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=== Syngeneic Model ===
=== Syngeneic Model ===
According to a 2015 review article, Lewis lung carcinoma is the only reproducible syngeneic lung cancer model, meaning that it is the only reproducible lung cancer model that utilizes a transplant that is immunologically compatible. Syngeneic models have proven to be useful in predicting clinical benefit of therapy in preclinical experiments. However, there has been criticism directed towards syngeneic model usage when attempting to translate therapies from another species to humans. For example, cancer therapies that exhibited promising results in mouse models can and have failed in clinical trials due to physiological differences in the activity of the targeted gene product. The activity of the mouse product did not translate to the activity of the human counterpart. tumor originated spontaneously as a carcinoma of the lung of a C57BL mouse.<nowiki><ref name= “Kellar”> {{cite journal | vauthors=Kellar A, Egan C, Morris D | date=2015 | title=Preclinical murine models for lung cancer: clinical trial applications | url= | journal=BioMed research international| volume= | issue=2015 | pages= | doi= | pmc= | pmid= | access-date = }} </ref></nowiki>
According to a 2015 review article, Lewis lung carcinoma is the only reproducible syngeneic lung cancer model, meaning that it is the only reproducible lung cancer model that utilizes a transplant that is immunologically compatible. Syngeneic models have proven to be useful in predicting clinical benefit of therapy in preclinical experiments. However, there has been criticism directed towards syngeneic model usage when attempting to translate therapies from another species to humans. For example, cancer therapies that exhibited promising results in mouse models can and have failed in clinical trials due to physiological differences in the activity of the targeted gene product. The activity of the mouse product did not translate to the activity of the human counterpart. tumor originated spontaneously as a carcinoma of the lung of a C57BL mouse.<ref name=":0">{{Cite journal|last=Kellar|first=Amelia|last2=Egan|first2=Cay|last3=Morris|first3=Don|date=2015|title=Preclinical Murine Models for Lung Cancer: Clinical Trial Applications|url=http://dx.doi.org/10.1155/2015/621324|journal=BioMed Research International|language=en|volume=2015|pages=1–17|doi=10.1155/2015/621324|issn=2314-6133}}</ref>


=== Orthotopic Model ===
=== Orthotopic Model ===
Lewis lung carcinoma can also be utilized as an orthotopic model.<ref><nowiki><ref name="Kellar"></nowiki></ref></ref> Orthotopic models focus upon correctly modeling the tumor microenvironment by injecting or implanting tumors into the corresponding organ that they originated from (i.e. implanting a Lewis lung carcinoma into the lung of another C57BL mouse). Because of this fidelity to mimicking the tumor microenvironment, orthotopic models are considered to be more physiologically relevant in representing human tumorigenesis. However, the creation of such models is a typically more involved and technically challenging process. They also require more complex imaging modalities for data collection.<ref><nowiki><ref name= “Qiu”> {{cite journal | vauthors=Qiu W, Su GH | date=2013 | title=Development of orthotopic pancreatic tumor mouse models | url= | journal=InPancreatic Cancer | volume= | issue= | pages=215-223 | doi= | pmc= | pmid= | access-date = }} </ref></nowiki></ref>
Lewis lung carcinoma can also be utilized as an orthotopic model.<ref name=":0" /> Orthotopic models focus upon correctly modeling the tumor microenvironment by injecting or implanting tumors into the corresponding organ that they originated from (i.e. implanting a Lewis lung carcinoma into the lung of another C57BL mouse). Because of this fidelity to mimicking the tumor microenvironment, orthotopic models are considered to be more physiologically relevant in representing human tumorigenesis. However, the creation of such models is a typically more involved and technically challenging process. They also require more complex imaging modalities for data collection.<ref>{{Cite journal|last=Qiu|first=Wanglong|last2=Su|first2=Gloria H.|date=2013|title=Development of orthotopic pancreatic tumor mouse models|url=https://www.ncbi.nlm.nih.gov/pubmed/23359156|journal=Methods in Molecular Biology (Clifton, N.J.)|volume=980|pages=215–223|doi=10.1007/978-1-62703-287-2_11|issn=1940-6029|pmc=PMC4049460|pmid=23359156}}</ref>


