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2015-01-02

Fig 1. Preclinical evidence demonstrates that CDDP-induced antitumor immunomodulation occurs via four mechanisms. TIL, tumor-infiltrating lymphocytes.

Fig 1. Preclinical evidence demonstrates that CDDP-induced antitumor immunomodulation occurs via four mechanisms. TIL, tumor-infiltrating lymphocytes.
  • de Biasi AR, Villena-Vargas J, Adusumilli PS

  • Clin Cancer Res. 2014 Nov 1;20(21):5384-5391.

2015-01-05

Fig 1. Neuropsychological pyramid (adapted from the original pyramid by Yehuda Ben-Yishay, PhD, at NYU School of Medicine). Functions are inter-related such that neurobehavioral problems are theorized to underlie and therefore exacerbate neurocognitive problems.

Fig 1. Neuropsychological pyramid (adapted from the original pyramid by Yehuda Ben-Yishay, PhD, at NYU School of Medicine). Functions are inter-related such that neurobehavioral problems are theorized to underlie and therefore exacerbate neurocognitive problems.
  • Wu LM, Austin J, Valdimarsdottir H, Isola L, Rowley SD, Diefenbach MA, Cammarata M, Redd WH, Rini C

  • Psychooncology. 2014 Dec;23(12):1406-14.

2015-01-06

Graphical Abstract.

Graphical Abstract.
  • Harris KK, Fay A, Yan HG, Kunwar P, Socci ND, Pottabathini N, Juventhala RR, Djaballah H, Glickman MS

  • ACS Chem Biol. 2014 Nov 21;9(11):2572-83.

2015-01-07

Fig 1. a) Composition of a SERS-active gold nanoparticle featuring an all-inclusive near-IR-active surface coating SERS substrate. b) Transmission electron microscopy (TEM) image of Au@IR-pHPMA.

Fig 1. a) Composition of a SERS-active gold nanoparticle featuring an all-inclusive near-IR-active surface coating SERS substrate. b) Transmission electron microscopy (TEM) image of Au@IR-pHPMA.
  • Iacono P, Karabeber H, Kircher MF

  • Angew Chem Int Ed Engl. 2014 Oct 27;53(44):11756-61.

2015-01-08

Fig 1. EGFR signaling pathways and receptor cross-talk. Activation of EGFR propagates downstream progrowth signals through the MAPK pathway (RAS–RAF–MEK–ERK) and PI3K–AKT–mTOR pathway. Targets for potential combinatorial therapeutic strategies to overcome resistance are noted.

Fig 1. EGFR signaling pathways and receptor cross-talk. Activation of EGFR propagates downstream progrowth signals through the MAPK pathway (RAS–RAF–MEK–ERK) and PI3K–AKT–mTOR pathway. Targets for potential combinatorial therapeutic strategies to overcome resistance are noted.
  • Yu HA, Riely GJ, Lovly CM

  • Clin Cancer Res. 2014 Dec 1;20(23):5898-5907.

2015-01-09

Fig 1. NRAS/Nras expression is required for maintenance of AML harboring oncogenic mutations.

Fig 1. NRAS/Nras expression is required for maintenance of AML harboring oncogenic mutations.
  • Burgess MR, Hwang E, Firestone AJ, Huang T, Xu J, Zuber J, Bohin N, Wen T, Kogan SC, Haigis KM, Sampath D, Lowe S, Shannon K, Li Q

  • Blood. 2014 Dec 18;124(26):3947-55.

2015-01-12

Fig 1. The impact of H3.3 K27M mutation on neural precursors.

Fig 1. The impact of H3.3 K27M mutation on neural precursors.
  • Funato K, Major T, Lewis PW, Allis CD, Tabar V

  • Science. 2014 Dec 19;346(6216):1529-33.

2015-01-13

Fig 1. Outline of methods.

Fig 1. Outline of methods.
  • Frees AE, Rajaram N, McCachren SS 3rd, Fontanella AN, Dewhirst MW, Ramanujam N

  • PLoS One. 2014 Dec 19;9(12):e115529.
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2015-01-14

Fig 1. An 82-year-old woman with metastatic colorectal cancer.

Fig 1. An 82-year-old woman with metastatic colorectal cancer.
  • Petre EN, Sofocleous CT, Solomon SB

  • Hematol Oncol Clin North Am. 2015 Feb;29(1):117-133.

2015-01-15

Fig 1a. The level of expression of the patient’s mismatched HLA-C allotype associates with transplant outcome.

Fig 1a. The level of expression of the patient’s mismatched HLA-C allotype associates with transplant outcome.
  • Petersdorf EW, Gooley TA, Malkki M, Bacigalupo AP, Cesbron A, Du Toit E, Ehninger G, Egeland T, Fischer GF, Gervais T, Haagenson MD, Horowitz MM, Hsu K, Jindra P, Madrigal A, Oudshoorn M, Ringdén O, Schroeder ML, Spellman SR, Tiercy JM, Velardi A, Witt CS, O'Huigin C, Apps R, Carrington M; International Histocompatibility Working Group in Hematopoietic Cell Transplantation

  • Blood. 2014 Dec 18;124(26):3996-4003.

2015-01-16

Graphical abstract: Here, we show that hypoxia upregulates γ-secretase activity through a direct interaction with Hif-1α, revealing an unconventional function for Hif-1α as an enzyme subunit, which is distinct from its canonical role as a transcription factor. Moreover, hypoxia-induced cell invasion and metastasis are alleviated by either γ-secretase inhibitors or a dominant-negative Notch coactivator, indicating that γ-secretase/Notch signaling plays an essential role in controlling these cellular processes.

Graphical abstract: Here, we show that hypoxia upregulates γ-secretase activity through a direct interaction with Hif-1α, revealing an unconventional function for Hif-1α as an enzyme subunit, which is distinct from its canonical role as a transcription factor. Moreover, hypoxia-induced cell invasion and metastasis are alleviated by either γ-secretase inhibitors or a dominant-negative Notch coactivator, indicating that γ-secretase/Notch signaling plays an essential role in controlling these cellular processes.
  • Villa JC, Chiu D, Brandes AH, Escorcia FE, Villa CH, Maguire WF, Hu CJ, de Stanchina E, Simon MC, Sisodia SS, Scheinberg DA, Li YM

  • Cell Rep. 2014 Aug 21;8(4):1077-92
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2015-01-19

Fig 1. Resection of colorectal liver metastases (CRLM) is safe and curative. Displayed is the 10-year follow-up on patients who underwent resection of CRLM from 1985 to 1994 at Memorial Sloan Kettering. There were 102 actual 10-year survivors, and 97% of the 102 were disease free at the last follow-up.

