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1. Botchkarev VA: Molecular mechanisms of chemotherapy-induced hair loss. J Investig Dermatol Symp Proc; 2003 Jun;8(1):72-5
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  • [Title] Molecular mechanisms of chemotherapy-induced hair loss.
  • Hair loss (alopecia) is a much-feared side-effect of many chemotherapy protocols and is one of the most psychological devastating aspects of cancer therapy.
  • So far, no satisfactory strategy for suppressing chemotherapy-induced alopecia is at hand.
  • During the last decade, some progress in understanding molecular mechanisms of chemotherapy-induced hair loss has been achieved using rodent models.
  • However, the pathobiology of the response of human hair follicle to chemotherapy remains largely unknown.
  • Here, we review molecular mechanisms that control apoptosis in the hair follicle induced by chemotherapy and delineate the basic strategy for pharmacological inhibition of this devastating side-effect of cancer treatment.
  • We focus on the roles of p53 and its target genes that are essential in mediating responses of hair follicle cells.
  • We assume that local pharmacological inhibition of p53 activity may serve as an effective treatment to prevent chemotherapy-induced hair loss.
  • Sufficient pharmacological inhibition of chemotherapy-induced hair loss may require a combination of inhibitors to block complementary or redundant pathways of apoptosis in hair follicles.

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  • (PMID = 12894998.001).
  • [ISSN] 1087-0024
  • [Journal-full-title] The journal of investigative dermatology. Symposium proceedings
  • [ISO-abbreviation] J. Investig. Dermatol. Symp. Proc.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tumor Suppressor Protein p53
  • [Number-of-references] 44
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2. Botchkarev VA, Komarova EA, Siebenhaar F, Botchkareva NV, Komarov PG, Maurer M, Gilchrest BA, Gudkov AV: p53 is essential for chemotherapy-induced hair loss. Cancer Res; 2000 Sep 15;60(18):5002-6
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  • [Title] p53 is essential for chemotherapy-induced hair loss.
  • Anticancer drugs stimulate apoptosis in the hair follicles (HF) and cause hair loss, the most common side effect of chemotherapy.
  • In a mouse model for chemotherapy-induced hair loss, we demonstrate that p53 is essential for this process: in contrast to wild-type mice, p53-deficient mice show neither hair loss nor apoptosis in the HF keratinocytes that maintained active proliferation after cyclophosphamide treatment.
  • These observations indicate that local pharmacological inhibition of p53 may be useful to prevent chemotherapy-associated hair loss.
  • [MeSH-major] Alopecia / chemically induced. Antineoplastic Agents, Alkylating / toxicity. Cyclophosphamide / toxicity. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Animals. Antigens, CD95 / biosynthesis. Antigens, CD95 / genetics. Apoptosis / drug effects. Apoptosis / physiology. Down-Regulation / drug effects. Female. Hair Follicle / cytology. Hair Follicle / drug effects. Hair Follicle / metabolism. Insulin-Like Growth Factor Binding Protein 3 / biosynthesis. Insulin-Like Growth Factor Binding Protein 3 / genetics. Mice. Mice, Inbred C57BL. Mice, Knockout. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Proto-Oncogene Proteins c-bcl-2 / genetics. Up-Regulation / drug effects

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  • (PMID = 11016618.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA75179
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Antineoplastic Agents, Alkylating; 0 / Insulin-Like Growth Factor Binding Protein 3; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 8N3DW7272P / Cyclophosphamide
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3. Botchkarev VA, Komarova EA, Siebenhaar F, Botchkareva NV, Sharov AA, Komarov PG, Maurer M, Gudkov AV, Gilchrest BA: p53 Involvement in the control of murine hair follicle regression. Am J Pathol; 2001 Jun;158(6):1913-9
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  • [Title] p53 Involvement in the control of murine hair follicle regression.
  • p53 is a transcription factor mediating a variety of biological responses including apoptotic cell death. p53 was recently shown to control apoptosis in the hair follicle induced by ionizing radiation and chemotherapy, but its role in the apoptosis-driven physiological hair follicle regression (catagen) remains to be elucidated.
  • Here, we show that p53 protein is strongly expressed and co-localized with apoptotic markers in the regressing hair follicle compartments during catagen.
  • In contrast to wild-type mice, p53 knockout mice show significant retardation of catagen accompanied by significant decrease in the number of apoptotic cells in the hair matrix.
  • Furthermore, p53 null hair follicles are characterized by alterations in the expression of markers that are encoded by p53 target genes and are implicated in the control of catagen (Bax, Bcl-2, insulin-like growth factor binding protein-3).
  • These data suggest that p53 is involved in the control of apoptosis in the hair follicle during physiological regression and imply that p53 antagonists may be useful for the management of hair growth disorders characterized by premature entry into catagen, such as androgenetic alopecia, alopecia areata, and telogen effluvium.