== Characterization ==
== Characterization ==
Generally, Lewis lung carcinoma is highly metastatic in immunocompetent mice.<ref><nowiki><ref name= “Bugge”> {{cite journal | vauthors=Bugge TH, Kombrinck KW, Xiao Q, Holmbäck K, Daugherty CC, Witte DP, Degen JL | date=1997 | title=Growth and dissemination of Lewis lung carcinoma in plasminogen-deficient mice | url= | journal=Blood | volume=90 | issue=11 | pages=4522-31 | doi= | pmc= | pmid= | access-date = }} </ref></nowiki></ref> If subcutaneously injected into mice, it is known to avidly metastasize to the lung. In fact, a 1996 study found that the carcinoma predominantly metastasized into the lungs after tail vein injections.<ref><nowiki><ref name= “Anderson”> {{cite journal | vauthors=Anderson IC, Shipp MA, Docherty AJ, Teicher BA | date=1996 | title=Combination therapy including a gelatinase inhibitor and cytotoxic agent reduces local invasion and metastasis of murine Lewis lung carcinoma | url= | journal=Cancer Research | volume=56 | issue=4 | pages=715-8 | doi= | pmc= | pmid= | access-date = }} </ref></nowiki></ref> Lewis lung carcinoma has the appearance of a semi-firm homogeneous mass that is not grossly hemorrhagic.<ref>Cancer Chemother Rep 2 1972 Nov;(3)1:325</ref>
Generally, Lewis lung carcinoma is highly metastatic in immunocompetent mice.<ref name=":1">{{Cite journal|last=Bugge|first=T. H.|last2=Kombrinck|first2=K. W.|last3=Xiao|first3=Q.|last4=Holmbäck|first4=K.|last5=Daugherty|first5=C. C.|last6=Witte|first6=D. P.|last7=Degen|first7=J. L.|date=1997-12-01|title=Growth and dissemination of Lewis lung carcinoma in plasminogen-deficient mice|url=https://www.ncbi.nlm.nih.gov/pubmed/9373263|journal=Blood|volume=90|issue=11|pages=4522–4531|issn=0006-4971|pmid=9373263}}</ref> If subcutaneously injected into mice, it is known to avidly metastasize to the lung. In fact, a 1996 study found that the carcinoma predominantly metastasized into the lungs after tail vein injections.<ref>{{Cite journal|last=Anderson|first=I. C.|last2=Shipp|first2=M. A.|last3=Docherty|first3=A. J.|last4=Teicher|first4=B. A.|date=1996-02-15|title=Combination therapy including a gelatinase inhibitor and cytotoxic agent reduces local invasion and metastasis of murine Lewis lung carcinoma|url=https://www.ncbi.nlm.nih.gov/pubmed/8631001|journal=Cancer Research|volume=56|issue=4|pages=715–718|issn=0008-5472|pmid=8631001}}</ref> Lewis lung carcinoma has the appearance of a semi-firm homogeneous mass that is not grossly hemorrhagic.<ref>Cancer Chemother Rep 2 1972 Nov;(3)1:325</ref>


A 1997 research study documented the tumor progression after subcutaneous injection into the dorsal subcutis for 107 wild type, 129/Black Swiss mice. These mice were selected for their genetic background proximity to C57BL/6J mice. They observed the progression as being characterized by skin ulceration followed by ulcer hemorrhaging. Not only that, there was also basal hemorrhaging and/or edema.<ref><ref name= “Bugge”></ref></ref>
A 1997 research study documented the tumor progression after subcutaneous injection into the dorsal subcutis for 107 wild type, 129/Black Swiss mice. These mice were selected for their genetic background proximity to C57BL/6J mice. They observed the progression as being characterized by skin ulceration followed by ulcer hemorrhaging. Not only that, there was also basal hemorrhaging and/or edema.<ref name=":1" />