Fig 1. Resection of colorectal liver metastases (CRLM) is safe and curative. Displayed is the 10-year follow-up on patients who underwent resection of CRLM from 1985 to 1994 at Memorial Sloan Kettering. There were 102 actual 10-year survivors, and 97% of the 102 were disease free at the last follow-up.
  • Smith JJ, D'Angelica MI

  • Hematol Oncol Clin North Am. 2015 Feb;29(1):61-84.

2015-01-20

Graphical Abstract.

Graphical Abstract.
  • Rampal R, Alkalin A, Madzo J, Vasanthakumar A, Pronier E, Patel J, Li Y, Ahn J, Abdel-Wahab O, Shih A, Lu C, Ward PS, Tsai JJ, Hricik T, Tosello V, Tallman JE, Zhao X, Daniels D, Dai Q, Ciminio L, Aifantis I, He C, Fuks F, Tallman MS, Ferrando A, Nimer S, Paietta E, Thompson CB, Licht JD, Mason CE, Godley LA, Melnick A, Figueroa ME, Levine RL

  • Cell Rep. 2014 Dec 11;9(5):1841-55.
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2015-01-21

Abstract.

Abstract.
  • Davis TD, Gerry CJ, Tan DS

  • ACS Chem Biol. 2014 Nov 21;9(11):2535-44.

2015-01-22

Fig 1. Transcriptional changes in the cancer-bearing stroma at the primary and secondary cancer sites identify a myeloid cell infiltration signature that is also found in human samples of breast cancer. Venn diagrams summarizing transcriptional changes in each model of cancer-bearing tissues of tumor-bearing mice versus naïve non-tumor-bearing mice (n = 3 mice per group; PT primary tumor, LN met lymph node metastasis). Cut-offs used for gene list generation: p value with FDR <0.05, fold >2. A core group of 34 probes differentially expressed probes in host cells (murine) at all sites in all models. Highlighted genes are expressed in cells of myeloid lineages (blue) and pseudogenes (gray)

Fig 1. Transcriptional changes in the cancer-bearing stroma at the primary and secondary cancer sites identify a myeloid cell infiltration signature that is also found in human samples of breast cancer. Venn diagrams summarizing transcriptional changes in each model of cancer-bearing tissues of tumor-bearing mice versus naïve non-tumor-bearing mice (n = 3 mice per group; PT primary tumor, LN met lymph node metastasis). Cut-offs used for gene list generation: p value with FDR <0.05, fold >2. A core group of 34 probes differentially expressed probes in host cells (murine) at all sites in all models. Highlighted genes are expressed in cells of myeloid lineages (blue) and pseudogenes (gray)
  • Drews-Elger K, Iorns E, Dias A, Miller P, Ward TM, Dean S, Clarke J, Campion-Flora A, Rodrigues DN, Reis-Filho JS, Rae JM, Thomas D, Berry D, El-Ashry D, Lippman ME

  • Breast Cancer Res Treat. 2014 Nov;148(1):41-59.

2015-01-23

Fig 1. Mechanisms of action of anti-angiogenesis therapy. Angiogenesis occurs when the balance of pro-angiogenic factors outweighs the anti-angiogenic factors. Vascular endothelial growth factors (VEGF), platelet derived growth factor (PDGF), tumor necrosis factor-alpha (TNFα), plasminogen activators, matrix metalloproteases (MMPs), transforming growth factor alpha (TGFα), angiogenin, integrin ανβ3, and angiopoietin 1 and 2 (Ang1, Ang2) are all pro-angiogenic cytokines and proteins, many of which are now specific drug targets. Targeting the cancer stem cell is another mechanism that may halt tumor growth. The anti-angiogenic cytokines, including tissue inhibitors of metalloproteases (TIMPs), thrombospondin, interleukin-4 (IL-4), IL-12, IL-18, interferon (IFN), angiostatin, endostatin, troponin-1, and platelet factor-4, act as intrinsic brakes on angiogenesis.

Fig 1. Mechanisms of action of anti-angiogenesis therapy. Angiogenesis occurs when the balance of pro-angiogenic factors outweighs the anti-angiogenic factors. Vascular endothelial growth factors (VEGF), platelet derived growth factor (PDGF), tumor necrosis factor-alpha (TNFα), plasminogen activators, matrix metalloproteases (MMPs), transforming growth factor alpha (TGFα), angiogenin, integrin ανβ3, and angiopoietin 1 and 2 (Ang1, Ang2) are all pro-angiogenic cytokines and proteins, many of which are now specific drug targets. Targeting the cancer stem cell is another mechanism that may halt tumor growth. The anti-angiogenic cytokines, including tissue inhibitors of metalloproteases (TIMPs), thrombospondin, interleukin-4 (IL-4), IL-12, IL-18, interferon (IFN), angiostatin, endostatin, troponin-1, and platelet factor-4, act as intrinsic brakes on angiogenesis.
  • Thomas AA, Omuro A

  • Curr Treat Options Oncol. 2014 Dec;15(4):551-66.

2015-01-26

Fig 2. Centre image: black line TVP, blue GTV-PET, red points volume of TVP/GTV-PET overlap, yellow points volume of increased choline uptake on PET located outside the tumour changes on the pathology slice (GTV-PET − TVP), green volume of tumour changes on the pathology slices located outside of the changes on PET (or false-negative PET regions, TVP − GTV-PET). The other four images show the TVP (pink) and GTV-PET (blue) for a microcarcinoma (top left and top right), a macrocarcinoma (bottom left) and a peripheral carcinoma (bottom right)

Fig 2. Centre image: black line TVP, blue GTV-PET, red points volume of TVP/GTV-PET overlap, yellow points volume of increased choline uptake on PET located outside the tumour changes on the pathology slice (GTV-PET − TVP), green volume of tumour changes on the pathology slices located outside of the changes on PET (or false-negative PET regions, TVP − GTV-PET). The other four images show the TVP (pink) and GTV-PET (blue) for a microcarcinoma (top left and top right), a macrocarcinoma (bottom left) and a peripheral carcinoma (bottom right)
  • Grosu AL, Weirich G, Wendl C, Prokic V, Kirste S, Geinitz H, Souvatzoglou M, Gschwend JE, Schwaiger M, Molls M, Weber WA, Treiber U, Krause BJ.

  • Eur J Nucl Med Mol Imaging. 2014 Dec;41(12):2242-8.

2015-01-27

Fig 3. IR-induced chromosome segregation errors lead to widespread chromosomal damage.

Fig 3. IR-induced chromosome segregation errors lead to widespread chromosomal damage.
  • Bakhoum SF, Kabeche L, Wood MD, Laucius CD, Qu D, Laughney AM, Reynolds GE, Louie RJ, Phillips J, Chan DA, Zaki BI, Murnane JP, Petritsch C, Compton DA

  • Nat Commun. 2015 Jan 21;6:5990.

