Name: the colon-26 carcinoma tumor-bearing mouse as a model for the study of cancer cachexia
Uploaded: 2016-11-30T14:00:00.000+00:00
Duration: 8 min 55 s
Description: Watch this Scientific Journal Video about The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia at JoVE.com

We thank Richard Lieber and Shannon Bremner for their ImageJ macro and instructions. While at Thomas Jefferson University, this work was supported by the Pennsylvania Department of Health CURE Grant TJU No. 080-37038-AI0801. Subsequently, this study was supported by a grant to AB from the National Institutes of Health (R21CA190028), and by grants to TAZ from the National Institutes of Health (R01CA122596, R01CA194593), the IU Simon Cancer Center, the Lustgarten Foundation, the Lilly Foundation, Inc., and the IUPUI Pancreas Signature Center.

<ol>
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The authors have nothing to disclose.

특히 최근의 단계에서, 결장암이 불량한 결과 및 환자의 삶의 질에서의 감소에 대한 책임이 악액질의 발전과 관련된다. 많은 연구는 암에 이차적 상태의 치료에 초점을 맞추고있다; 그러나,이 방향으로 많은 노력에도 불구하고, 여전히 암 악액질 (21)에 대한 승인 된 치료가 없습니다. 동물 모델 결과의 번역을 최대화하기 위해 가능한 한 가깝게 인간 병리 닮은 따라서, 필수적이다. <p cl...

근육 낭비는 암, 패혈증, 간, 간경변, 심장 및 신장 질환, 만성 폐쇄성 폐 질환, 에이즈 등의 다양한 임상 조건의 심각한 합병증이다. 특히, 근육 쇠약 한 암 환자의 50 % 이상에서 명백하다. 인해 및 / 또는로부터 골격근 단백질 분해 시스템의 과도한 활성화로 증가 단백질 분해로부터 암 결과 골격근 상실 단백질 합성 (6) 감소 하였다. 지방 분해는 지방 조직의 붕괴를 초래 또한 명백하다. 임상 악액질 감소 된 품질 및 수명의 길이와 연관된 20 사망 원인으로 추정된다 - 암 환자 (7)의 30 %. 최대한 가깝게 인간 질환과 유사한 실험 모델의 사용은 유익 할 것이다. 최적의 동물 모델 높은 재현성과 다를 치료에서 제한된 간섭 및 예측 인자 특징일반적으로 임상 상태 (8)과 관련된 다이어트, 성별, 유전 적 배경. 새로운 방법은 암의 발달에 민감한 유전자 변형 마우스를 사용하는 것이지만, 지금까지 암 악액질은 암 세포 또는 발암 주입 이식 특징 동물 모델에서 주로 연구되어왔다. C26 암종 베어링 마우스 암 악액질 2,5의 잘 특징으로 널리 사용 모델을 나타내는 (도 26 - 결장 선암 함). 주로 고급 지방 및 단백질 이화 9 체 근육 감량 C26에서 종양의 성장 결과. 일반적으로, 몸 전체 중량 대비 10 % 종양 중량은 골격근 질량 20-25 %의 감소 및 지방 3,10의 큰 고갈과 연관된다. 비장 비대 및 또한 급성기 반응의 활성화 및 프로 infla의 높이와 함께, 종양 성장을 관찰mmatory 사이토 카인 수준 3,11. 이들 중, 이곳은 IL-6 사이토 카인이 아마 악액질 (12)의 유일한 유도제없는 경우에도 C26 모델에서 근육 쇠약을 매개에서 중요한 역할을하는 것으로 알려져있다. 상승 된 IL-6는 JAK / STAT3 경로의 활성화를 통해 근육 위축이 발생하고,이 전사 인자를 억제하는 근육 3,4- 낭비를 방지 할 수있다. C26에 의한 근육 낭비하는 동안, 근육 위축의 많은 조건에서와 같이 근육 질량이없는 세포 사멸 또는 섬유 (13)의 손실을 크게 근육 섬유에서 근육 단백질 함량의 감소를 통해 손실됩니다. C26 악액질에서 작은 단면적을 향한 이동은 당분 및 산화 섬유 둘 모두에서 관찰된다. 이는 또한 감소 된 근력 5와 일치한다. 전세계 여러 그룹은 암 CAC 대한 근 소모성 새로운 중재자 또는 임상 적 약물을 발견하기 위해 C26 모델의 장점을 찍은hexia. 그러나,이 모델의 사용을위한 다양한 방법이 획득 된 데이터의 일관성에 관한 문제를 제기하고 다른 실험 조건에서 재현성 장벽 포즈보고되었다. 여기에서 우리는 표준화 및 재현성 데이터를 산출 암 악액질의 연구를위한이 모델의 전형적인 사용을보고합니다.