The cells were anaplastic, varying in size and shape; and they appeared to have little cytoplasm. The nuclei of the cells were highly distorted and prominent.<ref><ref name= “Bugge”></ref></ref>
The cells were anaplastic, varying in size and shape; and they appeared to have little cytoplasm. The nuclei of the cells were highly distorted and prominent.<ref name=":1" />
⚫
The tumors were highly vascularized and metastasized to different sites, including the lungs, lymph nodes, liver, pleural cavity, diaphragm, pericardium, cardiac muscle, pancreas, adipose tissue, and esophagus. In cases of lung metastasis, large tumor masses underwent necrosis, with some of them hemorrhaging and even fewer exhibiting acute inflammation. Smaller metastases positioned themselves to be eccentric or concentric to vessels. In large tumor nodules, the cells grew, without patterning, into confluent sheets. The nodules had capillaries predominantly forming and supplying blood to the surface. The capillaries were fine and thin-walled. The nodules did exhibit expansion, interfering with and invading the space of surrounding tissues. This caused tissue degeneration.<ref><ref name= “Bugge”></ref></ref>

⚫
The tumors were highly vascularized and metastasized to different sites, including the lungs, lymph nodes, liver, pleural cavity, diaphragm, pericardium, cardiac muscle, pancreas, adipose tissue, and esophagus. In cases of lung metastasis, large tumor masses underwent necrosis, with some of them hemorrhaging and even fewer exhibiting acute inflammation. Smaller metastases positioned themselves to be eccentric or concentric to vessels. In large tumor nodules, the cells grew, without patterning, into confluent sheets. The nodules had capillaries predominantly forming and supplying blood to the surface. The capillaries were fine and thin-walled. The nodules did exhibit expansion, interfering with and invading the space of surrounding tissues. This caused tissue degeneration.<ref name=":1" />


== Clinical Research ==
== Clinical Research ==
The Lewis lung carcinoma tumor model’s role in cancer has been its use for research into tumor metastasis and angiogenesis properties. The model is also useful for chemotherapeutic testing ''in vivo''. Navelbine and carboplatin, two chemotherapeutics currently on the market, were tested in C57BL mice with Lewis lung carcinoma tumors in their hind flank. Tumor regression reached 72.7% in the navelbine trials, with the carboplatin trials showing that 30-50 percent of the population had a prolonged tumor survival after treatment with carboplatin and paclitaxel. <ref><ref name= “Kellar”></ref></ref>
The Lewis lung carcinoma tumor model’s role in cancer has been its use for research into tumor metastasis and angiogenesis properties. The model is also useful for chemotherapeutic testing ''in vivo''. Navelbine and carboplatin, two chemotherapeutics currently on the market, were tested in C57BL mice with Lewis lung carcinoma tumors in their hind flank. Tumor regression reached 72.7% in the navelbine trials, with the carboplatin trials showing that 30-50 percent of the population had a prolonged tumor survival after treatment with carboplatin and paclitaxel.<ref name=":0" />


A 2017 study by Lee at al. looked at the effect of melittin, a polypeptide found in bee venom, on tumor-associated macrophages in a Lewis lung carcinoma model. Melittin has a background in research as a possible cancer drug due to its activity against malignant cells. Tumor-associated macrophages facilitate tumor progression through the promotion of angiogenesis and immunosuppression. In the ''in vivo'' tests, melittin inhibited rapid tumor growth and was correlated with decreased angiogenesis marker levels, VEGF and CD31.<ref><nowiki><ref name= “Lee”> {{cite journal | vauthors=Lee C, Bae SJ, Joo H, Bae H | date=2017 | title=Melittin suppresses tumor progression by regulating tumor-associated macrophages in a Lewis lung carcinoma mouse model | url= | journal=Oncotarget | volume=8 | issue=33 | pages=54951 | doi= | pmc= | pmid= | access-date = }} </ref></nowiki></ref>
A 2017 study by Lee at al. looked at the effect of melittin, a polypeptide found in bee venom, on tumor-associated macrophages in a Lewis lung carcinoma model. Melittin has a background in research as a possible cancer drug due to its activity against malignant cells. Tumor-associated macrophages facilitate tumor progression through the promotion of angiogenesis and immunosuppression. In the ''in vivo'' tests, melittin inhibited rapid tumor growth and was correlated with decreased angiogenesis marker levels, VEGF and CD31.<ref>{{Cite journal|last=Lee|first=Chanju|last2=Bae|first2=Sung-Joo S.|last3=Joo|first3=Hwansoo|last4=Bae|first4=Hyunsu|date=2017-08-15|title=Melittin suppresses tumor progression by regulating tumor-associated macrophages in a Lewis lung carcinoma mouse model|url=https://www.ncbi.nlm.nih.gov/pubmed/28903394|journal=Oncotarget|volume=8|issue=33|pages=54951–54965|doi=10.18632/oncotarget.18627|issn=1949-2553|pmc=PMC5589633|pmid=28903394}}</ref>