2015-01-28

Fig 2. Evaluation of LRAT proximal promoter methylation in CRC tissue specimens.

Fig 2. Evaluation of LRAT proximal promoter methylation in CRC tissue specimens.
  • Cheng YW, Pincas H, Huang J, Zachariah E, Zeng Z, Notterman DA, Paty P, Barany F

  • Med Oncol. 2014 Nov;31(11):254.

2015-01-29

Fig 1. Summary of peptide identifications from OvCa tumor and PDX breast tumor samples. Bar graphs show the numbers of identified peptides from each PDX breast tumor (A) and OvCa tumor (C). The intensities of identified peptides (log10 values) from PDX (B) and OvCa (D) tumor samples are plotted against their monoisotopic masses (Da), showing a similar peptide intensity range but different mass ranges. The distributions of the precursor proteins in terms of number of unique peptidome peptide identifications are shown in pie graphs for the PDX samples (E) and OvCa samples (F).

Fig 1. Summary of peptide identifications from OvCa tumor and PDX breast tumor samples. Bar graphs show the numbers of identified peptides from each PDX breast tumor (A) and OvCa tumor (C). The intensities of identified peptides (log10 values) from PDX (B) and OvCa (D) tumor samples are plotted against their monoisotopic masses (Da), showing a similar peptide intensity range but different mass ranges. The distributions of the precursor proteins in terms of number of unique peptidome peptide identifications are shown in pie graphs for the PDX samples (E) and OvCa samples (F).
  • Xu Z, Wu C, Xie F, Slysz GW, Tolic N, Monroe ME, Petyuk VA, Payne SH, Fujimoto GM, Moore RJ, Fillmore TL, Schepmoes AA, Levine DA, Townsend RR, Davies SR, Li S, Ellis M, Boja E, Rivers R, Rodriguez H, Rodland KD, Liu T, Smith RD

  • J Proteome Res.2015;14(1):422–433

2015-01-30

Fig 1.  Expression of Ror2 promotes in vivo tumor growth and invasion. A&C) Tabulated rates of successful injection and growth of all 786-0 xenograft tumors are shown. B) Average tumor size (cm) with error bars showing stdev for resulting xenograft tumors following paired orthotropic injections of 786-0 cells containing either the control empty vector, pcDNA6 or hRor2 exhibited a trend to increased in vivo tumor growth with Ror2 overexpression. D) Average tumor size (mm) with error bars showing stdev for resulting xenograft tumors following subcutaneous injection of 786-0 cells containing either the control empty vector, GFP, wild-type Ror2, or Ror2-DM showed a significant increase in in vivo tumor growth with wild-type Ror2 overexpression. P-values were calculated using an Anova one-way analysis (*<.05 **<.01). E) Representative image of an orthotopic xenograft consisting of 786-0 vector control cells. F) Increased invasion of local tissues was evident with Ror2 expression, with arrows highlighting areas of continued invasion into the spleen.

Fig 1. Expression of Ror2 promotes in vivo tumor growth and invasion. A&C) Tabulated rates of successful injection and growth of all 786-0 xenograft tumors are shown. B) Average tumor size (cm) with error bars showing stdev for resulting xenograft tumors following paired orthotropic injections of 786-0 cells containing either the control empty vector, pcDNA6 or hRor2 exhibited a trend to increased in vivo tumor growth with Ror2 overexpression. D) Average tumor size (mm) with error bars showing stdev for resulting xenograft tumors following subcutaneous injection of 786-0 cells containing either the control empty vector, GFP, wild-type Ror2, or Ror2-DM showed a significant increase in in vivo tumor growth with wild-type Ror2 overexpression. P-values were calculated using an Anova one-way analysis (*<.05 **<.01). E) Representative image of an orthotopic xenograft consisting of 786-0 vector control cells. F) Increased invasion of local tissues was evident with Ror2 expression, with arrows highlighting areas of continued invasion into the spleen.
  • Rasmussen NR, Debebe Z, Wright TM, Brooks SA, Sendor AB, Brannon AR, Hakimi AA, Hsieh JJ, Choueiri TK, Tamboli P, Maranchie JK, Hinds P, Wallen EM, Simpson C, Norris JL, Janzen WP, Rathmell WK

  • PLoS One. 2014 Dec 26;9(12):e116101.
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2015-02-02

Fig 2. A schematic representation of various databases that might be used to move towards providing hypothesis for selection of pharmacological agents. CCLE Cancer Cell Line Encyclopedia, GDSC genomics of drug sensitivity in cancer, NCI-60 the sixty cell lines of the US National Cancer Institute, TCGA The Cancer Genome Atlas

Fig 2. A schematic representation of various databases that might be used to move towards providing hypothesis for selection of pharmacological agents. CCLE Cancer Cell Line Encyclopedia, GDSC genomics of drug sensitivity in cancer, NCI-60 the sixty cell lines of the US National Cancer Institute, TCGA The Cancer Genome Atlas
  • Reinhold WC, Varma S, Rajapakse VN, Luna A, Sousa FG, Kohn KW, Pommier YG

  • Hum Genet. 2015 Jan;134(1):3-11.

2015-02-03

Fig 1. Cumulative incidence of first infection over time in myeloma patients and their matched controls.

Fig 1. Cumulative incidence of first infection over time in myeloma patients and their matched controls.
  • Blimark C, Holmberg E, Mellqvist UH, Landgren O, Björkholm M, Hultcrantz M, Kjellander C, Turesson I, Kristinsson SY

  • Haematologica. 2015 Jan;100(1):107-13.
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2015-02-04

Fig 1. Screening platform for the isolation of genes that mediate metastatic reactivation. (A) Schematic representation of the metastatic capabilities of the mouse mammary carcinoma cells constituting the progression series used here. (B) 4TO7-TGL cells transduced with empty vector or Coco were inoculated i.v. into syngeneic mice. Mice were killed after 21 d. Lung sections were subjected to immunofluorescent staining of GFP (tumor cells) and PECAM-1 (endothelial cells), followed by confocal analysis and 3D reconstruction. (C) Design of the tail-vein cDNA screen. After transduction with the 4T1 libraries, the 4TO7 cells are injected i.v. in syngeneic mice. Candidate mediators of metastasis are recovered from lung metastases.

