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2016-04-01

Fig 2. Differentiation of human ES-cell-derived ENC precursors into enteric neuron subtypes.

Fig 2. Differentiation of human ES-cell-derived ENC precursors into enteric neuron subtypes.
  • Fattahi F, Steinbeck JA, Kriks S, Tchieu J, Zimmer B, Kishinevsky S, Zeltner N, Mica Y, El-Nachef W, Zhao H, de Stanchina E

  • Nature. 2016 Mar 3;531(7592):105-9.

2016-04-04

Fig 1. A conceptual framework for interactive data retrieval.

Fig 1. A conceptual framework for interactive data retrieval.
  • Hruby GW, Matsoukas K, Cimino JJ, Weng C

  • J Biomed Inform. 2016 Mar 10. pii: S1532-0464(16)00044-7.

2016-04-05

Fig 1. Models of the hematopoietic hierarchy.

Fig 1. Models of the hematopoietic hierarchy.
  • Woolthuis CM, Park CY

  • Blood. 2016 Mar 10;127(10):1242-8.

2016-04-06

Fig 3. Dynamic and Active Interaction between the Radial Glial Fiber and the Periventricular Vessel in the MGE/PoA.

Fig 3. Dynamic and Active Interaction between the Radial Glial Fiber and the Periventricular Vessel in the MGE/PoA.
  • Tan X, Liu WA, Zhang XJ, Shi W, Ren SQ, Li Z, Brown KN, Shi SH

  • Dev Cell. 2016 Mar 21;36(6):624-38.

2016-04-07

Fig 3. Mechanisms of poor tumor T cell infiltration.

Fig 3. Mechanisms of poor tumor T cell infiltration.
  • Zou W, Wolchok JD, Chen L

  • Sci Transl Med. 2016 Mar 2;8(328):328rv4.

2016-04-08

Fig 2. Radiation oncologists per 100,000 residents stratified by HSA.

Fig 2. Radiation oncologists per 100,000 residents stratified by HSA.
  • Lin CC, Bruinooge SS, Kirkwood MK, Hershman DL, Jemal A, Guadagnolo BA, James BY, Hopkins S, Goldstein M, Bajorin D, Giordano SH

  • Int J Radiat Oncol Biol Phys. 2016 Mar 15;94(4):719-28.

2016-04-11

Fig 2. The hypoxia-inducible transcription factor (HIF) pathway in clear cell renal cancer. In normal epithelial cells, ubiquitination of HIF-α by the E3 ubiquitin ligase leads to degradation via the 26 proteasome.

Fig 2. The hypoxia-inducible transcription factor (HIF) pathway in clear cell renal cancer. In normal epithelial cells, ubiquitination of HIF-α by the E3 ubiquitin ligase leads to degradation via the 26 proteasome.
  • Schödel J, Grampp S, Maher ER, Moch H, Ratcliffe PJ, Russo P, Mole DR

  • Eur Urol. 2016 Apr;69(4):646-57.

2016-04-12

Fig 2. Modes of Sensing and Provision of Effector Function by Tissue-Resident Innate, Innate-like and Adaptive Lymphocytes.

Fig 2. Modes of Sensing and Provision of Effector Function by Tissue-Resident Innate, Innate-like and Adaptive Lymphocytes.
  • Fan X, Rudensky AY

  • Cell. 2016 Mar 10;164(6):1198-211.

2016-04-13

Fig 1. Lymph node drainage basins in gallbladder cancer.

Fig 1. Lymph node drainage basins in gallbladder cancer.
  • Qadan M, Kingham TP

  • Surg Clin North Am. 2016 Apr;96(2):229-45.

2016-04-14

Fig 7. DKK1 Enforces a Quiescent Immune Evasive State. (A) Growth of H2087-LCC cells depleted of DKK1 in athymic nude mice. Data are total number of LCC cells detected per lung after 3 months post-tail vein injection ± SEM. N = 5–6 mice per group, scoring representative serial sections of the entire lung for each mouse.(B) Relative mRNA expression of NK cell activating ligands and death receptors in H2087-LCC cells upon DKK1 depletion. Relative quantification is normalized to LCC1 or LCC2 control.(C) H2087 and HCC1954-LCC cells depleted of DKK1 are more susceptible to NK-cell-mediated cytotoxicity compared to their controls. Data are mean percentage of cytolysis ± SEM for three replicates. ∗∗p < 0.01, Student’s t test.(D) Depletion of NK cells by anti-asialo-GM1 in athymic nude mice injected with shDKK1 bearing H2087-LCC2 cells. Whole body photon flux, 2 months post-injection. N = 5–6 mice per group. ∗∗p < 0.01, Mann-Whitney test.(E) Growth of H2087-LCC cells depleted of DKK1 in NSG mice. Whole body photon flux, 2 months post-injection. N = 5–6 mice per group. ∗∗p < 0.01, ∗∗∗p < 0.001, Mann-Whitney test.(F) Representative immunofluorescence images of metastatic lesions in the lungs of NSG mice in (E). Scale bar, 50 μm.(G) Growth of H2087-LCC cells depleted of Sox2 in NSG mice. Whole body photon flux, 2 months post-injection. N = 5–6 mice per group. ∗p < 0.05, ∗∗∗p < 0.001, Mann-Whitney test.(H) A model summarizing the central tenets of latency recapitulated in the present latency competent cancer cell models.