Another 2017 study by Zhang et al. utilized Lewis lung carcinoma bearing mice to show that Toll-like receptor 4 mediates cancer-induced muscle wasting. It does so by directly activating muscle catabolism and stimulating an innate immune response in the mice.<ref><nowiki><ref name= “Zhang”> {{cite journal | vauthors=Zhang G, Liu Z, Ding H, Miao H, Garcia JM, Li YP | date=2017 | title=Toll-like receptor 4 mediates Lewis lung carcinoma-induced muscle wasting via coordinate activation of protein degradation pathways | url= | journal=Scientific reports | volume=7 | issue=1 | pages=2273 | doi= | pmc= | pmid= | access-date = }} </ref></nowiki></ref>
Another 2017 study by Zhang et al. utilized Lewis lung carcinoma bearing mice to show that Toll-like receptor 4 mediates cancer-induced muscle wasting. It does so by directly activating muscle catabolism and stimulating an innate immune response in the mice.<ref>{{Cite journal|last=Zhang|first=Guohua|last2=Liu|first2=Zhelong|last3=Ding|first3=Hui|last4=Miao|first4=Hongyu|last5=Garcia|first5=Jose M.|last6=Li|first6=Yi-Ping|date=2017-05-23|title=Toll-like receptor 4 mediates Lewis lung carcinoma-induced muscle wasting via coordinate activation of protein degradation pathways|url=https://www.ncbi.nlm.nih.gov/pubmed/28536426|journal=Scientific Reports|volume=7|issue=1|pages=2273|doi=10.1038/s41598-017-02347-2|issn=2045-2322|pmc=PMC5442131|pmid=28536426}}</ref>


Jing et al. discovered in 2017 that the targeting of CD169<sup>+</sup> macrophages in order to inhibit tumor Lewis lung carcinoma growth also caused depletion of bone and bone marrow in mice. This depletion disrupted bone homeostasis and caused bone weight loss and a bone density decrease in mice. Not only that, erythropoietic activity was severely impaired. Therefore, the use of CD169<sup>+</sup> macrophage targeting cancer therapies requires careful consideration of pitfalls.<ref><nowiki><ref name= “Jing”> {{cite journal | vauthors=Jing W, Zhang L, Qin F, Li X, Guo X, Li Y, Qiu C, Zhao Y | date=2017 | title=Targeting macrophages for cancer therapy disrupts bone homeostasis and impairs bone marrow erythropoiesis in mice bearing Lewis lung carcinoma tumors | url= | journal=Cellular Immunology | volume= | issue= | pages= | doi= | pmc= | pmid= | access-date = }} </ref></nowiki></ref>
Jing et al. discovered in 2017 that the targeting of CD169<sup>+</sup> macrophages in order to inhibit tumor Lewis lung carcinoma growth also caused depletion of bone and bone marrow in mice. This depletion disrupted bone homeostasis and caused bone weight loss and a bone density decrease in mice. Not only that, erythropoietic activity was severely impaired. Therefore, the use of CD169<sup>+</sup> macrophage targeting cancer therapies requires careful consideration of pitfalls.<ref>{{Cite journal|last=Jing|first=Weiqiang|last2=Zhang|first2=Li|last3=Qin|first3=Fei|last4=Li|first4=XiuXiu|last5=Guo|first5=Xing|last6=Li|first6=Yue|last7=Qiu|first7=Chunhong|last8=Zhao|first8=Yunxue|title=Targeting macrophages for cancer therapy disrupts bone homeostasis and impairs bone marrow erythropoiesis in mice bearing Lewis lung carcinoma tumors|url=https://doi.org/10.1016/j.cellimm.2017.09.006|journal=Cellular Immunology|doi=10.1016/j.cellimm.2017.09.006}}</ref>