Fig 1. Screening platform for the isolation of genes that mediate metastatic reactivation. (A) Schematic representation of the metastatic capabilities of the mouse mammary carcinoma cells constituting the progression series used here. (B) 4TO7-TGL cells transduced with empty vector or Coco were inoculated i.v. into syngeneic mice. Mice were killed after 21 d. Lung sections were subjected to immunofluorescent staining of GFP (tumor cells) and PECAM-1 (endothelial cells), followed by confocal analysis and 3D reconstruction. (C) Design of the tail-vein cDNA screen. After transduction with the 4T1 libraries, the 4TO7 cells are injected i.v. in syngeneic mice. Candidate mediators of metastasis are recovered from lung metastases.
  • Gao H, Chakraborty G, Lee-Lim AP, Mavrakis KJ, Wendel HG, Giancotti FG

  • Proc Natl Acad Sci U S A. 2014 Nov 18;111(46):16532-7.
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2015-02-05

Fig 1. Comparison of immunostaining for H3K27me3 and H3.3 K27M in wild-type and H3F3A K27M mutant pediatric GBM. a, b Representative images from a H3F3A K27M wild-type tumor, H3K27me3 (40×, a) and H3.3 K27M (40×, b). c–f. Representative images from two different H3F3A K27M mutant tumors, H3K27me3 (40×, c and 60×, e) and H3.3 K27M (40×, d and 60×, f). Arrowheads indicate endothelial cells in blood vessels

Fig 1. Comparison of immunostaining for H3K27me3 and H3.3 K27M in wild-type and H3F3A K27M mutant pediatric GBM. a, b Representative images from a H3F3A K27M wild-type tumor, H3K27me3 (40×, a) and H3.3 K27M (40×, b). c–f. Representative images from two different H3F3A K27M mutant tumors, H3K27me3 (40×, c and 60×, e) and H3.3 K27M (40×, d and 60×, f). Arrowheads indicate endothelial cells in blood vessels
  • Venneti S, Santi M, Felicella MM, Yarilin D, Phillips JJ, Sullivan LM, Martinez D, Perry A, Lewis PW, Thompson CB, Judkins AR

  • Acta Neuropathol. 2014 Nov;128(5):743-53.
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2015-02-06

Fig 1. Effects of Adipose Tissue on Insulin Signaling and Lipid Metabolism.

Fig 1. Effects of Adipose Tissue on Insulin Signaling and Lipid Metabolism.
  • Iyengar NM1, Hudis CA, Dannenberg AJ

  • Annu Rev Med. 2015 Jan 14;66:297-309.

2015-02-09

Fig 1. Cytoskeletal remodeling and the immunological synapse. Schematic diagram showing IS initiation (top) and maturation (bottom) both from the side (right) and from the perspective of the APC (left).

Fig 1. Cytoskeletal remodeling and the immunological synapse. Schematic diagram showing IS initiation (top) and maturation (bottom) both from the side (right) and from the perspective of the APC (left).
  • Le Floc'h A, Huse M

  • Cell Mol Life Sci. 2015 Feb;72(3):537-56.

2015-02-10

Fig 1. Dermoscopic and Histopathologic Features of Lymphatic Invasion in Case 1.

Fig 1. Dermoscopic and Histopathologic Features of Lymphatic Invasion in Case 1.
  • Fonseca M, Marchetti MA, Kiuru MH, Marghoob AA, Halpern AC

  • JAMA Dermatol. 2015 Jan 1;151(1):103-5.

2015-02-11

Fig 1. Binary and ternary complexes. (A) miRNA leads hAgo2 to target mRNA to repress its translation. (B) hAgo2–guide RNA binary and (C) hAgo2–guide RNA–target RNA ternary complexes: hAgo2 domains N, PAZ, MID, PIWI, and linkers Graphic abstract: L1 and L2 are shown; guide RNA (blue) in the binary complex and guide RNA (purple) and target RNA (green) in the ternary complex are shown.

Fig 1. Binary and ternary complexes. (A) miRNA leads hAgo2 to target mRNA to repress its translation. (B) hAgo2–guide RNA binary and (C) hAgo2–guide RNA–target RNA ternary complexes: hAgo2 domains N, PAZ, MID, PIWI, and linkers Graphic abstract: L1 and L2 are shown; guide RNA (blue) in the binary complex and guide RNA (purple) and target RNA (green) in the ternary complex are shown.
  • Patel DJ

  • Science. 2014 Oct 31;346(6209):542-3

2015-02-12

Fig 1. RNA extracted from freshly isolated monocytes and T cells from peripheral blood of patients treated with either anti–PD-1 (n = 6), anti–CTLA-4 (n = 5), Combo therapy with anti–PD-1 and anti–CTLA-4 concurrently (Combo, n = 6), and Seq anti–PD-1 in patients with prior anti–CTLA-4 (Seq, n = 3) was analyzed using the Affymetrix GeneChip Human Transcriptome 2.0 exon array.

Fig 1. RNA extracted from freshly isolated monocytes and T cells from peripheral blood of patients treated with either anti–PD-1 (n = 6), anti–CTLA-4 (n = 5), Combo therapy with anti–PD-1 and anti–CTLA-4 concurrently (Combo, n = 6), and Seq anti–PD-1 in patients with prior anti–CTLA-4 (Seq, n = 3) was analyzed using the Affymetrix GeneChip Human Transcriptome 2.0 exon array.
  • Das R, Verma R, Sznol M, Boddupalli CS, Gettinger SN, Kluger H, Callahan M, Wolchok JD, Halaban R, Dhodapkar MV, Dhodapkar KM

  • J Immunol. 2015 Feb 1;194(3):950-9.

2015-02-13

Fig 1. PC-[18F]FLT-1, a PET radiotracer designed to exhibit a H2O2-dependent cellular accumulation of [18F]FLT.

Fig 1. PC-[18F]FLT-1, a PET radiotracer designed to exhibit a H2O2-dependent cellular accumulation of [18F]FLT.
  • Carroll V, Michel BW, Blecha J, VanBrocklin H, Keshari K, Wilson D, Chang CJ

  • J Am Chem Soc. 2014 Oct 22;136(42):14742-5

2015-02-16

Fig 3. Expression levels of selected ten splice variants in brain regions of four mouse strains. Expression levels of (−1)/(Log2 (E−ΔC(t))) of selected variants is plotted across regions using MS excel. Pfc: prefrontal cortex; Str: striatum; Tha: thalamus; Hyp: hypothalamus; Hip: hippocampus; PAG: periaqueductal gray; BS: brainstem; Cb: cerebellum; Spc: spinal cord; WB: whole brain. 129:129P3/J; B6: C56BL/6J; SJL: SJL/J; SWR: SWR/J.

Fig 3. Expression levels of selected ten splice variants in brain regions of four mouse strains. Expression levels of (−1)/(Log2 (E−ΔC(t))) of selected variants is plotted across regions using MS excel. Pfc: prefrontal cortex; Str: striatum; Tha: thalamus; Hyp: hypothalamus; Hip: hippocampus; PAG: periaqueductal gray; BS: brainstem; Cb: cerebellum; Spc: spinal cord; WB: whole brain. 129:129P3/J; B6: C56BL/6J; SJL: SJL/J; SWR: SWR/J.
  • Xu J, Lu Z, Xu M, Rossi GC, Kest B, Waxman AR, Pasternak GW, Pan YX

  • PLoS One. 2014 Oct 24;9(10):e111267
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2015-02-17

Fig 1a. SNA (upper panels) and PNA (lower panels) staining on B cells 11 days after mice received one of the indicated single intravenous doses of 3F-NeuAc.

