n=5 (n=patient's number).With the comparison of non-cancer patient's artery *p < 0.01, with the artery comparison of cancer week ++p < 0.01, its E maxand pEC 50be respectively 130% ± 6% and 8.09 ± 0.10; The E of concentration-shrinkage curve that the cancer week artery of ET-1 induction shrinks maxand pEC 50be respectively 248% ± 34% and 8.73 ± 0.04, be significantly higher than the E of colon cancer artery and normal artery shrinkage curve max(P < 0.01, P < 0.01), n=5.
2.55-HT is to cancer artery, cancer week artery and the effect of normal artery.5-HT only causes weak contraction, E to normal artery maxbe 3% ± 1%; The E that colon cancer artery shrinks maxbe 2% ± 1%; The E of cancer week artery contraction maxit is 2% ± 1%, n=5 (concentration-contraction amount effect curve that Figure 45-HT causes at colorectal cancer patients cancer artery, all arteries of cancer and non-cancer patient edge artery.Numeric representation n=5 (n=patient's number).
3 conclusions:
Tumor tissue growth is fast, needs more blood supply; The vessel density of tumor tissues is high, and tumor vascular distribution and structure and normal person's blood vessel have notable difference, and tumor vessel is unordered, tortuous, expansion, plucked, branch are many; Tumor vessel tube wall iuntercellular gap length, opening are many, lack supporting structure in pipe, basilar memebrane fracture or disappearance.The new vessels of tumour lacks innervation and the architecture basics to vaso-active substance reaction, is no longer further divided into corresponding artery and vein after formation, and contractile function is poor [1].Thereby the function of tumour artery certainly exists difference with normal artery.Chen Dingzhang etc. [8]observe colon, rectal neoplasm patient's inferior mesenteric artery hemodynamic parameter and normal person and relatively have significant difference, colon tumor patient's inferior mesenteric artery internal diameter, blood flow rate and volume of blood flow are higher than normal person, and PI significantly reduces.
The present invention has tested the contraction activity of several frequently seen vaso-active substance to colon cancer artery, finds that the effect of ET-1 pinned sheepshank intestinal cancer artery is significantly better than NA, the E of ET-1 max(130% ± 6%) is NA E max(74% ± 5%) 1.76 times, it is negligible that 5-HT shrinks the effect of cancer artery, and S6c can not shrink artery.The all arteries of the contraction of colon cancer artery and cancer and non-cancer patient's artery compare, and find that potassium ion does not have significant difference to the contraction of 3 kinds of arteries.Colon cancer artery is obviously weaker than cancer surrounding tissue artery to the contraction of ET-1 and NA, is also weaker than non-cancer patient's artery.The resistance of prompting cancer artery is little, and blood flow is fast; Cancer week, the Artery resistance of tissue was large, and blood flow is slow, has robber's flow phenomenon.
The main exciting eparterial α acceptor of NA, vasoconstriction, colon cancer artery reduces the reactivity of NA, α receptor down-regulated on prompting cancer arterial smooth muscle.ET-1 is one of vaso-excitor material the strongest in body, the ET on can exciting vascular smooth muscle cell aand ET bacceptor [9], vasoconstriction.S6c is ET bthe specific agonist of acceptor, S6c does not cause contraction to cancer artery and non-cancer patient's edge artery, points out on normal artery and cancer arterial smooth muscle and does not express ET bacceptor.ET aacceptor does not have specific agonist, but S6c specifically with ET bafter receptors bind, S6c-ET bcompound can enter in cell, internalization, degraded gradually, final vascular smooth muscle surface ET bacceptor disappears completely, now adds vessel retraction that ET-1 causes all by ET areceptor-mediated [10].Therefore, ET aacceptor (instead of ET bacceptor) in the contraction of cancer artery, play important regulating action.ET athe change of the effect of acceptor to cancer artery is similar to the variation of α function of receptors, the contraction of colon cancer artery is significantly reduced to prompting colon cancer artery ET compared with the contraction of all arteries of cancer areceptor down-regulated.
Experiment shows, ET athe contraction of receptor-mediated colon cancer artery is far better than α acceptor; Colon cancer arterial smooth muscle ET aacceptor and α acceptor contractile function decline and cause vasodilation and all vessel retraction increased functionality of cancer to cause that Oligemia is conducive to the blood supply of cancer affected part position, adapt to the growth of cancerous tissue.
List of references:
[1] Chen Xinyi, Xu Li, Zhang Yanming, Sun Tao. Developing study on neoangiogenesis of malignant tumor [J]. cancer progression, 2005,3 (6): 528-33.
[1]CHEN?Xin-yi，XU?Li，ZHANG?Yan-ming，SUN?Tao.Developing?study?on?neoangiogenesis?of?malignant?tumor[J].Oncology?Progress.2005，3(6)：528-33.
[2] Dong Lei, Zhang Chuansen, Guan Yifan, etc. the blood flow rate of hepatocellular carcinoma feeding artery and the relation of microvessel density [J]. Chinese Journal of Oncology, 2005,27 (9): 538-40.
[2]DONG?Lei，ZHANG?Chuan-sen，GUAN?Yi-fan，et?al.Correlation?between?blood?flow?velocity?of?feeding?arteries?and?microvessel?density?of?hepatocellular?carcinoma[J].Chin?J?Oncol.2005，27(9)：538-40.
[3]Rogatsch?H，Hittmair?A，Reissigl?A，et?al.Microvessel?density?in?core?biopsies?of?prostatic?adenocarcinoma：a?stage?predictor[J].J?Pathol.1997，182(2)：205-10.
[4]Maeda?K，Chung?YS，Takatsuka?S，et?al.Tumor?angiogenesis?as?a?predictor?of?recurrence?in?gastric?carcinoma[J].J?Clin?Oncol.1995，13(2)：477-81.
[5]Weidner?N.Tumoural?vascularity?as?a?prognostic?factor?in?cancer?patients：the?evidence?continues?to?grow[J].JPathol.1998，184(2)：119-22.
[6]Cao?YX，He?LC，Xu?CB，et?al.Alteration?in?contractile?response?to?noradrenaline，5-hydroxytryptamine，sarafotoxin6c，and?angiotensin?II?in?rat?mesenteric?artery?during?organ?culture[J].ACAD?J?XJTU，2004，16(2)：155-9.
[7]Cao?YX，Zheng?JP，He?JY，et?al.Induces?vasodilatation?of?rat?mesenteric?artery?in?vitro?mainly?by?inhibiting?receptor-mediated?Ca(2+)-influx?and?Ca(2+)-release[J].Arch?Pharm?Res，2005，28(6)：709-15.
[8] Chen Dingzhang, Zhou Xiaodong, Shi Jing, etc. colon tumor and inflammatory patients inferior mesenteric artery blood flow change and meaning [J]. clinical ultrasound medicine magazine, 2005,7 (6): 401-3.
[8]CHEN?Ding-zhang，ZHOU?Xiao-dong，SHI?Jing，et?al.Colour?Doppler?study?on?the?hemodynamic?changes?and?the?significance?in?the?inferior?mesenteric?arteries?in?colon?tumor?[J].Ultrasound?in?Clin?Med.2005，7(6)：401-3.
[9]Lodge?NJ，Zhang?R，Halaka?NN，Moreland?S.Functional?role?of?endothelin?ETA?and?ETB?receptors?in?venous?and?arterial?smooth?muscle[J].Eur?J?Pharmacol.1995，287(3)：279-85.
[10] Luo Guogang, Ma Aiqun, Xu Cangbao, waits .ERK1/2 path to participate in ETA and the receptor-mediated in vitro superior mesenteric artery of ETB shrinks research [J]. Chinese Pharmacological Bulletin, 2005,21 (3): 343-7.
[10]LUO?Guo-gang，MA?Ai-qun，XU?Cang-ba，et?al.Involvement?of?ERK1/2pathway?in?endothelin?ETA?and?ETB?Receptor-mediated?contraction?in?isolated?rat?mesenteric?artery[J].Chinese?Pharm?acological?B?ulletin.2005，21(3)：343-7。