In 1975, Munson discovered that [[cannabinoids]] suppress Lewis lung carcinoma cell growth. The mechanism of this action was shown to be inhibition of DNA synthesis<ref>{{cite journal |pmid=616322 |year = 1977 | title=In vivo effects of cannabinoids on macromolecular biosynthesis in Lewis lung carcinomas. |journal = Cancer Biochem Biophys. |volume=2 |issue=2 |author=Friedman MA |pages=51–4}}</ref> Cannabinoids increase the life span of mice carrying Lewis lung tumors and decrease primary tumor size.<ref>{{cite journal |pmid=16250836 |year = 2005 | title=Cannabinoids and cancer. |journal = Mini Rev Med Chem. |doi=10.2174/138955705774329555 |volume=5 |issue=10 |author=Kogan NM |pages=941–52}}</ref> There are multiple modes of action.<ref>{{cite journal |pmid=12958205|year=2003| title=Inhibitory effects of cannabinoid CB1 receptor stimulation on tumor growth and metastatic spreading: actions on signals involved in angiogenesis and metastasis. |journal= FASEB J|doi=10.1096/fj.02-1129fje|volume=17|issue=12|vauthors=Portella G, Laezza C, Laccetti P, De Petrocellis L, Di Marzo V, Bifulco M |pages=1771–3}}</ref>
In 1975, Munson discovered that [[cannabinoids]] suppress Lewis lung carcinoma cell growth. The mechanism of this action was shown to be inhibition of DNA synthesis<ref>{{cite journal |pmid=616322 |year = 1977 | title=In vivo effects of cannabinoids on macromolecular biosynthesis in Lewis lung carcinomas. |journal = Cancer Biochem Biophys. |volume=2 |issue=2 |author=Friedman MA |pages=51–4}}</ref> Cannabinoids increase the life span of mice carrying Lewis lung tumors and decrease primary tumor size.<ref>{{cite journal |pmid=16250836 |year = 2005 | title=Cannabinoids and cancer. |journal = Mini Rev Med Chem. |doi=10.2174/138955705774329555 |volume=5 |issue=10 |author=Kogan NM |pages=941–52}}</ref> There are multiple modes of action.<ref>{{cite journal |pmid=12958205|year=2003| title=Inhibitory effects of cannabinoid CB1 receptor stimulation on tumor growth and metastatic spreading: actions on signals involved in angiogenesis and metastasis. |journal= FASEB J|doi=10.1096/fj.02-1129fje|volume=17|issue=12|vauthors=Portella G, Laezza C, Laccetti P, De Petrocellis L, Di Marzo V, Bifulco M |pages=1771–3}}</ref>

Revision as of 03:49, 21 April 2018

Lewis lung carcinoma is a tumor that spontaneously developed as an epidermoid carcinoma in the lung of a C57BL mouse. It was discovered in 1951 by Dr. Margaret Lewis of the Wistar Institute and became one of the first transplantable tumors.[1]

Models

Syngeneic Model

According to a 2015 review article, Lewis lung carcinoma is the only reproducible syngeneic lung cancer model, meaning that it is the only reproducible lung cancer model that utilizes a transplant that is immunologically compatible. Syngeneic models have proven to be useful in predicting clinical benefit of therapy in preclinical experiments. However, there has been criticism directed towards syngeneic model usage when attempting to translate therapies from another species to humans. For example, cancer therapies that exhibited promising results in mouse models can and have failed in clinical trials due to physiological differences in the activity of the targeted gene product. The activity of the mouse product did not translate to the activity of the human counterpart. tumor originated spontaneously as a carcinoma of the lung of a C57BL mouse.[2]