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  • (PMID = 11395365.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075179; United States / NCI NIH HHS / CA / CA75179
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bax protein, mouse; 0 / Insulin-Like Growth Factor Binding Protein 3; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein
  • [Other-IDs] NLM/ PMC1891974
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4. Sharov AA, Mardaryev AN, Sharova TY, Grachtchouk M, Atoyan R, Byers HR, Seykora JT, Overbeek P, Dlugosz A, Botchkarev VA: Bone morphogenetic protein antagonist noggin promotes skin tumorigenesis via stimulation of the Wnt and Shh signaling pathways. Am J Pathol; 2009 Sep;175(3):1303-14
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  • In contrast to wild-type mice, transgenic mice developed spontaneous hair follicle-derived tumors, which resemble human trichofolliculoma.
  • Global gene expression profiles revealed that in contrast to anagen hair follicles of wild-type mice, tumors of transgenic mice showed stage-dependent increases in the expression of genes encoding the selected components of Wnt and Shh pathways.
  • Specifically, expression of the Wnt ligands increased at the initiation stage of tumor formation, whereas expression of the Wnt antagonist and tumor suppressor Wnt inhibitory factor-1 decreased, as compared with fully developed tumors.
  • In contrast, expression of the components of Shh pathway increased in fully developed tumors, as compared with the tumor placodes.
  • Consistent with the expression data, pharmacological treatment of transgenic mice with Wnt and Shh antagonists resulted in the stage-dependent inhibition of tumor initiation, and progression, respectively.
  • Furthermore, BMP signaling stimulated Wnt inhibitory factor-1 expression and promoter activity in cultured tumor cells and HaCaT keratinocytes, as well as inhibited Shh expression, as compared with the corresponding controls.
  • Thus, tumor suppressor activity of the BMPs in skin epithelium depends on the local concentrations of noggin and is mediated at least in part via stage-dependent antagonizing of Wnt and Shh signaling pathways.

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  • (PMID = 19700758.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / K01 AR056771; United States / NIAMS NIH HHS / AR / AR 49778; United States / NIAMS NIH HHS / AR / R56 AR049778; United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/E023010/1; United States / NIAMS NIH HHS / AR / R01 AR049778
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Morphogenetic Proteins; 0 / Carrier Proteins; 0 / Hedgehog Proteins; 0 / SHH protein, human; 0 / Shh protein, mouse; 0 / Wnt Proteins; 148294-77-3 / noggin protein
  • [Other-IDs] NLM/ PMC2731148
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5. Imai Y, Isoda K, Ito E, Hakamada A, Yamanishi K, Mizutani H: Primary cutaneous follicle center cell lymphoma of the scalp successfully treated with anti CD20 monoclonal antibody and CHOP combination therapy with no subsequent permanent loss of hair. J Dermatol; 2003 Sep;30(9):683-8
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  • [Title] Primary cutaneous follicle center cell lymphoma of the scalp successfully treated with anti CD20 monoclonal antibody and CHOP combination therapy with no subsequent permanent loss of hair.
  • We present a primary cutaneous follicle center cell lymphoma (PCFCCL) patient who was successfully treated with Rituximab, a new anti-CD20 monoclonal antibody.
  • A thirty-two-year-old male developed two asymptomatic tumors on the scalp.
  • Histopathologically, the tumors were composed of diffuse and nodular infiltration of centrocytes and centroblasts.
  • Immunohistopathologically, the tumor cells stained positively with anti-CD20 antibody and anti-kappa antibody, but not with anti-CD5, anti-CD10, or anti-Bcl-2 antibody.
  • Radiation therapy is effective in treating PCFCCL; however, it usually results in the permanent loss of hair.
  • He has had no recurrence in more than 12 months and no permanent loss of hair on the scalp.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Head and Neck Neoplasms / drug therapy. Lymphoma, Follicular / drug therapy