Fig 1a. SNA (upper panels) and PNA (lower panels) staining on B cells 11 days after mice received one of the indicated single intravenous doses of 3F-NeuAc.
  • Macauley MS, Arlian BM, Rillahan CD, Pang PC, Bortell N, Marcondes MC, Haslam SM, Dell A, Paulson JC

  • J Biol Chem. 2014 Dec 19;289(51):35149-58.

2015-02-18

Abstract  The acyclic ligands H4C3octapa and p-SCN-Bn-H4C3octapa were synthesized for the first time, using nosyl protection chemistry.

Abstract The acyclic ligands H4C3octapa and p-SCN-Bn-H4C3octapa were synthesized for the first time, using nosyl protection chemistry.
  • Price EW, Zeglis BM, Cawthray JF, Lewis JS, Adam MJ, Orvig C

  • Inorg Chem. 2014 Oct 6;53(19):10412-31

2015-02-19

Figure 1. Sperm retrieval rates (SRRs) stratified by testicular volume and serum FSH levels.

Figure 1. Sperm retrieval rates (SRRs) stratified by testicular volume and serum FSH levels.
  • Berookhim BM, Palermo GD, Zaninovic N, Rosenwaks Z, Schlegel PN

  • Fertil Steril. 2014 Nov;102(5):1282-6.

2015-02-20

Fig 2. Six-Year Interval Kaplan–Meier Curves for Multiple Myeloma (MM) Patient Overall Survival From Time of Diagnosis (1971-2006)

Abbreviations: ASCT = Autologous Stem Cell Transplant; MEL(200) = melphalan (200 mg/m2).

Fig 2. Six-Year Interval Kaplan–Meier Curves for Multiple Myeloma (MM) Patient Overall Survival From Time of Diagnosis (1971-2006) Abbreviations: ASCT = Autologous Stem Cell Transplant; MEL(200) = melphalan (200 mg/m2).
  • Raje N, Faiman B, Harvey RD, Kurtin SE, Lonial S, Kumar SK, Cohen AD, Conde MA, Giralt SA, Recine MS, Tombler ER, Stadtmauer E, Jagannath S, Anderson KC; Managing Myeloma Continuing Education Initiative Advisory Group

  • Clin Lymphoma Myeloma Leuk. 2014 Oct;14(5):356-69

2015-02-23

Fig 1. Distribution of interval time from diagnosis to recurrence (thoracotomy) for 39 patients with recurrent osteosarcoma presenting as a single pulmonary metastasis.

Fig 1. Distribution of interval time from diagnosis to recurrence (thoracotomy) for 39 patients with recurrent osteosarcoma presenting as a single pulmonary metastasis.
  • Daw NC, Chou AJ, Jaffe N, Rao BN, Billups CA, Rodriguez-Galindo C, Meyers PA, Huh WW

  • Br J Cancer. 2015 Jan 20;112(2):278-82.

2015-02-24

Fig 2. Putative mechanisms for autocrine/paracrine activation of WNT signaling in synovial sarcoma. WNT signals through FZD/LRP6, inhibiting the APC–AXIN–GSK3B–CSNK1 destruction complex, leading to release and nuclear transport of β-catenin (CTNNB1). SS18–SSX integrates within SWI/SNF complexes, with potential interactions with developmental pathways, including NOTCH–HES, BMP–SMAD, Hedghog–GLI, MAPK–ETS, and LEF1–TLE1. Extensive cross-regulation between developmental pathways may lead to transcriptional activation of WNT ligands and/or derepression of WNT target genes. The sites of action of WNT inhibitors PRI-724 and LGK974 are indicated.

Fig 2. Putative mechanisms for autocrine/paracrine activation of WNT signaling in synovial sarcoma. WNT signals through FZD/LRP6, inhibiting the APC–AXIN–GSK3B–CSNK1 destruction complex, leading to release and nuclear transport of β-catenin (CTNNB1). SS18–SSX integrates within SWI/SNF complexes, with potential interactions with developmental pathways, including NOTCH–HES, BMP–SMAD, Hedghog–GLI, MAPK–ETS, and LEF1–TLE1. Extensive cross-regulation between developmental pathways may lead to transcriptional activation of WNT ligands and/or derepression of WNT target genes. The sites of action of WNT inhibitors PRI-724 and LGK974 are indicated.
  • Nielsen TO, Poulin NM, Ladanyi M

  • Cancer Discov. 2015 Feb;5(2):124-134. Epub 2015 Jan 22.

2015-02-25

Fig 3. Relative proportions and overlap among anterior pituitary deficiencies following cranial radiotherapy. ACTHD, adrenocorticotropic hormone deficiency; GHD, growth hormone deficiency; LH/FSHD, luteinizing hormone/follicle-stimulating hormone deficiency; TSHD, thyroid-stimulating hormone deficiency.

Fig 3. Relative proportions and overlap among anterior pituitary deficiencies following cranial radiotherapy. ACTHD, adrenocorticotropic hormone deficiency; GHD, growth hormone deficiency; LH/FSHD, luteinizing hormone/follicle-stimulating hormone deficiency; TSHD, thyroid-stimulating hormone deficiency.
  • Chemaitilly W, Li Z, Huang S, Ness KK, Clark KL, Green DM, Barnes N, Armstrong GT, Krasin MJ, Srivastava DK, Pui CH, Merchant TE, Kun LE, Gajjar A, Hudson MM, Robison LL, Sklar CA

  • J Clin Oncol. 2015 Feb 10;33(5):492-500.

2015-02-26

Fig 2. Relative frequency of thymoma histotypes by center volume and geographic region. A, Frequency of thymoma subtypes, ordered by size of center and geographic region. B, The frequency of thymoma subtypes by region and by high- and low-volume centers. “High volume centers” are those contributing more than 50% of the total cases per region. WHO, World Health Organization.

Fig 2. Relative frequency of thymoma histotypes by center volume and geographic region. A, Frequency of thymoma subtypes, ordered by size of center and geographic region. B, The frequency of thymoma subtypes by region and by high- and low-volume centers. “High volume centers” are those contributing more than 50% of the total cases per region. WHO, World Health Organization.
  • Weis CA, Yao X, Deng Y, Detterbeck FC, Marino M, Nicholson AG, Huang J, Ströbel P, Antonicelli A, Marx A; Contributors to the ITMIG Retrospective Database

  • J Thorac Oncol. 2015 Feb;10(2):367-72.