Orthotopic Model

Lewis lung carcinoma can also be utilized as an orthotopic model.[2] Orthotopic models focus upon correctly modeling the tumor microenvironment by injecting or implanting tumors into the corresponding organ that they originated from (i.e. implanting a Lewis lung carcinoma into the lung of another C57BL mouse). Because of this fidelity to mimicking the tumor microenvironment, orthotopic models are considered to be more physiologically relevant in representing human tumorigenesis. However, the creation of such models is a typically more involved and technically challenging process. They also require more complex imaging modalities for data collection.[3]

Characterization

Generally, Lewis lung carcinoma is highly metastatic in immunocompetent mice.[4] If subcutaneously injected into mice, it is known to avidly metastasize to the lung. In fact, a 1996 study found that the carcinoma predominantly metastasized into the lungs after tail vein injections.[5] Lewis lung carcinoma has the appearance of a semi-firm homogeneous mass that is not grossly hemorrhagic.[6]

A 1997 research study documented the tumor progression after subcutaneous injection into the dorsal subcutis for 107 wild type, 129/Black Swiss mice. These mice were selected for their genetic background proximity to C57BL/6J mice. They observed the progression as being characterized by skin ulceration followed by ulcer hemorrhaging. Not only that, there was also basal hemorrhaging and/or edema.[4]

The cells were anaplastic, varying in size and shape; and they appeared to have little cytoplasm. The nuclei of the cells were highly distorted and prominent.[4]

The tumors were highly vascularized and metastasized to different sites, including the lungs, lymph nodes, liver, pleural cavity, diaphragm, pericardium, cardiac muscle, pancreas, adipose tissue, and esophagus. In cases of lung metastasis, large tumor masses underwent necrosis, with some of them hemorrhaging and even fewer exhibiting acute inflammation. Smaller metastases positioned themselves to be eccentric or concentric to vessels. In large tumor nodules, the cells grew, without patterning, into confluent sheets. The nodules had capillaries predominantly forming and supplying blood to the surface. The capillaries were fine and thin-walled. The nodules did exhibit expansion, interfering with and invading the space of surrounding tissues. This caused tissue degeneration.[4]

Clinical Research

The Lewis lung carcinoma tumor model’s role in cancer has been its use for research into tumor metastasis and angiogenesis properties. The model is also useful for chemotherapeutic testing in vivo. Navelbine and carboplatin, two chemotherapeutics currently on the market, were tested in C57BL mice with Lewis lung carcinoma tumors in their hind flank. Tumor regression reached 72.7% in the navelbine trials, with the carboplatin trials showing that 30-50 percent of the population had a prolonged tumor survival after treatment with carboplatin and paclitaxel.[2]

A 2017 study by Lee at al. looked at the effect of melittin, a polypeptide found in bee venom, on tumor-associated macrophages in a Lewis lung carcinoma model. Melittin has a background in research as a possible cancer drug due to its activity against malignant cells. Tumor-associated macrophages facilitate tumor progression through the promotion of angiogenesis and immunosuppression. In the in vivo tests, melittin inhibited rapid tumor growth and was correlated with decreased angiogenesis marker levels, VEGF and CD31.[7]

Another 2017 study by Zhang et al. utilized Lewis lung carcinoma bearing mice to show that Toll-like receptor 4 mediates cancer-induced muscle wasting. It does so by directly activating muscle catabolism and stimulating an innate immune response in the mice.[8]

Jing et al. discovered in 2017 that the targeting of CD169+ macrophages in order to inhibit tumor Lewis lung carcinoma growth also caused depletion of bone and bone marrow in mice. This depletion disrupted bone homeostasis and caused bone weight loss and a bone density decrease in mice. Not only that, erythropoietic activity was severely impaired. Therefore, the use of CD169+ macrophage targeting cancer therapies requires careful consideration of pitfalls.[9]

In 1975, Munson discovered that cannabinoids suppress Lewis lung carcinoma cell growth. The mechanism of this action was shown to be inhibition of DNA synthesis[10] Cannabinoids increase the life span of mice carrying Lewis lung tumors and decrease primary tumor size.[11] There are multiple modes of action.[12]