<table><tbody><tr><td>Cell culture Flasks</td><td>Falcon - Becton Dickinson</td><td>35-5001</td><td></td></tr><tr><td>DMEM</td><td>Cellgro</td><td>10-017-CV</td><td></td></tr><tr><td>FBS</td><td>Gibco</td><td>26140</td><td></td></tr><tr><td>Streptomycin-Penicillin&amp;nbsp;</td><td>Cellgro</td><td>30-002-CI</td><td></td></tr><tr><td>CD2F1 mice</td><td>Harlan</td><td>060</td><td></td></tr><tr><td>Anesthesia apparatus</td><td>EZ-Anesthesia</td><td>EZ-7000</td><td></td></tr><tr><td>2-Methyl Butane</td><td>Sigma-Aldrich</td><td>M32631</td><td></td></tr><tr><td>OCT</td><td>Tissue-Tek</td><td>4583</td><td></td></tr><tr><td>Cryostat</td><td>Leica</td><td>CM1850</td><td></td></tr><tr><td>Cork disks</td><td>Electron Microscopy Sciences</td><td>63305</td><td></td></tr><tr><td>Superfrost plus glass slides</td><td>VWR</td><td>48311-703</td><td></td></tr><tr><td>Anti-Laminin Rabbit polyclonal antibody</td><td>Sigma-Aldrich</td><td>L9393</td><td></td></tr><tr><td>Anti-Dystrophin Mouse Monoclonal antibody</td><td>Vector Laboratories</td><td>VP-D508</td><td></td></tr><tr><td>Alexa Flour 594 anti-mouse IgG</td><td>Life Technologies</td><td>A11062</td><td></td></tr><tr><td>Alexa Flour 594 anti-rabbit IgG</td><td>Life Technologies</td><td>A21211</td><td></td></tr><tr><td>Hematoxylin</td><td>Sigma-Aldrich</td><td>GHS216</td><td></td></tr><tr><td>Eosin</td><td>Sigma-Aldrich</td><td>HT110332</td><td></td></tr><tr><td>Xylene</td><td>Acros Organics</td><td>422680025</td><td></td></tr><tr><td>Cytoseal-XYL</td><td>Thermo</td><td>8312-4</td><td></td></tr><tr><td>Microscope</td><td>Zeiss</td><td>Observer.Z1&amp;nbsp;</td><td></td></tr><tr><td>Bamboo Tablet</td><td>Wacom</td><td>CTH-661</td><td></td></tr><tr><td>Prism 7.0 for Mac OS X</td><td>GraphPad Software, Inc.</td><td></td><td></td></tr><tr><td>Excel for Mac 2011</td><td>Microsoft Corp.</td><td></td><td></td></tr><tr><td>ImageJ</td><td>US National Institutes of Health</td><td>IJ1.46</td><td>http://rsbweb.nih.gov/ij/download.html</td></tr><tr><td>Microtainer</td><td>BD</td><td>365873</td><td></td></tr></tbody></table>

the colon-26 carcinoma tumor-bearing mouse as a model for the study of cancer cachexia