Claims (2)

1. the reactivity of colon cancer artery to contracting blood vessel medium.
2. the reactivity to contracting blood vessel medium according to the artery of colon cancer shown in claim 1, is characterized in that: α acceptor and ET aacceptor is the main contracting blood vessel acceptor of normal artery, α acceptor and the ET of colon cancer artery athe contracting blood vessel function of acceptor is obviously weaker than cancer week artery.
CN201410206440.2A 2014-05-16 2014-05-16 Reactivity of colon cancer artery to vasoconstrictive medium Pending CN103983763A (en)

Priority Applications (1)

Application Number Priority Date Filing Date Title
CN201410206440.2A CN103983763A (en) 2014-05-16 2014-05-16 Reactivity of colon cancer artery to vasoconstrictive medium

Applications Claiming Priority (1)

Application Number Priority Date Filing Date Title
CN201410206440.2A CN103983763A (en) 2014-05-16 2014-05-16 Reactivity of colon cancer artery to vasoconstrictive medium

Publications (1)

Publication Number Publication Date
CN103983763A true CN103983763A (en) 2014-08-13

Family

ID=51275815

Family Applications (1)

Application Number Title Priority Date Filing Date
CN201410206440.2A Pending CN103983763A (en) 2014-05-16 2014-05-16 Reactivity of colon cancer artery to vasoconstrictive medium