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  • (PMID = 14578559.001).
  • [ISSN] 0385-2407
  • [Journal-full-title] The Journal of dermatology
  • [ISO-abbreviation] J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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6. Bol DK, Rowley RB, Ho CP, Pilz B, Dell J, Swerdel M, Kiguchi K, Muga S, Klein R, Fischer SM: Cyclooxygenase-2 overexpression in the skin of transgenic mice results in suppression of tumor development. Cancer Res; 2002 May 1;62(9):2516-21
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  • [Title] Cyclooxygenase-2 overexpression in the skin of transgenic mice results in suppression of tumor development.
  • Significant evidence has accumulated suggesting that the inducible form of cyclooxygenase (COX-2), a central enzyme in the prostaglandin biosynthetic pathway, plays an important role in tumor development.
  • Administration of a specific COX-2 inhibitor restored hair growth, indicating that the alopecia was attributable to elevated COX-2 enzymatic activity.
  • Unexpectedly, COX-2 overexpression was found to protect, rather than sensitize, K14.COX2 mice to skin tumor development induced by an initiation/promotion protocol.
  • K14.COX2 transgenics developed tumors at a much lower frequency than did their littermate controls (3.3% versus 93%, respectively, on a FVB background and approximately 25% versus 100%, respectively, on an ICR background) and presented with significantly reduced tumor burdens (average, 0.03 versus 12.7 tumors/mouse, respectively, on a FVB background and 0.5 versus 7.1 tumors/mouse, respectively, on an ICR background).
  • Mice fed a COX-2 inhibitor in utero and as weanlings up to the time of promotion also showed a significant resistance to tumor development.
  • These results clearly raise questions regarding the role of COX-2 and elevated prostaglandin levels in skin tumor development.
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene. Alopecia / drug therapy. Alopecia / enzymology. Animals. Carcinogens. Celecoxib. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Cyclooxygenase Inhibitors / pharmacology. Dinoprostone / metabolism. Female. Hair Follicle / drug effects. Humans. Male. Membrane Proteins. Mice. Mice, Inbred ICR. Mice, Transgenic. Phenotype. Pyrazoles. Sulfonamides / pharmacology. Tetradecanoylphorbol Acetate

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  • (PMID = 11980643.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-16672; United States / NCI NIH HHS / CA / CA-34443
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Pyrazoles; 0 / Sulfonamides; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; JCX84Q7J1L / Celecoxib; K7Q1JQR04M / Dinoprostone; NI40JAQ945 / Tetradecanoylphorbol Acetate
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7. Amoh Y, Li L, Yang M, Jiang P, Moossa AR, Katsuoka K, Hoffman RM: Hair follicle-derived blood vessels vascularize tumors in skin and are inhibited by Doxorubicin. Cancer Res; 2005 Mar 15;65(6):2337-43
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  • [Title] Hair follicle-derived blood vessels vascularize tumors in skin and are inhibited by Doxorubicin.
  • We have recently shown that the neural-stem cell marker nestin is expressed in hair follicle stem cells and the blood vessel network interconnecting hair follicles in the skin of transgenic mice with nestin regulatory element-driven green fluorescent protein (ND-GFP).
  • The hair follicles were shown to give rise to the nestin-expressing blood vessels in the skin.
  • In the present study, we visualized tumor angiogenesis by dual-color fluorescence imaging in ND-GFP transgenic mice after transplantation of the murine melanoma cell line B16F10 expressing red fluorescent protein.
  • ND-GFP was highly expressed in proliferating endothelial cells and nascent blood vessels in the growing tumor.
  • Progressive angiogenesis during tumor growth was readily visualized during tumor growth by GFP expression.
  • Doxorubicin inhibited the nascent tumor angiogenesis as well as tumor growth in the ND-GFP mice transplanted with B16F10-RFP.
  • This model is useful for direct visualization of tumor angiogenesis and evaluation of angiogenic inhibitors.
  • [MeSH-major] Doxorubicin / pharmacology. Hair Follicle / blood supply. Melanoma, Experimental / blood supply. Skin Neoplasms / blood supply
  • [MeSH-minor] Animals. Cell Growth Processes / drug effects. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Intermediate Filament Proteins / genetics. Intermediate Filament Proteins / metabolism. Mice. Mice, Transgenic. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / pathology. Nerve Tissue Proteins / genetics. Nerve Tissue Proteins / metabolism. Nestin. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism

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  • (PMID = 15781648.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA099258; United States / NCI NIH HHS / CA / CA101600; United States / NCI NIH HHS / CA / CA103563
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intermediate Filament Proteins; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Recombinant Fusion Proteins; 147336-22-9 / Green Fluorescent Proteins; 80168379AG / Doxorubicin
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8. Emmenegger U, Man S, Shaked Y, Francia G, Wong JW, Hicklin DJ, Kerbel RS: A comparative analysis of low-dose metronomic cyclophosphamide reveals absent or low-grade toxicity on tissues highly sensitive to the toxic effects of maximum tolerated dose regimens. Cancer Res; 2004 Jun 1;64(11):3994-4000
Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

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  • [Title] A comparative analysis of low-dose metronomic cyclophosphamide reveals absent or low-grade toxicity on tissues highly sensitive to the toxic effects of maximum tolerated dose regimens.
  • The survival benefits of traditional maximum tolerated dose (MTD) cytotoxic therapy have been modest for the treatment of most types of metastatic malignancy and, moreover, often come with increased acute and chronic toxicity.
  • Recent studies have demonstrated that the frequent administration of comparatively low doses of cytotoxic agents, with no extended breaks [low-dose metronomic (LDM) chemotherapy], may not only be at least as efficient as MTD therapy but also less toxic.
  • This coincides with an apparent selectivity for "activated" endothelial cells of the tumor vasculature.
  • However, the impact of LDM chemotherapy on the most sensitive target cell populations normally affected by MTD therapy (i.e., bone marrow progenitors, gut mucosa, and hair follicle cells) has not been analyzed in experimental detail.
  • Of note was the finding of sustained lymphopenia, which is not unexpected given the use of CTX as immunosuppressive drug.
  • LDM offers clear safety advantages over conventional MTD chemotherapy and therefore would appear to be ideal for long-term combination therapy with targeted antiangiogenic drugs.
  • [MeSH-minor] Animals. Blood Cell Count. Body Weight / drug effects. Bone Marrow / drug effects. Cell Division / drug effects. Female. Intestinal Mucosa / cytology. Intestinal Mucosa / drug effects. Lymphopenia / chemically induced. Male. Maximum Tolerated Dose. Mice. Mice, Inbred BALB C. Mice, Nude. Mice, SCID. Neovascularization, Physiologic / drug effects. Wound Healing / drug effects

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  • (PMID = 15173013.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-41233
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide
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9. DeBloom J 2nd, Severson J, Gaspari A, Scott G: Follicular mycosis fungoides: a case report and review of the literature. J Cutan Pathol; 2001 Jul;28(6):318-24
Hazardous Substances Data Bank. METHOTREXATE .

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  • Unlike classic MF where atypical lymphocytes show a predilection for the epidermis (epidermotropism), follicular MF displays a malignant lymphocytic infiltrate tropic for hair follicles (folliculotropism).
  • [MeSH-major] Hair Follicle / pathology. Mycosis Fungoides / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Administration, Topical. Adult. Anti-Inflammatory Agents / therapeutic use. Antineoplastic Agents, Alkylating / therapeutic use. Biomarkers, Tumor / analysis. Dermatologic Agents / therapeutic use. Drug Therapy, Combination. Glucocorticoids. Humans. Immunohistochemistry. Male. Mechlorethamine / therapeutic use. Methotrexate / therapeutic use. T-Lymphocytes / chemistry. T-Lymphocytes / pathology. Treatment Outcome

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  • [CommentIn] J Cutan Pathol. 2002 Nov;29(10):625 [12453304.001]
  • (PMID = 11401680.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Biomarkers, Tumor; 0 / Dermatologic Agents; 0 / Glucocorticoids; 50D9XSG0VR / Mechlorethamine; YL5FZ2Y5U1 / Methotrexate
  • [Number-of-references] 21
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10. Letada PR, Sparling JD, Norwood C: Imiquimod in the treatment of alopecia universalis. Cutis; 2007 Feb;79(2):138-40
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  • [Title] Imiquimod in the treatment of alopecia universalis.
  • Imiquimod is used topically in the treatment of numerous dermatologic conditions.
  • Imiquimod modifies the immune response through cytokine induction of the T-cell helper subset, correlating with the expression of interferon alpha, tumor necrosis factor alpha, interferon gamma, and interleukins (ILs) 1 and 12.
  • Alopecia universalis is a severe form of alopecia thought to arise from T-cell mediated autoimmune disease of the hair follicle.
  • There have been no case reports noting a beneficial effect of topical imiquimod in the treatment of alopecia universalis.
  • We present a case of a 15-year-old adolescent girl with alopecia universalis since age 8 who experienced transient hair growth after topical application of imiquimod.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. Alopecia / drug therapy. Aminoquinolines / therapeutic use