References

  1. ^ Rashidi, Babak; Yang, Meng; Jiang, Ping; Baranov, Eugene; An, Zili; Wang, Xiaoen; Moossa, A. R.; Hoffman, R. M. (2000-01-01). "A highly metastatic Lewis lung carcinoma orthotopic green fluorescent protein model". Clinical & Experimental Metastasis. 18 (1): 57–60. doi:10.1023/A:1026596131504. ISSN 0262-0898.
  2. ^ a b c Kellar, Amelia; Egan, Cay; Morris, Don (2015). "Preclinical Murine Models for Lung Cancer: Clinical Trial Applications". BioMed Research International. 2015: 1–17. doi:10.1155/2015/621324. ISSN 2314-6133.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  3. ^ Qiu, Wanglong; Su, Gloria H. (2013). "Development of orthotopic pancreatic tumor mouse models". Methods in Molecular Biology (Clifton, N.J.). 980: 215–223. doi:10.1007/978-1-62703-287-2_11. ISSN 1940-6029. PMC 4049460. PMID 23359156.{{cite journal}}: CS1 maint: PMC format (link)
  4. ^ a b c d Bugge, T. H.; Kombrinck, K. W.; Xiao, Q.; Holmbäck, K.; Daugherty, C. C.; Witte, D. P.; Degen, J. L. (1997-12-01). "Growth and dissemination of Lewis lung carcinoma in plasminogen-deficient mice". Blood. 90 (11): 4522–4531. ISSN 0006-4971. PMID 9373263.
  5. ^ Anderson, I. C.; Shipp, M. A.; Docherty, A. J.; Teicher, B. A. (1996-02-15). "Combination therapy including a gelatinase inhibitor and cytotoxic agent reduces local invasion and metastasis of murine Lewis lung carcinoma". Cancer Research. 56 (4): 715–718. ISSN 0008-5472. PMID 8631001.
  6. ^ Cancer Chemother Rep 2 1972 Nov;(3)1:325
  7. ^ Lee, Chanju; Bae, Sung-Joo S.; Joo, Hwansoo; Bae, Hyunsu (2017-08-15). "Melittin suppresses tumor progression by regulating tumor-associated macrophages in a Lewis lung carcinoma mouse model". Oncotarget. 8 (33): 54951–54965. doi:10.18632/oncotarget.18627. ISSN 1949-2553. PMC 5589633. PMID 28903394.{{cite journal}}: CS1 maint: PMC format (link)
  8. ^ Zhang, Guohua; Liu, Zhelong; Ding, Hui; Miao, Hongyu; Garcia, Jose M.; Li, Yi-Ping (2017-05-23). "Toll-like receptor 4 mediates Lewis lung carcinoma-induced muscle wasting via coordinate activation of protein degradation pathways". Scientific Reports. 7 (1): 2273. doi:10.1038/s41598-017-02347-2. ISSN 2045-2322. PMC 5442131. PMID 28536426.{{cite journal}}: CS1 maint: PMC format (link)
  9. ^ Jing, Weiqiang; Zhang, Li; Qin, Fei; Li, XiuXiu; Guo, Xing; Li, Yue; Qiu, Chunhong; Zhao, Yunxue. "Targeting macrophages for cancer therapy disrupts bone homeostasis and impairs bone marrow erythropoiesis in mice bearing Lewis lung carcinoma tumors". Cellular Immunology. doi:10.1016/j.cellimm.2017.09.006.
  10. ^ Friedman MA (1977). "In vivo effects of cannabinoids on macromolecular biosynthesis in Lewis lung carcinomas". Cancer Biochem Biophys. 2 (2): 51–4. PMID 616322.
  11. ^ Kogan NM (2005). "Cannabinoids and cancer". Mini Rev Med Chem. 5 (10): 941–52. doi:10.2174/138955705774329555. PMID 16250836.
  12. ^ Portella G, Laezza C, Laccetti P, De Petrocellis L, Di Marzo V, Bifulco M (2003). "Inhibitory effects of cannabinoid CB1 receptor stimulation on tumor growth and metastatic spreading: actions on signals involved in angiogenesis and metastasis". FASEB J. 17 (12): 1771–3. doi:10.1096/fj.02-1129fje. PMID 12958205.{{cite journal}}: CS1 maint: unflagged free DOI (link)


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