Country Status (1)

Country Link
CN (1) CN103983763A (en)

Citations (1)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
US20070065866A1 (en) * 2002-12-23 2007-03-22 William Marsh Rice University Compositions and Methods for Suppressing Fibrocytes

Patent Citations (1)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
US20070065866A1 (en) * 2002-12-23 2007-03-22 William Marsh Rice University Compositions and Methods for Suppressing Fibrocytes

Non-Patent Citations (1)

* Cited by examiner, † Cited by third party
Title
祁光裕等: "结肠癌血管的肾上腺素受体和内皮素受体", 《西安交通大学学报》, vol. 27, no. 4, 31 August 2006 (2006-08-31) *

Similar Documents

Publication Publication Date Title
Li et al. Long noncoding RNA NEAT1 promotes proliferation and invasion via targeting miR-181a-5p in non-small cell lung cancer
Cruz-Bermúdez et al. Cancer-associated fibroblasts modify lung cancer metabolism involving ROS and TGF-β signaling
Zarour et al. Colorectal cancer liver metastasis: evolving paradigms and future directions
Frederiks et al. Renal cell carcinoma and oxidative stress: the lack of peroxisomes
Luo et al. Circ-ITCH correlates with small tumor size, decreased FIGO stage and prolonged overall survival, and it inhibits cells proliferation while promotes cells apoptosis in epithelial ovarian cancer
Zhan et al. Down-regulation of lysyl oxidase-like 2 (LOXL2) is associated with disease progression in lung adenocarcinomas
Dong et al. Overexpression of S100P promotes colorectal cancer metastasis and decreases chemosensitivity to 5-FU in vitro
Luo et al. CHI3L1 overexpression is associated with metastasis and is an indicator of poor prognosis in papillary thyroid carcinoma
Piao et al. LETM1 is a potential cancer stem-like cell marker and predicts poor prognosis in colorectal adenocarcinoma
Acun et al. HLJ1 (DNAJB4) gene is a novel biomarker candidate in breast cancer
Liu et al. Identification of a three-RNA binding proteins (RBPs) signature predicting prognosis for breast cancer
Tan et al. Silencing of CXCR4 inhibits tumor cell proliferation and neural invasion in human hilar cholangiocarcinoma
Zhuang et al. Aberrant expression of pim-3 promotes proliferation and migration of ovarian cancer cells
Sharma et al. Histomorphological spectrum of prostatic lesions: a retrospective analysis of transurethral resection of prostate specimens
Yoshida et al. Immunohistochemical detection of cervical lymph node micrometastases from T2N0 tongue cancer
Jiang et al. miR-885-5p inhibits invasion and metastasis in gastric cancer by targeting malic enzyme 1
Heng et al. A unique small cell lung carcinoma disease progression model shows progressive accumulation of cancer stem cell properties and CD44 as a potential diagnostic marker
CN103983763A (en) Reactivity of colon cancer artery to vasoconstrictive medium
Wang et al. Expression of long noncoding RNA NBAT1 is associated with the outcome of patients with non-small cell lung cancer
Han et al. Expression of TRAP1 in gastric cancer tissue and its correlation with malignant biology
Aiad et al. The prognostic and predictive significance of PARP-1 in locally advanced breast cancer of Egyptian patients receiving neoadjuvant chemotherapy
Xiao et al. Association of ultrasonographic features with NGX6 expression and prognosis in invasive ductal breast carcinoma
Chen et al. BTBD7 accelerates the epithelial-mesenchymal transition, proliferation and invasion of prostate cancer cells
CN106701762A (en) Inhibitor for P4HB gene expression and application of inhibitor
Bonzano et al. Omission of Radiation

Legal Events

Date Code Title Description
C06 Publication
PB01 Publication
C10 Entry into substantive examination
SE01 Entry into force of request for substantive examination
ASS Succession or assignment of patent right

Free format text: FORMER OWNER: LIN JIE WANG JUNJIE

Effective date: 20150225

Owner name: CHENZHOU FIRST PEOPLE S HOSPITAL

Free format text: FORMER OWNER: LI JIE

Effective date: 20150225

C41 Transfer of patent application or patent right or utility model
TA01 Transfer of patent application right

Effective date of registration: 20150225

Address after: Luo Jia Jing 423000 Chenzhou province Hunan City Beihu District No. 102

Applicant after: Chenzhou First People's Hospital

Address before: Luo Jia Jing 423000 Chenzhou province Hunan City Beihu District No. 102

Applicant before: Li Jie

Applicant before: Lin Jie

Applicant before: Wang Junjie

C02 Deemed withdrawal of patent application after publication (patent law 2001)
WD01 Invention patent application deemed withdrawn after publication

Application publication date: 20140813