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  • (PMID = 17388216.001).
  • [ISSN] 0011-4162
  • [Journal-full-title] Cutis
  • [ISO-abbreviation] Cutis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Aminoquinolines; 99011-02-6 / imiquimod
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11. Uchida N, Tsuzuki Y, Ando T, Mochida Y, Yoshikawa M, Sekihara M, Kobayashi M, Ide M, Ohno Y, Kuwano H: Malignant proliferating trichilemmal tumor in the skin over the breast: a case report. Breast Cancer; 2000 Jan;7(1):79-82
Hazardous Substances Data Bank. FLUOROURACIL .

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  • [Title] Malignant proliferating trichilemmal tumor in the skin over the breast: a case report.
  • A proliferating trichilemmal tumor is relatively uncommon.
  • We describe a 67-year-old woman with a malignant proliferating trichilemmal tumor in the skin over the breast.
  • Eight months postoperatively, a tumor appeared in her right axilla and progressively enlarged.
  • We subsequently excised the tumor.
  • To the best of our knowledge, only one case of a proliferating trichilemmal tumor occurring in the skin over the breast has been reported.
  • [MeSH-major] Breast Neoplasms / pathology. Hair Diseases / pathology. Hair Follicle / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Axilla. Carcinoma, Squamous Cell / diagnosis. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Diagnostic Errors. Doxorubicin / administration & dosage. Fadrozole / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Lymphatic Metastasis. Mastectomy, Radical. Mitomycin / administration & dosage. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / surgery

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  • (PMID = 11029776.001).
  • [ISSN] 1340-6868
  • [Journal-full-title] Breast cancer (Tokyo, Japan)
  • [ISO-abbreviation] Breast Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 50SG953SK6 / Mitomycin; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; H3988M64PU / Fadrozole; U3P01618RT / Fluorouracil
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12. Zöller M, Gupta P, Marhaba R, Vitacolonna M, Freyschmidt-Paul P: Anti-CD44-mediated blockade of leukocyte migration in skin-associated immune diseases. J Leukoc Biol; 2007 Jul;82(1):57-71
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  • CD44 plays an important role in leukocyte extravasation, which is fortified in autoimmune diseases and delayed-type hypersensitivity (DTH) reactions.
  • We wanted to explore this question in alopecia areata (AA), a hair-follicle centric autoimmune disease, and in a chronic eczema.
  • Aiming to support the therapeutic efficacy of a chronic eczema in AA by anti-CD44 treatment, it became essential to control whether a blockade of migration, preferentially of AA effector cells, could be achieved by CD44 isoform-specific antibodies.
  • In vivo, both antibodies interfered with T cell and monocyte extravasation into the skin; only anti-panCD44 prevented T cell homing into lymph nodes.
  • Thus, allergen treatment of AA likely can be supported by targeting AA T cells selectively via a panCD44-CD49d-bispecific antibody.
  • [MeSH-major] Alopecia Areata / drug therapy. Antibodies, Monoclonal / therapeutic use. Antigens, CD44 / drug effects. Chemotaxis, Leukocyte / drug effects
  • [MeSH-minor] Allergens / pharmacology. Allergens / therapeutic use. Animals. Cell Adhesion Molecules. Eczema / drug therapy. Immune System Diseases / drug therapy. Mice. Protein Isoforms / immunology. Skin Diseases / drug therapy