Cancer cachexia is the progressive loss of skeletal muscle mass and adipose tissue, negative nitrogen balance, anorexia, fatigue, inflammation, and activation of lipolysis and proteolysis systems. Cancer patients with cachexia benefit less from anti-neoplastic therapies and show increased mortality1. Several animal models have been established in order to investigate the molecular causes responsible for body and muscle wasting as a result of tumor growth. Here, we describe methodologies pertaining to a well-characterized model of cancer cachexia: mice bearing the C26 carcinoma2-4. Although this model is heavily used in cachexia research, different approaches make reproducibility a potential issue. The growth of the C26 tumor causes a marked and progressive loss of body and skeletal muscle mass, accompanied by reduced muscle cross-sectional area and muscle strength3-5. Adipose tissue is also lost. Wasting is coincident with elevated circulating levels of pro-inflammatory cytokines, particularly Interleukin-6 (IL-6)3, which is directly, although not entirely, responsible for C26 cachexia. It is well-accepted that a primary mechanism by which the C26 tumor induces muscle tissue depletion is the activation of skeletal muscle proteolytic systems. Thus, expression of muscle-specific ubiquitin ligases, such as atrogin-1/MAFbx and MuRF-1, represent an accepted method for the evaluation of the ongoing muscle catabolism2. Here, we present how to execute this model in a reproducible manner and how to excise several tissues and organs (the liver, spleen, and heart), as well as fat and skeletal muscles (the gastrocnemius, tibialis anterior, and quadriceps). We also provide useful protocols that describe how to perform muscle freezing, sectioning, and fiber size quantification.

(- 5 4 D) 지수 세포 성장 하였다 주사 후 8 D - C26 종양 성장 동력학은 제 7 래그 상을 나타낸다. 종양 덩어리는 최후 (도 1A-B는 약 2 g)을 ~ 체중의 10 %에 도달한다. 첫 번째 단계에서, 종양은 촉진하여 위치 될 수 있으며, 피부의 작은 돌기로 나타난다. 두 번째 단계에서, 종양은 피하 대량으로 관찰되었다. 드물게 종양은 개방 상처의 결과로, 궤양이된?...

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The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia

Mice bearing the Colon-26 (C26) carcinoma represent a classical model of cancer cachexia. Progressive muscle wasting occurs in association with tumor growth, over-expression of muscle-specific ubiquitin ligases, and reductions in muscle cross-sectional area. Fat loss is also observed. Cachexia is studied in a time-dependent manner with increasing severity of wasting.

콜론-26 암 종양 베어링 암 악액질의 연구를위한 모델로 마우스를

Cancer cachexia is the progressive loss of skeletal muscle mass and adipose tissue, negative nitrogen balance, anorexia, fatigue, inflammation, and ...

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JoVE Journal

Cancer Research

16.1K 조회수.  Indiana University School of Medicine. Mice bearing the Colon-26 (C26) carcinoma represent a classical model of cancer cachexia. Progressive muscle wasting occurs in association with tumor growth, over-expression of muscle-specific ubiquitin ligases, and reductions in muscle cross-sectional area. Fat loss is also observed. Cachexia is studied in a time-dependent manner with increasing severity of wasting. 

비디오: The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia

Advanced Animal Model of Colorectal Metastasis in Liver: Imaging Techniques and Properties of Metastatic Clones