2015-02-27

Fig 3. Dynamic monitoring of serial urinary cfDNA BRAFV600E-mutant allele burden in patients with systemic histiocytosis. A, gadolinium-enhanced T1 MRI images of ECD involvement of brain (green arrows), and 2[18F]fluoro-2-deoxy-d-glucose (FDG)–PET images of disease in the right atrium (asterisk) and testes (asterisk), pre-dabrafenib, and after 2 months of dabrafenib. B, urinary BRAFV600E cfDNA results throughout this same patient's therapy. C, urinary BRAFV600E cfDNA results of a patient with ECD treated with anakinra followed by a period of treatment cessation and then initiation of vemurafenib. D, maximal intensity projection images of FDG–PET scan images (top) demonstrating tibial infiltration by ECD pre-vemurafenib (left scan), following 10 weeks of vemurafenib (middle scan), and then 16 weeks after vemurafenib discontinuation (right scan) in a patient with ECD with accompanying urinary cfDNA results for each time point (bottom).

Fig 3. Dynamic monitoring of serial urinary cfDNA BRAFV600E-mutant allele burden in patients with systemic histiocytosis. A, gadolinium-enhanced T1 MRI images of ECD involvement of brain (green arrows), and 2[18F]fluoro-2-deoxy-d-glucose (FDG)–PET images of disease in the right atrium (asterisk) and testes (asterisk), pre-dabrafenib, and after 2 months of dabrafenib. B, urinary BRAFV600E cfDNA results throughout this same patient's therapy. C, urinary BRAFV600E cfDNA results of a patient with ECD treated with anakinra followed by a period of treatment cessation and then initiation of vemurafenib. D, maximal intensity projection images of FDG–PET scan images (top) demonstrating tibial infiltration by ECD pre-vemurafenib (left scan), following 10 weeks of vemurafenib (middle scan), and then 16 weeks after vemurafenib discontinuation (right scan) in a patient with ECD with accompanying urinary cfDNA results for each time point (bottom).
  • Hyman DM, Diamond EL, Vibat CR, Hassaine L, Poole JC, Patel M, Holley VR, Cabrilo G, Lu TT, Arcila ME, Chung YR, Rampal R, Lacouture ME, Rosen N, Meric-Bernstam F, Baselga J, Kurzrock R, Erlander MG, Janku F, Abdel-Wahab O.

  • Cancer Discov. 2015 Jan;5(1):64-71.

2015-03-02

Fig 3. Expression of p53 by immunohistochemistry. A, The staining pattern of a thymic carcinoma with wild-type TP53. Note scattered positive nuclei representing less than 10% of the tumor cells. B, The staining pattern of p53 in a thymic carcinoma with TP53 mutation. Note positive nuclei in more than 60% of tumor cells. There was a perfect correlation between mutation and immunohistochemistry staining pattern in these cases.

Fig 3. Expression of p53 by immunohistochemistry. A, The staining pattern of a thymic carcinoma with wild-type TP53. Note scattered positive nuclei representing less than 10% of the tumor cells. B, The staining pattern of p53 in a thymic carcinoma with TP53 mutation. Note positive nuclei in more than 60% of tumor cells. There was a perfect correlation between mutation and immunohistochemistry staining pattern in these cases.
  • Moreira AL, Won HH, McMillan R, Huang J, Riely GJ, Ladanyi M, Berger MF

  • J Thorac Oncol. 2015 Feb;10(2):373-80.

2015-03-03

Grading of complications leading to readmission in relation to morbidities encountered during the primary stay.

Grading of complications leading to readmission in relation to morbidities encountered during the primary stay.
  • Tamandl D, Butte JM, Allen PJ, D'Angelica MI, DeMatteo RP, Groeger JS, Jarnagin WR, Fong Y

  • Surgery. 2015 Feb;157(2):231-8.

2015-03-04

Predicted transmembrane domains for human Hhat. A, TMDs predicted for human Hhat by the indicated programs (top panel). TMDs predicted with high consistency by most programs are highlighted in green. Bottom panel, final topology model of Hhat. RL, re-entrant loop. B, schematic representation of FLAG epitope insert (red arrows) and HA epitope insert (blue arrows) constructs used to map the topology of Hhat.

Predicted transmembrane domains for human Hhat. A, TMDs predicted for human Hhat by the indicated programs (top panel). TMDs predicted with high consistency by most programs are highlighted in green. Bottom panel, final topology model of Hhat. RL, re-entrant loop. B, schematic representation of FLAG epitope insert (red arrows) and HA epitope insert (blue arrows) constructs used to map the topology of Hhat.
  • Matevossian A, Resh MD.

  • J Biol Chem. 2015 Jan 23;290(4):2235-43

2015-03-05

Fig 2. CD19-CAR expression and ex vivo expansion of Tol2-modified T-cells. (a) Surface expression of CD19-CAR on T-cells after nucleofection with pTol2-CD19-CAR with or without pCAGGS-mT2TP (TPase) plasmids was examined by flow cytometry. Values represent the percentages of CD3+ CD19-CAR+ and CD3− CD19-CAR+ cells. Data are representative of one of the three independent experiments using different donors. (b) CD19-CAR expression of Tol2-tranduced T-cells in the presence or absence of TPase as detected by western blotting with an anti-CD3ζ antibody. β-Actin was used as a loading control. (c) Growth rates of transduced T-cells with or without TPase. 3T3/CD19 cells were added weekly. Viable cells were enumerated by trypan blue exclusion. Data represent mean±s.d. from three different donors.

Fig 2. CD19-CAR expression and ex vivo expansion of Tol2-modified T-cells. (a) Surface expression of CD19-CAR on T-cells after nucleofection with pTol2-CD19-CAR with or without pCAGGS-mT2TP (TPase) plasmids was examined by flow cytometry. Values represent the percentages of CD3+ CD19-CAR+ and CD3− CD19-CAR+ cells. Data are representative of one of the three independent experiments using different donors. (b) CD19-CAR expression of Tol2-tranduced T-cells in the presence or absence of TPase as detected by western blotting with an anti-CD3ζ antibody. β-Actin was used as a loading control. (c) Growth rates of transduced T-cells with or without TPase. 3T3/CD19 cells were added weekly. Viable cells were enumerated by trypan blue exclusion. Data represent mean±s.d. from three different donors.
  • Tsukahara T, Iwase N, Kawakami K, Iwasaki M, Yamamoto C, Ohmine K, Uchibori R, Teruya T, Ido H, Saga Y, Urabe M, Mizukami H, Kume A, Nakamura M, Brentjens R, Ozawa K

  • Gene Ther. 2015 Feb;22(2):209-15.

