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Role of immune and inflammatory cells in lung cancer–associated PH

Published byJob West Modified over 6 years ago

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Presentation on theme: "Role of immune and inflammatory cells in lung cancer–associated PH"— Presentation transcript:

1 Fig. 5. Role of immune and inflammatory cells in lung cancer–associated PH.
Role of immune and inflammatory cells in lung cancer–associated PH. Representative photomicrographs and quantification of (A) CD3+ (lymphocytes) and (B) CD68+ (macrophages) cells in pulmonary vessels from nontumor (N) and tumor (T) SCC and AC tissues. Scale bars, 20 μm; n = 7. *P < 0.05, **P < 0.01, compared with nontumor tissues of SCC or AC. NSG mice were injected with saline (NSG-control), LLC1 (NSG-LLC1) cells, or A549 (NSG-A549) cells. Twelve and 20 days after injection, the NSG-control (n = 7), NSG-LLC1 (n = 9), and NSG-A549 (n = 9) lung tumor–bearing mice underwent echocardiographic and physiological measurements. (C) Representative photographs of mouse lungs. Scale bars, 2 mm. (D) Representative echocardiographic images and echocardiographic measurements of (E) NSG-A549 and (F) NSG-LLC1 lung tumor–bearing mice. Physiological measurements (RVSP and PO2), RV hypertrophy [RV/(LV + S)], and PVR of (G) NSG-A549 and (H) NSG-LLC1 lung tumor–bearing mice. Soni Savai Pullamsetti et al., Sci Transl Med 2017;9:eaai9048 Published by AAAS

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Supplemental Fig 1 Rt. Lung Tumor A B Murine lung cancer model. LLC were implanted as described in Fig 1. A) Representative histology showing the distribution.

Supplemental Fig 1 Rt. Lung Tumor A B Murine lung cancer model. LLC were implanted as described in Fig 1. A) Representative histology showing the distribution.
Fig. 1. TP is highly expressed in myeloma.

Fig. 1. TP is highly expressed in myeloma.
Fig. 2. LUM015 fluorescently labels tumor cells in mouse models of STS and breast cancer. LUM015 fluorescently labels tumor cells in mouse models of STS.

Fig. 2. LUM015 fluorescently labels tumor cells in mouse models of STS and breast cancer. LUM015 fluorescently labels tumor cells in mouse models of STS.
Fig. 6. AZD6738 induces DNA damage and apoptosis and exhibits antitumor efficacy in xenograft models of high-risk medulloblastoma and neuroblastoma. AZD6738.

Fig. 6. AZD6738 induces DNA damage and apoptosis and exhibits antitumor efficacy in xenograft models of high-risk medulloblastoma and neuroblastoma. AZD6738.
Fig. 3. Features of PH in KRasLA2 transgenic mice.

Fig. 3. Features of PH in KRasLA2 transgenic mice.
Fig. 4. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin expression. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin.

Fig. 4. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin expression. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin.
In vivo function of MeTro sealants using rat incision model of lungs

In vivo function of MeTro sealants using rat incision model of lungs
Fig. 6. Ex vivo and in vivo test to evaluate the sealing capability of the MeTro sealant using a porcine lung incision model. Ex vivo and in vivo test.

Fig. 6. Ex vivo and in vivo test to evaluate the sealing capability of the MeTro sealant using a porcine lung incision model. Ex vivo and in vivo test.
Fig. 7. Role of PDE5 up-regulation in lung cancer–associated PH.

Fig. 7. Role of PDE5 up-regulation in lung cancer–associated PH.
Fig. 1. BCAS1 expression identifies newly generated oligodendrocytes.

Fig. 1. BCAS1 expression identifies newly generated oligodendrocytes.
Fig. 5 Maraba induces antitumor T cell immunity.

Fig. 5 Maraba induces antitumor T cell immunity.
Fig. 6. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex vivo. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex.

Fig. 6. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex vivo. Combinatorial VCPI and OV M1 treatment is efficacious in vivo and ex.
Fig. 1 Localized treatment of TNBC cancers kills tumor cells and minimizes the metastatic burden. Localized treatment of TNBC cancers kills tumor cells.

Fig. 1 Localized treatment of TNBC cancers kills tumor cells and minimizes the metastatic burden. Localized treatment of TNBC cancers kills tumor cells.
Fig. 8. In vivo suppression of MM by CMLD

Fig. 8. In vivo suppression of MM by CMLD
Fig. 6. Increased efficacy of immunotherapy in lymphangiogenic B16 melanomas depends on CCR7 signaling before therapy and local activation and expansion.

Fig. 6. Increased efficacy of immunotherapy in lymphangiogenic B16 melanomas depends on CCR7 signaling before therapy and local activation and expansion.
Fig. 8. mRIPO elicits neutrophil influx followed by DC and T cell infiltration into tumors. mRIPO elicits neutrophil influx followed by DC and T cell infiltration.

Fig. 8. mRIPO elicits neutrophil influx followed by DC and T cell infiltration into tumors. mRIPO elicits neutrophil influx followed by DC and T cell infiltration.
Fig. 4 Infection-induced CLV dysfunction is associated with decreased LMC coverage. Infection-induced CLV dysfunction is associated with decreased LMC.

Fig. 4 Infection-induced CLV dysfunction is associated with decreased LMC coverage. Infection-induced CLV dysfunction is associated with decreased LMC.
Fig. 2. GPC3 expression in normal and tumor tissues.

Fig. 2. GPC3 expression in normal and tumor tissues.
Fig. 5. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic mice. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic.

Fig. 5. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic mice. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic.
Fig. 3. Paclitaxel promotes TMEM-dependent vascular permeability, cancer cell dissemination, and metastasis in breast cancer. Paclitaxel promotes TMEM-dependent.

Fig. 3. Paclitaxel promotes TMEM-dependent vascular permeability, cancer cell dissemination, and metastasis in breast cancer. Paclitaxel promotes TMEM-dependent.

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