Fig 7. DKK1 Enforces a Quiescent Immune Evasive State. (A) Growth of H2087-LCC cells depleted of DKK1 in athymic nude mice. Data are total number of LCC cells detected per lung after 3 months post-tail vein injection ± SEM. N = 5–6 mice per group, scoring representative serial sections of the entire lung for each mouse.(B) Relative mRNA expression of NK cell activating ligands and death receptors in H2087-LCC cells upon DKK1 depletion. Relative quantification is normalized to LCC1 or LCC2 control.(C) H2087 and HCC1954-LCC cells depleted of DKK1 are more susceptible to NK-cell-mediated cytotoxicity compared to their controls. Data are mean percentage of cytolysis ± SEM for three replicates. ∗∗p < 0.01, Student’s t test.(D) Depletion of NK cells by anti-asialo-GM1 in athymic nude mice injected with shDKK1 bearing H2087-LCC2 cells. Whole body photon flux, 2 months post-injection. N = 5–6 mice per group. ∗∗p < 0.01, Mann-Whitney test.(E) Growth of H2087-LCC cells depleted of DKK1 in NSG mice. Whole body photon flux, 2 months post-injection. N = 5–6 mice per group. ∗∗p < 0.01, ∗∗∗p < 0.001, Mann-Whitney test.(F) Representative immunofluorescence images of metastatic lesions in the lungs of NSG mice in (E). Scale bar, 50 μm.(G) Growth of H2087-LCC cells depleted of Sox2 in NSG mice. Whole body photon flux, 2 months post-injection. N = 5–6 mice per group. ∗p < 0.05, ∗∗∗p < 0.001, Mann-Whitney test.(H) A model summarizing the central tenets of latency recapitulated in the present latency competent cancer cell models.
  • Malladi S, Macalinao DG, Jin X, He L, Basnet H, Zou Y, de Stanchina E, Massagué J

  • Cell. 2016 Mar 24;165(1):45-60.

2016-04-15

Fig 2. A Metabolic Checkpoint Involving a UPRmt via SIRT7 Is Required for Stem Cell Maintenance.

Fig 2. A Metabolic Checkpoint Involving a UPRmt via SIRT7 Is Required for Stem Cell Maintenance.
  • Lin YF, Haynes CM

  • Molecular cell. 2016 Mar 3;61(5):677-82.

2016-04-18

Fig 1. Spinal cord dose-volume plot (A) from Gibbs et al1 and (B) with an approximated exponential DVH (dashed lines).

Fig 1. Spinal cord dose-volume plot (A) from Gibbs et al1 and (B) with an approximated exponential DVH (dashed lines).
  • Grimm J, Sahgal A, Soltys SG, Luxton G, Patel A, Herbert S, Xue J, Ma L, Yorke E, Adler JR, Gibbs IC

  • Semin Radiat Oncol. 2016 Apr;26(2):165-71.

2016-04-19

Fig 1. Kaplan–Meier curves showing estimates of metastasis-free survival in M0/Mx patients treated by surgery for sarcomatoid-variant renal cell carcinoma (sRCC).

Fig 1. Kaplan–Meier curves showing estimates of metastasis-free survival in M0/Mx patients treated by surgery for sarcomatoid-variant renal cell carcinoma (sRCC).
  • Nguyen DP, Vilaseca A, Vertosick EA, Corradi RB, Touijer KA, Benfante NE, Sjoberg DD, Russo P

  • World J Urol. 2016 Apr;34(4):539-44.

2016-04-20

Fig 2. In vitro functional study of fCNT-mediated siEGFP delivery to EGFP+ HeLa cells. (A) Representative time-lapse confocal microscopy images at 1, 24, and 60 hours. Fluorescence quantification from three ROIs of the cells. Scale bars, 50 μm. (B) Flow cytometry histogram overlay. (C and D) Western blot (C) and RT-PCR analysis (D) of EGFP expression by cells isolated at day 3 after transfection. Data in (A) and (D) are means ± SEM (n = 3). P values were determined by unpaired t test. h, hours; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.

Fig 2. In vitro functional study of fCNT-mediated siEGFP delivery to EGFP+ HeLa cells. (A) Representative time-lapse confocal microscopy images at 1, 24, and 60 hours. Fluorescence quantification from three ROIs of the cells. Scale bars, 50 μm. (B) Flow cytometry histogram overlay. (C and D) Western blot (C) and RT-PCR analysis (D) of EGFP expression by cells isolated at day 3 after transfection. Data in (A) and (D) are means ± SEM (n = 3). P values were determined by unpaired t test. h, hours; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.
  • Alidori S, Akhavein N, Thorek DL, Behling K, Romin Y, Queen D, Beattie BJ, Manova-Todorova K, Bergkvist M, Scheinberg DA, McDevitt MR

  • Sci Transl Med. 2016 Mar 23;8(331):331ra39.

2016-04-21

Fig 2. Lkb1 inactivation leads to a T-cell–suppressive tumor microenvironment with low PD-L1 expression in tumor cells. A, total counts of CD4 T cells (top) and CD8 T cells (bottom). **, P < 0.01. B, expression of checkpoint receptors in CD4 T cells (top) and CD8 T cells (bottom) in Kras (K) or Kras/Lkb1 (KL) tumors. *, P < 0.05; **, P < 0.01; ***, P < 0.001. C, IFNγ expression and proliferation marker (Ki-67) positivity for CD4 or CD8 T cells in Kras or Kras/Lkb1 tumors. Representative flow cytometry data (total CD3+ T cells) from each mouse model (left). Percentage of Ki-67+ and IFNγ+ in CD4 or CD8 T cells from Kras (n = 6) or Kras/Lkb1 (n = 6) mice. *, P < 0.05; **, P < 0.01. D, PD-L1 expression in gated CD45−EpCAM+ cells in Kras (n = 5) or Kras/Lkb1 (n = 5) tumors evaluated by flow cytometry. *, P = 0.0384. E, PD-L1 expression in KP (n = 3) versus KPL (n = 3) cell lines evaluated by flow cytometry. *, P = 0.0495. Data are representative of three independent experiments. F, PD-L1 expression in H441 or H1792 cells stably transfected with sh-nontarget (NT) or sh-LKB1. Data are representative of three independent experiments.