2015-03-06

AAVrh.10BevMab-directed expression of bevacizumab in the mouse CNS. (a) Diagram of the mouse brain illustrates regions for expression analysis and site of vector administration. R=right; L=left. (b) Relative quantification of AAVrh.10-directed bevacizumab mRNA expression per microgram of total RNA in each brain region and in peripheral organs (n=3). The limit of detection is denoted by the dashed line. Statistical difference by two-tailed t-test to R1 and R2, P<0.01 is marked with asterisk (*). There was no significant difference between R1 and R2 (P>0.4). (c) Time-dependent quantification of AAVrh.10-directed bevacizumab protein expression in each brain region compared with blood (n=4). The limit of detection denoted by the dashed line. R=right; L=left. Statistical difference by two-tailed t-test to (R1,R2) P<0.05 marked with asterisk (*) and P<0.01 (**). (d) AAVrh.10BevMab-mediated expression of bevacizumab in neurons of the mouse striatum. Shown is immunofluorescent assessment of coronal section of the CNS 4 weeks after administration of AAVrh.10BevMab. Detection of AAVrh.10BevMab-directed expression of bevacizumab was assessed with anti-human IgG antibody (anti-IgG, green), glia cells were assessed with anti-glial fibrillary acidic protein (anti-GFAP, purple) and neurons were assessed with neuronal nuclear antigen (NeuN, red). Bar=50 μm.

AAVrh.10BevMab-directed expression of bevacizumab in the mouse CNS. (a) Diagram of the mouse brain illustrates regions for expression analysis and site of vector administration. R=right; L=left. (b) Relative quantification of AAVrh.10-directed bevacizumab mRNA expression per microgram of total RNA in each brain region and in peripheral organs (n=3). The limit of detection is denoted by the dashed line. Statistical difference by two-tailed t-test to R1 and R2, P<0.01 is marked with asterisk (*). There was no significant difference between R1 and R2 (P>0.4). (c) Time-dependent quantification of AAVrh.10-directed bevacizumab protein expression in each brain region compared with blood (n=4). The limit of detection denoted by the dashed line. R=right; L=left. Statistical difference by two-tailed t-test to (R1,R2) P<0.05 marked with asterisk (*) and P<0.01 (**). (d) AAVrh.10BevMab-mediated expression of bevacizumab in neurons of the mouse striatum. Shown is immunofluorescent assessment of coronal section of the CNS 4 weeks after administration of AAVrh.10BevMab. Detection of AAVrh.10BevMab-directed expression of bevacizumab was assessed with anti-human IgG antibody (anti-IgG, green), glia cells were assessed with anti-glial fibrillary acidic protein (anti-GFAP, purple) and neurons were assessed with neuronal nuclear antigen (NeuN, red). Bar=50 μm.
  • Hicks MJ, Funato K, Wang L, Aronowitz E, Dyke JP, Ballon DJ, Havlicek DF, Frenk EZ, De BP, Chiuchiolo MJ, Sondhi D, Hackett NR, Kaminsky SM, Tabar V, Crystal RG

  • Cancer Gene Ther. 2015 Jan;22(1):1-8.

2015-03-09

Intraductal papillary mucinous neoplasm.

Intraductal papillary mucinous neoplasm.
  • Dudeja V, Allen PJ

  • Semin Oncol. 2015 Feb;42(1):70-85.

2015-03-10

Characteristics of the distribution of vertical couch displacement that occurred for each minute after initial beam-on are shown.

Characteristics of the distribution of vertical couch displacement that occurred for each minute after initial beam-on are shown.
  • Lovelock DM, Messineo AP, Cox BW, Kollmeier MA, Zelefsky MJ

  • Int J Radiat Oncol Biol Phys. 2015 Mar 1;91(3):588-94.

2015-03-11

Fig 1. An example sequence of colored circles for each of the three stimulus types (high-, low-, and zero-probability predictor conditions).

Fig 1. An example sequence of colored circles for each of the three stimulus types (high-, low-, and zero-probability predictor conditions).
  • Jost E, Conway CM, Purdy JD, Walk AM, Hendricks MA

  • Brain Res. 2015 Feb 9;1597:95-107.

2015-03-12

Postoperative day 8 axial CT slices of the single major complication.

Postoperative day 8 axial CT slices of the single major complication.
  • Tewari SO, Getrajdman GI, Petre EN, Sofocleous CT, Siegelbaum RH, Erinjeri JP, Weiser MR, Thornton RH

  • J Vasc Interv Radiol. 2015 Feb;26(2):182-8.

2015-03-13

Fig 2. Crater-shaped topography of a Mohs surgical wound.

Fig 2. Crater-shaped topography of a Mohs surgical wound.
  • Flores ES, Cordova M, Kose K, Phillips W, Rossi A, Nehal K, Rajadhyaksha M

  • J Biomed Opt. 2015 Jun 1;20(6):61103.
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2015-03-16

Synopsis. 


A chemical screen and systems approach reveal SYK-STAT3 signaling as a druggable target in basal-like breast cancers. The study supports the systems-based notion that targeting a cell state, rather than a mutational state, can lead to therapeutic target discovery.

Synopsis. A chemical screen and systems approach reveal SYK-STAT3 signaling as a druggable target in basal-like breast cancers. The study supports the systems-based notion that targeting a cell state, rather than a mutational state, can lead to therapeutic target discovery.
  • Muellner MK, Mair B, Ibrahim Y, Kerzendorfer C, Lechtermann H, Trefzer C, Klepsch F, Müller AC, Leitner E, Macho-Maschler S, Superti-Furga G, Bennett KL, Baselga J, Rix U, Kubicek S, Colinge J, Serra V, Nijman SM

  • Mol Syst Biol. 2015 Feb 19;11(2):789.
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2015-03-17

Structure of chimeric antigen receptors (CARs).

Structure of chimeric antigen receptors (CARs).
  • Park JH, Brentjens RJ

  • J Clin Oncol. 2015 Feb 20;33(6):651-3.

2015-03-18

Fig 1. Comparison of corresponding sections from (a) PAC-MRI and (b) ERC-MRI transverse T2W fast spin-echo sequences on which a radiologist outlined the prostate circumference during calculation of the prostate volume.

Fig 1. Comparison of corresponding sections from (a) PAC-MRI and (b) ERC-MRI transverse T2W fast spin-echo sequences on which a radiologist outlined the prostate circumference during calculation of the prostate volume.
  • Mazaheri Y, Afaq AA, Jung SI, Goldman DA, Wang L, Aslan H, Zelefsky MJ, Akin O, Hricak H

  • Clin Radiol. 2015 Apr;70(4):379-86.

2015-03-19

Candidate therapeutic targets and driver oncogenic events.