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  • (PMID = 17442857.001).
  • [ISSN] 0741-5400
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Allergens; 0 / Antibodies, Monoclonal; 0 / Antigens, CD44; 0 / Cell Adhesion Molecules; 0 / Protein Isoforms
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13. Liu X, Alexander V, Vijayachandra K, Bhogte E, Diamond I, Glick A: Conditional epidermal expression of TGFbeta 1 blocks neonatal lethality but causes a reversible hyperplasia and alopecia. Proc Natl Acad Sci U S A; 2001 Jul 31;98(16):9139-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To study the role of transforming growth factor type beta1 (TGFbeta1) in epidermal growth control and disease, we have generated a conditional expression system by using the bovine keratin 5 promoter to drive expression of the tetracycline-regulated transactivators tTA and rTA, and a constitutively active mutant of TGFbeta1 linked to the tetO target sequence for the transactivator.
  • Maximal expression of TGFbeta1 during gestation caused embryonic lethality, whereas partial suppression allowed full-term development with neonatal lethality characterized by runting, epidermal hypoproliferation, and blocked hair follicle growth.
  • With complete suppression, phenotypically normal double transgenic (DT) mice were born.
  • Acute induction of TGFbeta1 in the epidermis of adult mice inhibited basal and follicular keratinocyte proliferation and reentry of telogen hair follicles into anagen.
  • Readministration of doxycycline to tTA DT mice caused hair regrowth within 14 days.
  • The mRNA and protein for Smad7, an inhibitor of TGFbeta signaling, were up-regulated in the epidermis and hair follicles of alopecic skin and rapidly induced in rTA mice in parallel with the TGFbeta1 transgene, suggesting that the hyperproliferative phenotype may result in part from development of a sustained negative feedback loop.

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  • (PMID = 11481479.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Smad7 Protein; 0 / Smad7 protein, mouse; 0 / Trans-Activators; 0 / Transforming Growth Factor beta; N12000U13O / Doxycycline
  • [Other-IDs] NLM/ PMC55386
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14. Battistella M, Mateus C, Lassau N, Chami L, Boukoucha M, Duvillard P, Cribier B, Robert C: Sunitinib efficacy in the treatment of metastatic skin adnexal carcinomas: report of two patients with hidradenocarcinoma and trichoblastic carcinoma. J Eur Acad Dermatol Venereol; 2010 Feb;24(2):199-203
MedlinePlus Health Information. consumer health - Skin Cancer.

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  • [Title] Sunitinib efficacy in the treatment of metastatic skin adnexal carcinomas: report of two patients with hidradenocarcinoma and trichoblastic carcinoma.
  • BACKGROUND: Adnexal carcinomas are rare and diverse cutaneous tumours.
  • Sunitinib, an oral tyrosine kinase inhibitor, is reportedly effective for the treatment of various solid cancers.
  • The second patient had a metastatic malignant hair follicle tumour (trichoblastic carcinoma) and achieved a partial remission with sunitinib, and disease stabilized after 10 months.
  • Dynamic contrast-enhanced ultrasound (DCE-US) performed to evaluate tumour vascularization during treatment depicted a dramatic and early decrease in the tumour blood volume.
  • DCE-US using linear raw data may have an early predictive value for tumour response to sunitinib.
  • Further studies involving larger cohorts of patients are warranted in order to confirm the efficacy of sunitinib in these rare tumours.
  • [MeSH-major] Acrospiroma / drug therapy. Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Indoles / therapeutic use. Neoplasm Metastasis. Pyrroles / therapeutic use. Skin Neoplasms / drug therapy
  • [MeSH-minor] Adult. Female. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 19522717.001).
  • [ISSN] 1468-3083
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Indoles; 0 / Pyrroles; 0 / sunitinib
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15. Singer AJ, McClain SA, Hacht G, Batchkina G, Simon M: Semapimod reduces the depth of injury resulting in enhanced re-epithelialization of partial-thickness burns in swine. J Burn Care Res; 2006 Jan-Feb;27(1):40-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Studies suggest that tumor necrosis factor alpha (TNF-alpha) plays a role in burn pathogenesis.
  • [MeSH-major] Burns / drug therapy. Hydrazones / pharmacology. Immunosuppressive Agents / pharmacology. Wound Healing / drug effects
  • [MeSH-minor] Animals. Anti-Infective Agents, Local / pharmacology. Bandages. Cicatrix / pathology. Epidermis / metabolism. Female. Hair Follicle / pathology. Infusions, Intravenous. Necrosis. Random Allocation. Silver Sulfadiazine / pharmacology. Swine. Thrombosis / pathology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16566536.001).
  • [ISSN] 1559-047X
  • [Journal-full-title] Journal of burn care & research : official publication of the American Burn Association
  • [ISO-abbreviation] J Burn Care Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents, Local; 0 / Hydrazones; 0 / Immunosuppressive Agents; 0 / Tumor Necrosis Factor-alpha; 9SGW2H1K8P / semapimod; W46JY43EJR / Silver Sulfadiazine
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16. Surguladze D, Deevi D, Claros N, Corcoran E, Wang S, Plym MJ, Wu Y, Doody J, Mauro DJ, Witte L, Busam KJ, Pytowski B, Rodeck U, Tonra JR: Tumor necrosis factor-alpha and interleukin-1 antagonists alleviate inflammatory skin changes associated with epidermal growth factor receptor antibody therapy in mice. Cancer Res; 2009 Jul 15;69(14):5643-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor necrosis factor-alpha and interleukin-1 antagonists alleviate inflammatory skin changes associated with epidermal growth factor receptor antibody therapy in mice.
  • Cancer patients receiving epidermal growth factor receptor (EGFR) antibody therapy often experience an acneiform rash of uncertain etiology in skin regions rich in pilosebaceous units.
  • Here, we show that a monoclonal antibody targeting murine EGFR, ME1, caused a neutrophil-rich hair follicle inflammation in mice, similar to that reported in patients.
  • This effect was preceded by the appearance of lipid-filled hair follicle distensions adjacent to enlarged sebaceous glands.
  • The cytokine tumor necrosis factor-alpha (TNFalpha), localized immunohistochemically to this affected region of the pilosebaceous unit, was specifically up-regulated by ME1 in skin but not in other tissues examined.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Dermatitis / prevention & control. Interleukin-1 / antagonists & inhibitors. Receptor, Epidermal Growth Factor / immunology. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Animals. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Disease Models, Animal. Enzyme-Linked Immunosorbent Assay. Etanercept. Exanthema / chemically induced. Exanthema / prevention & control. Female. Humans. Immunoglobulin G / pharmacology. Interleukin 1 Receptor Antagonist Protein / pharmacology. Mice. Mice, SCID. Receptors, Tumor Necrosis Factor. Reverse Transcriptase Polymerase Chain Reaction. Skin / drug effects. Skin / metabolism. Skin / pathology