Fig 2. Lkb1 inactivation leads to a T-cell–suppressive tumor microenvironment with low PD-L1 expression in tumor cells. A, total counts of CD4 T cells (top) and CD8 T cells (bottom). **, P < 0.01. B, expression of checkpoint receptors in CD4 T cells (top) and CD8 T cells (bottom) in Kras (K) or Kras/Lkb1 (KL) tumors. *, P < 0.05; **, P < 0.01; ***, P < 0.001. C, IFNγ expression and proliferation marker (Ki-67) positivity for CD4 or CD8 T cells in Kras or Kras/Lkb1 tumors. Representative flow cytometry data (total CD3+ T cells) from each mouse model (left). Percentage of Ki-67+ and IFNγ+ in CD4 or CD8 T cells from Kras (n = 6) or Kras/Lkb1 (n = 6) mice. *, P < 0.05; **, P < 0.01. D, PD-L1 expression in gated CD45−EpCAM+ cells in Kras (n = 5) or Kras/Lkb1 (n = 5) tumors evaluated by flow cytometry. *, P = 0.0384. E, PD-L1 expression in KP (n = 3) versus KPL (n = 3) cell lines evaluated by flow cytometry. *, P = 0.0495. Data are representative of three independent experiments. F, PD-L1 expression in H441 or H1792 cells stably transfected with sh-nontarget (NT) or sh-LKB1. Data are representative of three independent experiments.
  • Koyama S, Akbay EA, Li YY, Aref AR, Skoulidis F, Herter-Sprie GS, Buczkowski KA, Liu Y, Awad MM, Denning WL, Diao L, Wang J, Parra-Cuentas ER, Wistuba II, Soucheray M, Thai T, Asahina H, Kitajima S, Altabef A, Cavanaugh JD, Rhee K, Gao P, Zhang H, Fecci PE, Shimamura T, Hellmann MD, Heymach JV, Hodi FS, Freeman GJ, Barbie DA, Dranoff G, Hammerman PS, Wong KK

  • Cancer Res. 2016 Mar 1;76(5):999-1008

2016-04-22

Fig 1. Schematic of the PI3K/mTOR signaling pathway. Figure legend: upon receptor tyrosine kinase (RTK) stimulation, PI3K phosphorylates the lipid moiety PIP2, creating PIP3. AKT is recruited to the membrane, where it is phosphorylated and activated by the mTORC2 complex and PDK. AKT phosphorylates and inhibits the TCS complex, which permits the activation of mTORC1 by RHEB GTPase. The RTK pathway also actives the RAS-ERK pathway and feeds into TSC1/2 regulation. PTEN is a phosphatase and converts PIP2 back to PIP2, inhibiting PI3K signals.

Fig 1. Schematic of the PI3K/mTOR signaling pathway. Figure legend: upon receptor tyrosine kinase (RTK) stimulation, PI3K phosphorylates the lipid moiety PIP2, creating PIP3. AKT is recruited to the membrane, where it is phosphorylated and activated by the mTORC2 complex and PDK. AKT phosphorylates and inhibits the TCS complex, which permits the activation of mTORC1 by RHEB GTPase. The RTK pathway also actives the RAS-ERK pathway and feeds into TSC1/2 regulation. PTEN is a phosphatase and converts PIP2 back to PIP2, inhibiting PI3K signals.
  • Myers AP, Filiaci VL, Zhang Y, Pearl M, Behbakht K, Makker V, Hanjani P, Zweizig S, Burke JJ 2nd, Downey G, Leslie KK, Van Hummelen P, Birrer MJ, Fleming GF

  • Gynecol Oncol. 2016 Apr;141(1):43-8

2016-04-25

Fig 1. FRET K48 di-Ub assay.

Fig 1. FRET K48 di-Ub assay.
  • Wu K, Chong RA, Yu Q, Bai J, Spratt DE, Ching K, Lee C, Miao H, Tappin I, Hurwitz J, Zheng N

  • Proc Natl Acad Sci U S A. 2016 Mar 21.

2016-04-26

Fig 2. Immune checkpoint inhibitors: releasing the brakes on the immune system.

Fig 2. Immune checkpoint inhibitors: releasing the brakes on the immune system.
  • Dizon DS, Krilov L, Cohen E, Gangadhar T, Ganz PA, Hensing TA, Hunger S, Krishnamurthi SS, Lassman AB, Markham MJ, Mayer E

  • J Clin Oncol. 2016 Mar 20;34(9):987-1011.

2016-04-27

Fig 2. Comparative genomic analysis of B. fragilis strains reveals multiple independent acquisitions of T6SS loci and numerous putative effector/immunity cassettes.

Fig 2. Comparative genomic analysis of B. fragilis strains reveals multiple independent acquisitions of T6SS loci and numerous putative effector/immunity cassettes.
  • Wexler AG, Bao Y, Whitney JC, Bobay LM, Xavier JB, Schofield WB, Barry NA, Russell AB, Tran BQ, Goo YA, Goodlett DR

  • Proc Natl Acad Sci U S A. 2016 Mar 29;113(13):3639-44.