Patients with a limited number of hepatic metastases and slow rates of progression can be successfully treated with local treatment approaches1,2. However, little is known about the heterogeneity of liver metastases, and animal models capable of evaluating the development of individual metastatic colonies are needed. Here, we present an advanced model of hepatic metastases that provides the ability to quantitatively visualize the development of individual tumor clones in the liver and estimate their growth kinetics and colonization efficiency. We generated a panel of monoclonal derivatives of HCT116 human colorectal cancer cells stably labeled with luciferase and tdTomato and possessing different growth properties. With a splenic injection followed by a splenectomy, the majority of these clones are able to generate hepatic metastases, but with different frequencies of colonization and varying growth rates. Using the In Vivo&#160;Imaging System (IVIS), it is possible to visualize and quantify metastasis development with in vivo luminescent and ex vivo fluorescent imaging. In addition, Diffuse Luminescent Imaging Tomography (DLIT) provides a 3D distribution of liver metastases in vivo. Ex vivo fluorescent imaging of harvested livers provides quantitative measurements of individual hepatic metastatic colonies, allowing for the evaluation of the frequency of liver colonization and the growth kinetics of metastases. Since the model is similar to clinically observed liver metastases, it can serve as a modality for detecting genes associated with liver metastasis and for testing potential ablative or adjuvant treatments for liver metastatic disease.

The ability of metastatic clones to colonize distant sites depends on their proliferation capacity and/or their ability to survive in the host microenvironment without significant proliferation. Here, we present an animal model that allows quantitative visualization of both types of liver colonization by metastatic clones.

고급 동물의 간에서 대장 전이의 모델 : 이미징 기술 및 전이성 클론의 특성

Patients with a limited number of hepatic metastases and slow rates of progression can be successfully treated with local treatment approaches1,2. ...

연구

암 연구학

Isolation of Circulating Tumor Cells in an Orthotopic Mouse Model of Colorectal Cancer

Despite the advantages of easy applicability and cost-effectiveness, subcutaneous mouse models have severe limitations and do not accurately simulate tumor biology and tumor cell dissemination. Orthotopic mouse models have been introduced to overcome these limitations; however, such models are technically demanding, especially in hollow organs such as the large bowel. In order to produce uniform tumors which reliably grow and metastasize, standardized techniques of tumor cell preparation and injection are critical. 
We have developed an orthotopic mouse model of colorectal cancer (CRC) which develops highly uniform tumors and can be used for tumor biology studies as well as therapeutic trials. Tumor cells from either primary tumors, 2-dimensional (2D) cell lines or 3-dimensional (3D) organoids are injected into the cecum and, depending on the metastatic potential of the injected tumor cells, form highly metastatic tumors. In addition, CTCs can be found regularly. We here describe the technique of tumor cell preparation from both 2D cell lines and 3D organoids as well as primary tumor tissue, the surgical and injection techniques as well as the isolation of CTCs from the tumor-bearing mice, and present tips for troubleshooting.

We describe the establishment of orthotopic colorectal tumors via injection of tumor cells or organoids into the cecum of mice and the subsequent isolation of circulating tumor cells (CTCs) from this model.

대장 암 정위 마우스 모델에서의 순환 종양 세포의 분리

Despite the advantages of easy applicability and cost-effectiveness, subcutaneous mouse models have severe limitations and do not accurately simulate ...

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

Despite the advantages of easy applicability and cost-effectiveness, colorectal cancer mouse models based on tumor cell injection have severe limitations and do not accurately simulate tumor biology and tumor cell dissemination. Genetically engineered mouse models have been introduced to overcome these limitations; however, such models are technically demanding, especially in large organs such as the colon in which only a single tumor is desired.
As a result, an immunocompetent, genetically engineered mouse model of colorectal cancer was developed which develops highly uniform tumors and can be used for tumor biology studies as well as therapeutic trials. Tumor development is initiated by surgical, segmental infection of the distal colon with adeno-cre virus in compound conditionally mutant mice. The tumors can be easily detected and monitored via colonoscopy. We here describe the surgical technique of segmental adeno-cre infection of the colon, the surveillance of the tumor via high-resolution colonoscopy and present the resulting colorectal tumors.

A protocol for the establishment of a genetically engineered mouse model of colorectal cancer by segmental adeno-cre infection and its surveillance via high-resolution colonoscopy is presented.

산발성 대장 암의 유 전적으로 조작 된 마우스 모델

Despite the advantages of easy applicability and cost-effectiveness, colorectal cancer mouse models based on tumor cell injection have severe limitations ...

