Host control of metastasis in CZ, C3 and [CZ x C3] F1 mice.

<p>Host control of metastasis in CZ, C3 and [CZ x C3] F1 mice.</p

Activation of NFAT and secretion of MMP-2 are critical for invasion by metastatic bone tumor cells.

<p>A) Immunoblot for NFAT c1 in tumor cell lysates. B) Normalized luciferase activity of an NFAT reporter in tumor cells. C) Inhibition of invasion by CZ II tumor cells. Left: cells ± TIMP-2. Middle: cells ± NFAT siRNA. Right: immunoblots on cells ± NFAT siRNA.</p

Metastatic tumor cells invade Matrigel via an MMP-2-mediated pathway.

<p>A) Migration assay was carried out as in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1000733#ppat-1000733-g002" target="_blank">Figure 2A</a> except the upper surface of the filter was coated with Matrigel. B) Upper – Zymography with gelatin as ‘in gel’ substrate and conditioned media from each of the tumor lines. Lower – Immunoblot for MMP-2 in tumor cell lysates.</p

Primary and metastatic bone tumors from CZ mice.

<p>A) A primary bone tumor (P) on the head of the femur of a CZ mouse. B) H&E stained section of the same tumor showing invasion of adjacent muscle and destruction of bone by invading tumor cells. C) Metastatic nodule (Mx) on the surface of the lung of the same animal. D) H&E stained section of the lung metastasis from the same animal showing osteiod. E) Occult metastatic lesion with osteoid in the lung of a different CZ animal. F) H&E stained section of a liver metastasis showing osteoid in a CZ animal inoculated with osteosarcoma cells.</p

Additional file 4: of Isoform-specific deletion of PKM2 constrains tumor initiation in a mouse model of soft tissue sarcoma

Table S1. Raw data for LC-MS metabolomics on KP M2+/+ and KP M2-/- sarcomas. Related to Fig. 5. This table contains all the LC-MS metabolomics data. Includes normalization and statistical analysis for each measured metabolite. (XLSX 140 kb

Additional file 3: of Isoform-specific deletion of PKM2 constrains tumor initiation in a mouse model of soft tissue sarcoma

Figure S3. (A) Representative images of IF for tdTomato, PKM1 or PKM2, and EdU on KP M2 +/+ or KP M2 −/− sarcoma cell lines. (B) Cumulative populaion doublings of KP M2 +/+ or KP M2 −/− sarcoma cell lines, n = 3 KP M2 +/+ cell lines and n = 4 KP M2 −/− cell lines. (C) Sarcoma weight in grams. (JPG 2694 kb

Additional file1: of Isoform-specific deletion of PKM2 constrains tumor initiation in a mouse model of soft tissue sarcoma

Figure S1. Quantification of PKM1 and PKM2 staining intensities shown as percent of tissue cores scored in 16 normal human skeletal muscle samples (A) and 48 primary human rhabdomyosarcomas (B). Score 0 = no staining, Score 1 = weak, Score 2 = positive, or Score 3 = strong. (C) Representative images of IHC for PKM1 and PKM2 in KP mouse sarcoma tissue. Corresponding H&E images are shown. Scale bars, 20 μm. (JPG 1314 kb

Effect of laser on the humoral immune response to a model vaccine.

<p>A, Serum ovalbumin- (OVA)-specific IgG titers 3, 6, and 12 weeks following vaccination with 40 µg OVA with or without laser illumination. Endpoint titer of OVA-specific serum IgG was determined by ELISA. Plates were coated with OVA. <i>n</i> = 33, 19, 15, 12 and 11, 5 and 6, 6 and 6 for no OVA, OVA i.d., OVA +Alum i.d., OVA i.d. + PW 532 nm 1 and 4 minutes, OVA i.d. + PW 1064 nm 1 and 4 minutes, OVA i.d. + CW 1064 nm 1 and 4 minutes, respectively. Error bars show means ± s.e.m. *<i>P</i><0.05, **<i>P</i><0.01 and ***<i>P</i><0.001 as compared to OVA i.d. B, The relationships between anti-OVA antibody titers following 1–4 minutes PW 532 nm, PW 1064 nm and CW 1064 nm laser-treated groups at 6 weeks (logIgG) and maximal skin surface temperature (Tm) was not statistically significant; a Pearson's correlation coefficient <i>r</i> = −0.237 (<i>P</i> = 0.08), where log(IgG) = −0.193Tm+10.75 (linear regression, R² = 0.056). <i>n</i> = 20, 17, 18, for OVA i.d. + PW 532 nm 1–4 minutes, OVA i.d. + PW 1064 nm 1–4 minutes, OVA i.d. + CW 1064 nm 1–4 minutes.</p

NIR laser safety study in humans.

<p>A, Schedule of laser treatment and follow-up skin appearance documentation. Five healthy adults aged 20 to 46 years old with either skin phototype V or VI were enrolled. B, A plastic grid was used to separate the laser exposure sites. An aqueous gel was applied in each section of the grid to enhance the dissipation of heat from the skin's surface. The bar indicates 1 inch. C and D, Representative images of the laser-exposed skin are shown at (C) 1 hour and (D) 2 days after completion of the treatment. No detectable skin damage on visual inspection was observed following laser exposure at any irradiance used.</p

Reported sensations and signs of skin damage on each NIR laser dose.

<p>Consenting human subjects were exposed to a range of laser doses from 0.5 to 3.7 W/cm² (16 doses) each up to 120 seconds. Sensations felt by subjects were classified as mild (warmth, tingling, itching, pinprick/needle sensations), moderate (hotness, dull pain), or severe (burning, sharp pain), and recorded. The operator also recorded any signs of skin damage.</p>1<p>Warmth</p>2<p>Hotness</p>3<p>Burning</p>4<p>Pinprick/needle sensations</p>5<p>Dull pain</p>6<p>Sharp pain</p>7<p>Tingling</p>8<p>Itching</p>9<p>Skin appearance change; No changes in skin appearance or damage were noted on all exposures, except transient skin darkening (transient hyperpigmentation) occurred in some subjects, which was due to changes in capillary blood flow in the treated area. These changes were not observed during follow-up examination after 2 hours.</p>10<p>Skin damage</p