2016-04-28

Fig 1. The frequency, scope, and prognostic value of chromosome 17p alterations in human cancers.

Fig 1. The frequency, scope, and prognostic value of chromosome 17p alterations in human cancers.
  • Liu Y, Chen C, Xu Z, Scuoppo C, Rillahan CD, Gao J, Spitzer B, Bosbach B, Kastenhuber ER, Baslan T, Ackermann S

  • Nature. 2016 Mar 24;531(7595):471-5.

2016-04-29

Fig 1. Image-based assessment, diagnosis, treatment planning, and response after spine SBRT. (A) The patient had metastatic lung cancer presenting with a T12 metastasis with a well-defined mass-type tumour (green arrow) within the vertebral body, ipsilateral posterior elements, and minor disease extension to the posterior contralateral lamina on axial T2-weighted MRI. Left-sided anterior, lateral, and posterior epidural tumour extension (Bilsky 1B) and paraspinal disease were also seen. On T1-weighted imaging, the signal in the rest of the vertebral body was consistent with the presence of disease but was not conspicuous on T2-weighted imaging (white arrow). (B) A doughnut-type distribution was applied for SBRT and the patient received 24 Gy in two fractions. (C) 6 months after SBRT, axial T2-weighted MRI showed regression of the epidural and paraspinal disease (green arrow) with heterogeneous T2 hypointensity (white arrow) within the bone. What the signal change represented (disease, fibrosis, or necrosis) was unknown, but tumour regression led to a classification of stable disease and possible partial response. (D) At 12 months, axial T2-weighted MRI showed some minor increase in left-sided epidural and paraspinal disease (green arrow) and more homogeneous T2 hypointensity in the vertebral body and bilateral posterior elements (white arrow). The patient was asymptomatic. Biospy confirmed tumour recurrence, resulting in a classification of progressive disease. This case highlights the challenges of interpreting signal changes after spine SBRT. SBRT=stereotactic body radiotherapy.

Fig 1. Image-based assessment, diagnosis, treatment planning, and response after spine SBRT. (A) The patient had metastatic lung cancer presenting with a T12 metastasis with a well-defined mass-type tumour (green arrow) within the vertebral body, ipsilateral posterior elements, and minor disease extension to the posterior contralateral lamina on axial T2-weighted MRI. Left-sided anterior, lateral, and posterior epidural tumour extension (Bilsky 1B) and paraspinal disease were also seen. On T1-weighted imaging, the signal in the rest of the vertebral body was consistent with the presence of disease but was not conspicuous on T2-weighted imaging (white arrow). (B) A doughnut-type distribution was applied for SBRT and the patient received 24 Gy in two fractions. (C) 6 months after SBRT, axial T2-weighted MRI showed regression of the epidural and paraspinal disease (green arrow) with heterogeneous T2 hypointensity (white arrow) within the bone. What the signal change represented (disease, fibrosis, or necrosis) was unknown, but tumour regression led to a classification of stable disease and possible partial response. (D) At 12 months, axial T2-weighted MRI showed some minor increase in left-sided epidural and paraspinal disease (green arrow) and more homogeneous T2 hypointensity in the vertebral body and bilateral posterior elements (white arrow). The patient was asymptomatic. Biospy confirmed tumour recurrence, resulting in a classification of progressive disease. This case highlights the challenges of interpreting signal changes after spine SBRT. SBRT=stereotactic body radiotherapy.
  • Thibault I, Chang EL, Sheehan J, Ahluwalia MS, Guckenberger M, Sohn MJ, Ryu S, Foote M, Lo SS, Muacevic A, Soltys SG, Chao S, Gerszten P, Lis E, Yu E, Bilsky M, Fisher C, Schiff D, Fehlings MG, Ma L, Chang S, Chow E, Parelukar WR, Vogelbaum MA, Sahgal A

  • Lancet Oncol. 2015 Dec;16(16):e595-603

2016-05-02

Fig 1. P values of gene-by-environment interactions for the gene CELF4 region.

Fig 1. P values of gene-by-environment interactions for the gene CELF4 region.
  • Wang X, Sun CL, Quiñones-Lombraña A, Singh P, Landier W, Hageman L, Mather M, Rotter JI, Taylor KD, Chen YD, Armenian SH

  • J Clin Oncol. 2016 Mar 10;34(8):863-70.

2016-05-03

Fig 4. Some of the many areas of current therapeutic interest in small cell lung cancer.

Fig 4. Some of the many areas of current therapeutic interest in small cell lung cancer.
  • Bunn PA, Minna JD, Augustyn A, Gazdar AF, Ouadah Y, Krasnow MA, Berns A, Brambilla E, Rekhtman N, Massion PP, Niederst M

  • J Thorac Oncol. 2016 Apr;11(4):453-74.