Orthotopic Mouse Model of Colorectal Cancer

The traditional subcutaneous tumor model is less than ideal for studying colorectal cancer. Orthotopic mouse models of colorectal cancer, which feature cancer cells growing in their natural location, replicate human disease with high fidelity. Two techniques can be used to establish this model. Both techniques are similar and require mouse anesthesia and laparotomy for exposure of the cecum. One technique involves injection of a colorectal cancer cell suspension into the cecal wall. Cancer cells are first grown in culture, harvested when subconfluent and prepared as a single cell suspension. A small volume of cells is injected slowly to avoid leakage. The other technique involves transplantation of a piece of subcutaneous tumor onto the cecum. A mouse with a previously established subcutaneous colorectal tumor is euthanized and the tumor is removed using sterile technique. The tumor piece is divided into small pieces for transplantation to another mouse. Prior to transplantation, the cecal wall is lightly damaged to facilitate tumor cell infiltration. The time to developing primary tumors and liver metastases will vary depending on the technique, cell line, and mouse species used. This orthotopic mouse model is useful for studying the natural progression of colorectal cancer and testing new therapeutic agents against colorectal cancer.

Two techniques can be used to establish this model: injection of a cancer cell suspension into the cecal wall or transplantation of a piece of subcutaneous tumor onto the cecum. This model is useful for studying the natural progression of colorectal cancer and testing new therapeutic agents against colorectal cancer.

대장암의 Orthotopic 마우스 모델

The traditional subcutaneous tumor model is less than ideal for studying colorectal cancer. Orthotopic mouse models of colorectal cancer, which feature ...

생물학

Modeling Colitis-Associated Cancer with Azoxymethane (AOM) and Dextran Sulfate Sodium (DSS)

Individuals with inflammatory bowel disease (IBD), such as Crohn's disease (CD) or ulcerative colitis (UC) are at increased risk of developing colorectal cancer (CRC) over healthy individuals. This risk is proportional to the duration and extent of disease, with a cumulative incidence as high as 30% in individuals with longstanding UC with widespread colonic involvement.1 Colonic dysplasia in IBD and colitis associated cancer (CAC) are believed to develop as a result of repeated cycles of epithelial cell injury and repair while these cells are bathed in a chronic inflammatory cytokine milieu.2 While spontaneous and colitis-associated cancers share the quality of being adenocarcinomas, the sequence of underlying molecular events is believed to be different.3 This distinction argues the need for specific animal models of CAC.
Several mouse models currently exist for the study of CAC. Dextran sulfate sodium (DSS), an agent with direct toxic effects on the colonic epithelium, can be administered in drinking water to mice in multiple cycles to create a chronic inflammatory state. With sufficient duration, some of these mice will develop tumors.4 Tumor development is hastened in this model if administered in a pro-carcinogenic setting. These include mice with genetic mutations in tumorigenesis pathways (APC, p53, Msh2), as well as mice pre-treated with genotoxic agents (azoxymethane [AOM], 1,2-dimethylhydrazine [DMH]).5 
The combination of DSS with AOM as a model for colitis associated cancer has gained popularity for its reproducibility, potency, low price, and ease of use. Though they have a shared mechanism, AOM has been found to be more potent and stable in solution than DMH. While tumor development in other models generally requires several months, mice injected with AOM and subsequently treated with DSS develop adequate tumors in as little as 7-10 weeks.6, 7 Finally, AOM and DSS can be administered to mice of any genetic background (knock out, transgenic, etc.) without cross-breeding to a specific tumorigenic strain. Here, we demonstrate a protocol for inflammation-driven colonic tumorigenesis in mice utilizing a single injection of AOM followed by three seven-day cycles of DSS over a 10 week period. This model induces tumors with histological and molecular changes closely resembling those occurring in human CAC and provides a highly valuable model for the study of oncogenesis and chemoprevention in this disease.8

Modeling Colitis-Associated Cancer with Azoxymethane AOM and Dextran Sulfate Sodium DSS

We demonstrate a protocol in which administration of the genotoxic agent azoxymethane (AOM) followed by three cycles of the pro-inflammatory agent dextran sulfate sodium (DSS) rapidly and consistently generates colon tumors in mice with morphologic and molecular similarities to those seen in human colitis-associated cancer.