Candidate therapeutic targets and driver oncogenic events.
  • Collaborators (348)

  • Nature. 2015 Jan 29;517(7536):576-82.

2015-03-20

Fig 4. Sample result groups that have RHOC as a common downstream target.

Fig 4. Sample result groups that have RHOC as a common downstream target.
  • Barbur O, Gonen M, Askoy B, Schultz N, Ciriello G, Sander C, and Demir E

  • Genome Biology 2015, 16:45
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2015-03-23

Fig 3. Survival analysis of LSK-derived leukemia cells that were secondarily transplanted from the initiation experiment (Figure 2A) into sublethally irradiated mice, n = 31 Msi2fl/fl and n = 31 Msi2Δ/Δ, combined from transplant experiments in Supplemental Figure 3A.

Fig 3. Survival analysis of LSK-derived leukemia cells that were secondarily transplanted from the initiation experiment (Figure 2A) into sublethally irradiated mice, n = 31 Msi2fl/fl and n = 31 Msi2Δ/Δ, combined from transplant experiments in Supplemental Figure 3A.
  • Park SM, Gönen M, Vu L, Minuesa G, Tivnan P, Barlowe TS, Taggart J, Lu Y, Deering RP, Hacohen N, Figueroa ME, Paietta E, Fernandez HF, Tallman MS, Melnick A, Levine R, Leslie C, Lengner CJ, Kharas MG

  • J Clin Invest. 2015 Mar 2;125(3):1286-98.

2015-03-24

Patients who remain in remission per the investigator following treatment with brentuximab vedotin.

Patients who remain in remission per the investigator following treatment with brentuximab vedotin.
  • Gopal AK, Chen R, Smith SE, Ansell SM, Rosenblatt JD, Savage KJ, Connors JM, Engert A, Larsen EK8, Chi X, Sievers EL, Younes A

  • Blood. 2015 Feb 19;125(8):1236-43.

2015-03-25

Fig 6. RCM and histopathology correlation of residual basal cell carcinoma (BCC) in a Mohs surgical wound. (a) RCM video mosaic of a residual wound quadrant. (b) The inset shows magnified view of 1  mm×1  mm  area showing: (1) intact skin; (2) epidermal margin; (3) peripheral dermal margin and a portion of the deep dermal margin; and the wound edge (yellow dotted line). (c) Corresponding en face frozen section, showing nodular BCC (H&E, 20X). Tumor island circled in red.

Fig 6. RCM and histopathology correlation of residual basal cell carcinoma (BCC) in a Mohs surgical wound. (a) RCM video mosaic of a residual wound quadrant. (b) The inset shows magnified view of 1  mm×1  mm area showing: (1) intact skin; (2) epidermal margin; (3) peripheral dermal margin and a portion of the deep dermal margin; and the wound edge (yellow dotted line). (c) Corresponding en face frozen section, showing nodular BCC (H&E, 20X). Tumor island circled in red.
  • Flores ES, Cordova M, Kose K, Phillips W, Rossi A, Nehal K, Rajadhyaksha M

  • J Biomed Opt. 2015 Jun;20(6):61103

2015-03-26

Fig 1. Flow diagram of studies included in individual participant data meta-analysis of hormonal contraception and HIV acquisition.

Fig 1. Flow diagram of studies included in individual participant data meta-analysis of hormonal contraception and HIV acquisition.
  • Morrison CS, Chen PL, Kwok C, Baeten JM, Brown J, Crook AM, Van Damme L, Delany-Moretlwe S, Francis SC, Friedland BA, Hayes RJ, Heffron R, Kapiga S, Karim QA, Karpoff S, Kaul R, McClelland RS, McCormack S, McGrath N, Myer L, Rees H, van der Straten A, Watson-Jones D, van de Wijgert JH, Stalter R, Low N

  • PLoS Med. 2015 Jan 22;12(1):e1001778.
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2015-03-27

Characterization of SERRS nanostars

Characterization of SERRS nanostars
  • Harmsen S, Huang R, Wall MA, Karabeber H, Samii JM, Spaliviero M, White JR, Monette S, O'Connor R, Pitter KL, Sastra SA, Saborowski M, Holland EC, Singer S, Olive KP, Lowe SW, Blasberg RG, Kircher MF

  • Sci Transl Med. 2015 Jan 21;7(271):271ra7

2015-03-30

Fig 1. NAC induces apoptosis in IL7R mutant DND-41 T-ALL cells and Ba/F3 cells transformed by a cysteine-containing IL7R mutant allele.

Fig 1. NAC induces apoptosis in IL7R mutant DND-41 T-ALL cells and Ba/F3 cells transformed by a cysteine-containing IL7R mutant allele.
  • Mansour MR, Reed C, Eisenberg AR, Tseng JC, Twizere JC, Daakour S, Yoda A, Rodig SJ, Tal N, Shochat C, Berezovskaya A, DeAngelo DJ, Sallan SE, Weinstock DM, Izraeli S, Kung AL, Kentsis A, Look AT

  • Br J Haematol. 2015 Jan;168(2):230-8.

2015-03-31

Fig 1. Prostate-specific antigen (PSA) relapse-free survival for all patients.

Fig 1. Prostate-specific antigen (PSA) relapse-free survival for all patients.
  • Cuaron J, Pei X, Cohen GN, Cox BW, Yamada Y, Zelefsky MJ, Kollmeier MA

  • Brachytherapy. 2015 Mar-Apr;14(2):179-84.

2015-04-01

Fig 1. Basic components and operation of electronic nicotine delivery systems (ENDS). When a user inhales from the ENDS device, airflow is detected by a sensor. The sensor activates a heating element that pulls the e-liquid stored in the cartridge into the vaporization chamber where it is aerosolized (ie, turned from e-liquid into a fine mist of liquid droplets, often referred to as a vapor). The aerosolized e-liquid is then inhaled by the user. In some models, activation of the sensor also powers the indicator light, which simulates the glow of burning tobacco. In manually operated models, the heating element is activated by pressing a button.

Fig 1. Basic components and operation of electronic nicotine delivery systems (ENDS). When a user inhales from the ENDS device, airflow is detected by a sensor. The sensor activates a heating element that pulls the e-liquid stored in the cartridge into the vaporization chamber where it is aerosolized (ie, turned from e-liquid into a fine mist of liquid droplets, often referred to as a vapor). The aerosolized e-liquid is then inhaled by the user. In some models, activation of the sensor also powers the indicator light, which simulates the glow of burning tobacco. In manually operated models, the heating element is activated by pressing a button.
  • Brandon TH, Goniewicz ML, Hanna NH, Hatsukami DK, Herbst RS, Hobin JA, Ostroff JS, Shields PG, Toll BA, Tyne CA, Viswanath K, Warren GW

  • J Clin Oncol. 2015 Mar 10;33(8):952-63.