2016-05-04

Fig 1. Monocyte functions during bacterial, fungal, and parasitic infections. Ly6Chi bone marrow monocytes arise from progressively committed hematopoietic progenitors that include MDPs and cMoPs. Ly6Chi monocytes exit the bone marrow and enter the circulation in response to CCR2 ligands and traffic to peripheral tissues (A–D). Ly6Clo monocytes exhibit vascular and endothelial surveillance functions.(A) During systemic listeriosis, Ly6Chi monocytes differentiate into TNF+ and iNOS+ effector cells in the spleen, termed Tip-DCs, under the influence of NK cell-derived IFN-γ⋅ Tip-DCs mediate cell-intrinsic and cell-extrinsic listerial killing through the production of reactive nitrogen and oxygen species and inflammatory cytokines and direct T cell differentiation. Memory T cells in turn potentiate Tip-DC and neutrophil-mediated listerial killing during recall infections. (B) Fungal conidia are engulfed by Ly6Chi monocytes or their Mo-DC derivatives and are killed directly in the lung or transported to lung-draining LNs for CD4 T cell priming by LN-resident DCs. Mo-DCs direct CD4 T cell differentiation by regulating T-bet expression and have the capacity to enhance neutrophil-mediated conidial killing through undefined mechanism(s). (C) During intestinal helminth infections, Ly6Chi monocyte-derived macrophages (Mo-Mac) promote inducible Treg development through the production of retinoic acid (RA) and dampen Th2 via PD-L2-dependent mechanisms. (D) During acute toxoplamosis, tissue-infiltrating Ly6Chi monocytes dampen neutrophil-dependent ileitis and tissue damage upon exposure to commensal bacteria via induction of PGE2 and IL-10. Ly6Chi monocytes are the major cell type infected by T. gondii and mediate proinflammatory responses and parasite killing as well.

Fig 1. Monocyte functions during bacterial, fungal, and parasitic infections. Ly6Chi bone marrow monocytes arise from progressively committed hematopoietic progenitors that include MDPs and cMoPs. Ly6Chi monocytes exit the bone marrow and enter the circulation in response to CCR2 ligands and traffic to peripheral tissues (A–D). Ly6Clo monocytes exhibit vascular and endothelial surveillance functions.(A) During systemic listeriosis, Ly6Chi monocytes differentiate into TNF+ and iNOS+ effector cells in the spleen, termed Tip-DCs, under the influence of NK cell-derived IFN-γ⋅ Tip-DCs mediate cell-intrinsic and cell-extrinsic listerial killing through the production of reactive nitrogen and oxygen species and inflammatory cytokines and direct T cell differentiation. Memory T cells in turn potentiate Tip-DC and neutrophil-mediated listerial killing during recall infections. (B) Fungal conidia are engulfed by Ly6Chi monocytes or their Mo-DC derivatives and are killed directly in the lung or transported to lung-draining LNs for CD4 T cell priming by LN-resident DCs. Mo-DCs direct CD4 T cell differentiation by regulating T-bet expression and have the capacity to enhance neutrophil-mediated conidial killing through undefined mechanism(s). (C) During intestinal helminth infections, Ly6Chi monocyte-derived macrophages (Mo-Mac) promote inducible Treg development through the production of retinoic acid (RA) and dampen Th2 via PD-L2-dependent mechanisms. (D) During acute toxoplamosis, tissue-infiltrating Ly6Chi monocytes dampen neutrophil-dependent ileitis and tissue damage upon exposure to commensal bacteria via induction of PGE2 and IL-10. Ly6Chi monocytes are the major cell type infected by T. gondii and mediate proinflammatory responses and parasite killing as well.
  • Lauvau G, Loke P, Hohl TM

  • Semin Immunol. 2016 Mar 25. pii: S1044-5323(16)00021-X

2016-05-05

Fig 1. Mammary gland-specific expression of dox-inducible miR30 shRNAs.

Fig 1. Mammary gland-specific expression of dox-inducible miR30 shRNAs.
  • Ebbesen SH, Scaltriti M, Bialucha CU, Morse N, Kastenhuber ER, Wen HY, Dow LE, Baselga J, Lowe SW

  • Proc Natl Acad Sci. 2016 Mar 15;113(11):3030-5.

2016-05-06

Fig 2. Immunohistochemical analysis of tumor cell-surface expression of PD-L1 from representative samples (20x).

Fig 2. Immunohistochemical analysis of tumor cell-surface expression of PD-L1 from representative samples (20x).
  • Johnson DB, Lovly CM, Flavin M, Panageas KS, Ayers GD, Zhao Z, Iams WT, Colgan M, DeNoble S, Terry CR, Berry EG

  • Cancer Immunol Res. 2015 Mar;3(3):288-95.
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2016-05-09

Fig 1. Longitudinal profiling of cell-free DNA to detect driver mutations in NSCLC before, during, and after treatment.

Fig 1. Longitudinal profiling of cell-free DNA to detect driver mutations in NSCLC before, during, and after treatment.
  • Tsui DW, Berger MF

  • Clin Cancer Res. 2016 Feb 15;22(4):790-2.

2016-05-10

Fig 2. Structure of an RtcB-GTP-(Mn2+)2 complex.

Fig 2. Structure of an RtcB-GTP-(Mn2+)2 complex.
  • Maughan WP, Shuman S

  • J Bacteriol. 2016 Mar 31;198(8):1294-304.

2016-05-11

Fig 4. (a) Docked poses of the lead molecule (±)-1 and the C10 analogues 10–15 and 17. Key hydrogen bonding interactions are given by the yellow dashed lines and hydrophobic interactions by the turquoise dashed lines. (b) Compound 10 docked in binding pocket.

Fig 4. (a) Docked poses of the lead molecule (±)-1 and the C10 analogues 10–15 and 17. Key hydrogen bonding interactions are given by the yellow dashed lines and hydrophobic interactions by the turquoise dashed lines. (b) Compound 10 docked in binding pocket.
  • Gadhiya S, Madapa S, Kurtzman T, Alberts IL, Ramsey S, Pillarsetty NK, Kalidindi T, Harding WW

  • Bioorg Med Chem. 2016 May 1;24(9):2060-71.