Azoxymethane (AOM)과 Dextran의 황산 나트륨 (DSS)와 모델링 대장염 - 관련 암

Individuals with inflammatory bowel disease (IBD), such as Crohn's disease (CD) or ulcerative colitis (UC) are at increased risk of developing colorectal ...

의학

Portal Vein Injection of Colorectal Cancer Organoids to Study the Liver Metastasis Stroma

Hepatic metastasis of colorectal cancer (CRC) is a leading cause of cancer-related death. Cancer-associated fibroblasts (CAFs), a major component of the tumor microenvironment, play a crucial role in metastatic CRC progression and predict poor patient prognosis. However, there is a lack of satisfactory mouse models to study the crosstalk between metastatic cancer cells and CAFs. Here, we present a method to investigate how liver metastasis progression is regulated by the metastatic niche and possibly could be restrained by stroma-directed therapy. Portal vein injection of CRC organoids generated a desmoplastic reaction, which faithfully recapitulated the fibroblast-rich histology of human CRC liver metastases. This model was tissue-specific with a higher tumor burden in the liver when compared to an intra-splenic injection model, simplifying mouse survival analyses. By injecting luciferase-expressing tumor organoids, tumor growth kinetics could be monitored by in vivo imaging. Moreover, this preclinical model provides a useful platform to assess the efficacy of therapeutics targeting the tumor mesenchyme. We describe methods to examine whether adeno-associated virus-mediated delivery of a tumor-inhibiting stromal gene to hepatocytes could remodel the tumor microenvironment and improve mouse survival. This approach enables the development and assessment of novel therapeutic strategies to inhibit hepatic metastasis of CRC.

Portal vein injection of colorectal cancer (CRC) organoids generates stroma-rich liver metastasis. This mouse model of CRC hepatic metastasis represents a useful tool to study tumor-stroma interactions and develop novel stroma-directed therapeutics such as adeno-associated virus-mediated gene therapies.

간 전이 스트로마를 연구하기 위해 대장암 오가노이드의 포털 정맥 주사

Hepatic metastasis of colorectal cancer (CRC) is a leading cause of cancer-related death. Cancer-associated fibroblasts (CAFs), a major component of the ...

Orthotopic Implantation of Patient-Derived Cancer Cells in Mice Recapitulates Advanced Colorectal Cancer

Over the last decade, more sophisticated preclinical colorectal cancer (CRC) models have been established using patient-derived cancer cells and 3D tumoroids. Since patient derived tumor organoids can retain the characteristics of the original tumor, these reliable preclinical models enable cancer drug screening and the study of drug resistance mechanisms. However, CRC related death in patients is mostly associated with the presence of metastatic disease. It is therefore essential to evaluate the efficacy of anti-cancer therapies in relevant in vivo models that truly recapitulate the key molecular features of human cancer metastasis. We have established an orthotopic model based on the injection of CRC patient-derived cancer cells directly into the cecum wall of mice. These tumor cells develop primary tumors in the cecum that metastasize to the liver and lungs, which is frequently observed in patients with advanced CRC. This CRC mouse model can be used to evaluate drug responses monitored by microcomputed tomography (&#181;CT), a clinically relevant small-scale imaging method that can easily identify primary tumors or metastases in patients. Here, we describe the surgical procedure and the required methodology to implant patient-derived cancer cells in the cecum wall of immunodeficient mice.

This protocol describes the orthotopic implantation of patient-derived cancer cells in the cecum wall of immunodeficient mice. The model recapitulates advanced colorectal cancer metastatic disease and allows for the evaluation of new therapeutic drugs in a clinically relevant scenario of lung and liver metastases.