2016-05-12

Fig 3. Immediate postablation treatment assessment with intraprocedural split-dose PET/CT in 65-y-old woman with metastatic colorectal cancer and rising level of carcinoembryonic antigen after partial liver resection.

Fig 3. Immediate postablation treatment assessment with intraprocedural split-dose PET/CT in 65-y-old woman with metastatic colorectal cancer and rising level of carcinoembryonic antigen after partial liver resection.
  • Solomon SB, Cornelis F

  • J Nucl Med. 2016 Apr;57(4):493-6.

2016-05-13

Fig 1. Treatment schema.

Fig 1. Treatment schema.
  • Yu AF, Manrique C, Pun S, Liu JE, Mara E, Fleisher M, Patil S, Jones LW, Steingart RM, Hudis CA, Dang CT

  • Oncologist. 2016 Apr;21(4):418-24.

2016-05-16

Fig 3. Bias-variance trade-off for fixed equilibration time versus automatic equilibration time selection.

Fig 3. Bias-variance trade-off for fixed equilibration time versus automatic equilibration time selection.
  • Chodera JD

  • J Chem Theory Comput. 2016 Apr 12;12(4):1799-805.

2016-05-17

Fig 1. Patterns of colorectal cancer screening by income among Medicare enrollees ages 65 to 80 years, 2000–2005.

Fig 1. Patterns of colorectal cancer screening by income among Medicare enrollees ages 65 to 80 years, 2000–2005.
  • Doubeni CA, Corley DA, Zauber AG

  • Gastroenterology. 2016 May;150(5):1052-5.
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2016-05-18

Single-cell RNA-seq to determine the cellular structure of the Flt3ITD/ITD;Dnmt3afl/flMxCre AML model.

Single-cell RNA-seq to determine the cellular structure of the Flt3ITD/ITD;Dnmt3afl/flMxCre AML model.
  • Meyer SE, Qin T, Muench DE, Masuda K, Venkatasubramanian M, Orr E, Suarez L, Gore SD, Delwel R, Paietta E, Tallman MS

  • Cancer Discov. 2016 May;6(5):501-15.

2016-05-19

Fig 4. Granulin is highly expressed in hepatic metastatic lesions and metastasis-associated macrophages are the main source of granulin secretion.

Fig 4. Granulin is highly expressed in hepatic metastatic lesions and metastasis-associated macrophages are the main source of granulin secretion.
  • Nielsen SR, Quaranta V, Linford A, Emeagi P, Rainer C, Santos A, Ireland L, Sakai T, Sakai K, Kim YS, Engle D

  • Nat Cell Biol. 2016 May;18(5):549-60.

2016-05-20

Fig 1. RNA-seq studies of hematopoiesis reveal stage-specific regulation of splicing during normal hematopoiesis.

Fig 1. RNA-seq studies of hematopoiesis reveal stage-specific regulation of splicing during normal hematopoiesis.
  • Inoue D, Bradley RK, Abdel-Wahab O

  • Genes Dev. 2016 May 1;30(9):989-1001.

2016-05-23

Fig 5. The benefit of quorum sensing under strong competition.

Fig 5. The benefit of quorum sensing under strong competition.
  • Schluter J, Schoech AP, Foster KR, Mitri S

  • PLoS Comput Biol. 2016 Apr 27;12(4):e1004848.
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2016-05-24

Fig 1. Performance characteristics of γPNAs.

Fig 1. Performance characteristics of γPNAs.
  • Nölling J, Rapireddy S, Amburg JI, Crawford EM, Prakash RA, Rabson AR, Tang YW, Singer A

  • MBio. 2016 Apr 19;7(2).
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2016-05-25

Fig 1. Unimolecular pentavalent vaccine.

Fig 1. Unimolecular pentavalent vaccine.
  • O’Cearbhaill RE, Ragupathi G, Zhu J, Wan Q, Mironov S, Yang G, Spassova MK, Iasonos A, Kravetz S, Ouerfelli O, Spriggs DR

  • Cancers (Basel). 2016 Apr 22;8(4). pii: E46.
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2016-05-26

Fig 1. The intestinal commensal microbiota provides colonization resistance against a wide range of pathogens by indirect and direct mechanisms.

Fig 1. The intestinal commensal microbiota provides colonization resistance against a wide range of pathogens by indirect and direct mechanisms.
  • Pamer EG

  • Science. 2016 Apr 29;352(6285):535-8.

2016-05-27

Fig 4. Butyrate induces acetylation of p53 at Lys-120 and binding of Lys-120-acetylated p53 with the Apaf-1 promoter.

Fig 4. Butyrate induces acetylation of p53 at Lys-120 and binding of Lys-120-acetylated p53 with the Apaf-1 promoter.
  • Yun T, Yu K, Yang S, Cui Y, Wang Z, Ren H, Chen S, Li L, Liu X, Fang M, Jiang X

  • J Biol Chem. 2016 Apr 1;291(14):7386-95.

2016-05-31

Fig 1. Nicastrin carrying entire lid deletion forms a stable, active γ-secretase complex.

Fig 1. Nicastrin carrying entire lid deletion forms a stable, active γ-secretase complex.
  • Zhang X, Sullivan E, Scimeca M, Wu X, Li YM, Sisodia SS

  • J Biol Chem. 2016 Mar 25;291(13):6748-53.

2016-06-01

Fig 10. Location of the gC1qR residues that disrupt trimer formation.

Fig 10. Location of the gC1qR residues that disrupt trimer formation.
  • Pednekar L, Valentino A, Ji Y, Tumma N, Valentino C, Kadoor A, Hosszu KK, Ramadass M, Kew RR, Kishore U, Peerschke EI

  • Mol Immunol. 2016 Apr 22;74:18-26.