생쥐에서 환자 유래 암세포의 정형외피 이식은 진행성 대장암을 재현합니다.

Over the last decade, more sophisticated preclinical colorectal cancer (CRC) models have been established using patient-derived cancer cells and 3D ...

Orthotopic NSCLC를 모델링하기 위한 다세포 스페로이드의 폐내 접종

Construction of An Orthotopic Xenograft Model of Non-Small Cell Lung Cancer Mimicking Disease Progression and Predicting Drug Activities

Non-small cell lung cancer (NSCLC) is a highly lethal disease with a complex and heterogeneous tumor microenvironment. Currently, common animal models based on subcutaneous inoculation of cancer cell suspensions do not recapitulate the tumor microenvironment in NSCLC. Herein we describe a murine orthotopic lung cancer xenograft model that employs the intrapulmonary inoculation of three-dimensional multicellular spheroids (MCS). Specifically, fluorescent human NSCLC cells (A549-iRFP) were cultured in low-attachment 96-well microplates with collagen for 3 weeks to form MCS, which were then inoculated intercostally into the left lung of athymic nude mice to establish the orthotopic lung cancer model.
Compared with the original A549 cell line, MCS of the A549-iRFP cell line responded similarly to anticancer drugs. The long-wavelength fluorescent signal of the A549-iRFP cells correlated strongly with common markers of cancer cell growth, including spheroid volume, cell viability, and cellular protein level, thus allowing dynamic monitoring of the cancer growth in vivo by fluorescent imaging. After inoculation into mice, the A549-iRFP MCS xenograft reliably progressed through phases closely resembling the clinical stages of NSCLC, including the expansion of the primary tumor, the emergence of neighboring secondary tumors, and the metastases of cancer cells to the contralateral right lung and remote organs. Moreover, the model responded to the benchmark antilung cancer drug, cisplatin with the anticipated toxicity and slower cancer progression. Therefore, this murine orthotopic xenograft model of NSCLC would serve as a platform to recapitulate the disease&#39;s progression and facilitate the development of potential anticancer drugs.

저자 스포트라이트: 항암제의 나노제형 개발을 위한 쥐 비소세포폐암 모델 확립

This study presents an orthotopic non-small cell lung cancer (NSCLC) model based on intrapulmonary inoculation of multicellular spheroids of fluorescent A549-iRFP cells. The model recapitulates clinical NSCLC stages and responds to cisplatin, according to dynamic in vivo monitoring of long-wavelength fluorescence.

비소세포폐암의 기형외형 이종이식 모델 구축: 질병 진행 모방 및 약물 활성성 예측

Non-small cell lung cancer (NSCLC) is a highly lethal disease with a complex and heterogeneous tumor microenvironment. Currently, common animal models ...

콜론-26 암 종양 베어링 암 악액질의 연구를위한 모델로 마우스를

요약

더 많은 비디오 탐색

이 비디오의 챕터

고급 동물의 간에서 대장 전이의 모델 : 이미징 기술 및 전이성 클론의 특성

대장 암 정위 마우스 모델에서의 순환 종양 세포의 분리

산발성 대장 암의 유 전적으로 조작 된 마우스 모델

대장암의 Orthotopic 마우스 모델

Azoxymethane (AOM)과 Dextran의 황산 나트륨 (DSS)와 모델링 대장염 - 관련 암

간 전이 스트로마를 연구하기 위해 대장암 오가노이드의 포털 정맥 주사

생쥐에서 환자 유래 암세포의 정형외피 이식은 진행성 대장암을 재현합니다.

비소세포폐암의 기형외형 이종이식 모델 구축: 질병 진행 모방 및 약물 활성성 예측

비소세포폐암의 기형외형 이종이식 모델 구축: 질병 진행 모방 및 약물 활성성 예측

비소세포폐암의 기형외형 이종이식 모델 구축: 질병 진행 모방 및 약물 활성성 예측