2016-06-02

Fig 6. Progeny virions and VP1 do not accumulate in vacuoles.

Fig 6. Progeny virions and VP1 do not accumulate in vacuoles.
  • Luo Y, Motamedi N, Magaldi TG, Gee GV, Atwood WJ, DiMaio D

  • MBio. 2016 Mar 22;7(2). pii: e00297-16.
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2016-06-03

Fig 1. rcellminer simplifies the exploration of CellMiner data in R.

Fig 1. rcellminer simplifies the exploration of CellMiner data in R.
  • Luna A, Rajapakse VN, Sousa FG, Gao J, Schultz N, Varma S, Reinhold W, Sander C, Pommier Y

  • Bioinformatics. 2016 Apr 15;32(8):1272-4.

2016-06-06

Fig 1. Scheduling PI3K inhibition for ER+ breast cancer: limitations and possible solutions.

Fig 1. Scheduling PI3K inhibition for ER+ breast cancer: limitations and possible solutions.
  • Toska E, Baselga J

  • Clin Cancer Res. 2016 May 1;22(9):2099-101.

2016-06-07

Fig 2. Maximum change in target lesion by best investigator-assessed confirmed response in patients receiving dabrafenib as second-line or later treatment.

Fig 2. Maximum change in target lesion by best investigator-assessed confirmed response in patients receiving dabrafenib as second-line or later treatment.
  • Planchard D, Kim TM, Mazieres J, Quoix E, Riely G, Barlesi F, Souquet PJ, Smit EF, Groen HJ, Kelly RJ, Cho BC

  • Lancet Oncol. 2016 May 31;17(5):642-50.

2016-06-08

Fig 7. Histopathologic analyses of the primary tumor and the ipsilateral submandibular and axillary LN tissues.

Fig 7. Histopathologic analyses of the primary tumor and the ipsilateral submandibular and axillary LN tissues.
  • Sharma SK, Nemieboka B, Sala E, Lewis JS, Zeglis BM

  • J Nucl Med. 2016 May;57(5):771-6.

2016-06-09

Fig 2. GDC-0032 is a more potent inhibitor of downstream AKT and mTOR signaling in head and neck cancer cell lines containing PIK3CA-activating alterations than in cell lines containing PTEN alterations.

Fig 2. GDC-0032 is a more potent inhibitor of downstream AKT and mTOR signaling in head and neck cancer cell lines containing PIK3CA-activating alterations than in cell lines containing PTEN alterations.
  • Zumsteg Z, Morse N, Krigsfeld G, Gupta G, Higginson D, Lee NY, Morris L, Ganly I, Shiao SL, Powell SN, Chung CH

  • Clin Cancer Res. 2016 Apr 15;22(8):2009-19.

2016-06-10

Fig 1. Diagram exemplifies clear cell kidney cancer evolution initiated with the VHL mutation, which was followed by mTOR pathway activation that could take places at unique temporospatial sequence within individual tumors. The early acquisitions of mTOR pathway activation through either genetic or epigenetic means as illustrated scenarios (1) and (2) could render such tumors dependent on continuous mTOR pathway hyperactivation and thereby more susceptible to mTORC1 inhibitors. River branch image adapted from Wei and Hsieh (2).

Fig 1. Diagram exemplifies clear cell kidney cancer evolution initiated with the VHL mutation, which was followed by mTOR pathway activation that could take places at unique temporospatial sequence within individual tumors. The early acquisitions of mTOR pathway activation through either genetic or epigenetic means as illustrated scenarios (1) and (2) could render such tumors dependent on continuous mTOR pathway hyperactivation and thereby more susceptible to mTORC1 inhibitors. River branch image adapted from Wei and Hsieh (2).
  • Voss MH, Hsieh JJ

  • Clin Cancer Res. 2016 May 15;22(10):2320-2.

2016-06-13

Fig 1. BOCTOPUS2 pipeline – HHblits is used to obtain a position specific scoring matrix (PSSM), 4 SVMs are used to predict the location of each residue. A per-residue profile is constructed by combining the output probabilities of SVMs. Then a filter is applied to detect the likely transmembrane β-barrel region. The resulting per-residue profile is used as an input to a Hidden Markov Model to predict the topology.

Fig 1. BOCTOPUS2 pipeline – HHblits is used to obtain a position specific scoring matrix (PSSM), 4 SVMs are used to predict the location of each residue. A per-residue profile is constructed by combining the output probabilities of SVMs. Then a filter is applied to detect the likely transmembrane β-barrel region. The resulting per-residue profile is used as an input to a Hidden Markov Model to predict the topology.
  • Hayat S, Peters C, Shu N, Tsirigos KD, Elofsson A

  • Bioinformatics. 2016 May 15;32(10):1571-3.

2016-06-15

Fig 1. Single-agent activity of PD-1/PD-L1 axis blockade in R/R disease across different tumor types. Although the data are preliminary and head-to-head comparison is difficult because of differences in enrollment criteria (e.g., the expression level of PD-L1 in the tumor and methods used to stain PD-L1), response to PD-1/PD-L1 axis inhibition appears especially high in patients with HL compared with those who have other tumor types, including NHLs.

Fig 1. Single-agent activity of PD-1/PD-L1 axis blockade in R/R disease across different tumor types. Although the data are preliminary and head-to-head comparison is difficult because of differences in enrollment criteria (e.g., the expression level of PD-L1 in the tumor and methods used to stain PD-L1), response to PD-1/PD-L1 axis inhibition appears especially high in patients with HL compared with those who have other tumor types, including NHLs.
  • Matsuki E, Younes A

  • Curr Treat Options Oncol. 2016 Jun;17(6):31.

2016-06-16

Fig 1. Considerations for designing neoadjuvant trials for drug development and approval.

Fig 1. Considerations for designing neoadjuvant trials for drug development and approval.
  • Funt SA, Chapman PB

  • Clin Cancer Res. 2016 May 15;22(10):2323-8.

2016-06-17

Fig 1. Histone modifications regulated by the JAK–STAT pathway.

Fig 1. Histone modifications regulated by the JAK–STAT pathway.
  • Liu F, Wang L, Perna F, Nimer SD

  • Nat Rev Cancer. 2016 May 25;16(6):359-72.

2016-06-20

Fig 6. Undecalcified whole-mount cryosection and autoradiography of osteoblastic (LNCaP) and osteolytic (PC3) intratibial prostate cancer xenograft models (n = 3–4 mice per group).

Fig 6. Undecalcified whole-mount cryosection and autoradiography of osteoblastic (LNCaP) and osteolytic (PC3) intratibial prostate cancer xenograft models (n = 3–4 mice per group).
  • Abou DS, Ulmert D, Doucet M, Hobbs RF, Riddle RC, Thorek DL

  • Journal of the National Cancer Institute. 2016 May 1;108(5):djv380.

2016-06-21

Fig 1. Schema interaction between tumor and immune cells.

Fig 1. Schema interaction between tumor and immune cells.
  • Ma W, Gilligan BM, Yuan J, Li T

  • J Hematol Oncol. 2016 May 27;9(1):47.
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2016-06-23

Fig 2. ATFS-1 promotes ∆mtDNA maintenance and mitochondrial biogenesis largely independent of Parkin.

Fig 2. ATFS-1 promotes ∆mtDNA maintenance and mitochondrial biogenesis largely independent of Parkin.
  • Lin YF, Schulz AM, Pellegrino MW, Lu Y, Shaham S, Haynes CM

  • Nature. 2016 May 2;533(7603):416-9.

2016-06-24

Fig 1. Use of A Methodology Based on ACMG Variant-Classification Guidelines to Identify Variants in 180 Clinically Relevant Genes in Individuals with Breast Cancer.

Fig 1. Use of A Methodology Based on ACMG Variant-Classification Guidelines to Identify Variants in 180 Clinically Relevant Genes in Individuals with Breast Cancer.
  • Maxwell KN, Hart SN, Vijai J, Schrader KA, Slavin TP, Thomas T, Wubbenhorst B, Ravichandran V, Moore RM, Hu C, Guidugli L, Wenz B, Domchek SM, Robson ME, Szabo C, Neuhausen SL, Weitzel JN, Offit K, Couch FJ, Nathanson KL

  • Am J Hum Genet. 2016 May 5;98(5):801-17.

2016-06-27

Fig 5. Study PIM4973 (ROVER) tumor response.

Fig 5. Study PIM4973 (ROVER) tumor response.
  • Powles T, Lackner MR, Oudard S, Escudier B, Ralph C, Brown JE, Hawkins RE2, Castellano D, Rini BI, Staehler MD, Ravaud A, Lin W, O'Keeffe B, Wang Y, Lu S, Spoerke JM, Huw LY, Byrtek M, Zhu R, Ware JA, Motzer RJ

  • J Clin Oncol. 2016 May 10;34(14):1660-8.

2016-06-28

Fig 6. Characteristics of gametically programmed DMRs.

Fig 6. Characteristics of gametically programmed DMRs.
  • Mitchell E, Klein SL, Argyropoulos KV, Sharma A, Chan RB, Toth JG, Barboza L, Bavley C, Bortolozzi A, Chen Q, Liu B

  • Nat Commun. 2016 May 13;7:11492.
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2016-06-29

Fig 1. Diagram exemplifies clear cell kidney cancer evolution initiated with the VHL mutation, which was followed by mTOR pathway activation that could take places at unique temporospatial sequence within individual tumors.

Fig 1. Diagram exemplifies clear cell kidney cancer evolution initiated with the VHL mutation, which was followed by mTOR pathway activation that could take places at unique temporospatial sequence within individual tumors.
  • Voss MH, Hsieh JJ

  • Clin Cancer Res. 2016 May 15;22(10):2320-2.

2016-06-30

Fig 1. Physiological Deficits at Sensory Afferent Terminals in vGluT1−/− Mice.

Fig 1. Physiological Deficits at Sensory Afferent Terminals in vGluT1−/− Mice.
  • Mende M, Fletcher EV, Belluardo JL, Pierce JP, Bommareddy PK, Weinrich JA, Kabir ZD, Schierberl KC, Pagiazitis JG, Mendelsohn AI, Francesconi A, Edwards RH, Milner TA, Rajadhyaksha AM, van Roessel PJ, Mentis GZ, Kaltschmidt JA

  • Neuron. 2016 Jun 15;90(6):1189-202.

2016-07-01

Fig 1. Granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor β chain (GM-CSFRβ) signaling is critical for survival, fungal clearance, and lung integrity during Aspergillus fumigatus challenge.

Fig 1. Granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor β chain (GM-CSFRβ) signaling is critical for survival, fungal clearance, and lung integrity during Aspergillus fumigatus challenge.
  • Kasahara S, Jhingran A, Dhingra S, Salem A, Cramer RA, Hohl TM

  • J Infect Dis. 2016 Apr 15;213(8):1289-98.
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