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  • (PMID = 19584274.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antibodies, Monoclonal; 0 / Immunoglobulin G; 0 / Interleukin 1 Receptor Antagonist Protein; 0 / Interleukin-1; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; OP401G7OJC / Etanercept
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17. Tang L, Cao L, Bernardo O, Chen Y, Sundberg JP, Lui H, Chung S, Shapiro J: Topical mechlorethamine restores autoimmune-arrested follicular activity in mice with an alopecia areata-like disease by targeting infiltrated lymphocytes. J Invest Dermatol; 2003 Mar;120(3):400-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Alopecia areata is an autoimmune disease targeted at hair follicles with infiltrated T lymphocytes probably playing an important role in the pathogenesis.
  • After 10 wk of mechlorethamine therapy, a full pelage of hair covered the treated side in all the mice and was maintained during the study, whereas the vehicle-treated sides showed either no change or continued hair loss.
  • In vitro cell viability assay showed that lymphocytes were much more sensitive to the cytotoxic effects of mechlorethamine than skin and hair follicular cells.
  • RNase protection assay and real-time reverse transcription polymerase chain reaction showed that tumor necrosis factor alpha/beta, interleukin-12, and interferon-gamma were inhibited by mechlorethamine upon successful treatment.
  • [MeSH-major] Alkylating Agents / administration & dosage. Alopecia Areata / drug therapy. Alopecia Areata / physiopathology. Autoimmune Diseases / drug therapy. Autoimmune Diseases / physiopathology. Hair Follicle / physiopathology. Lymphocytes / drug effects. Mechlorethamine / administration & dosage
  • [MeSH-minor] Animals. Cell Movement. Interferon-gamma / antagonists & inhibitors. Interleukin-12 / antagonists & inhibitors. Lymphotoxin-alpha / antagonists & inhibitors. Mice. Mice, Inbred C3H. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • Hazardous Substances Data Bank. NITROGEN MUSTARD N-OXIDE HYDROCHLORIDE .
  • Hazardous Substances Data Bank. MECHLORETHAMINE .
  • Hazardous Substances Data Bank. MECHLORETHAMINE HYDROCHLORIDE .
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  • (PMID = 12603852.001).
  • [ISSN] 0022-202X
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR43801
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Lymphotoxin-alpha; 0 / Tumor Necrosis Factor-alpha; 187348-17-0 / Interleukin-12; 50D9XSG0VR / Mechlorethamine; 82115-62-6 / Interferon-gamma
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18. Yi HS, Sym SJ, Park J, Cho EK, Ha SY, Shin DB, Lee JH: Recurrent and metastatic trichilemmal carcinoma of the skin over the thigh: a case report. Cancer Res Treat; 2010 Sep;42(3):176-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Trichilemmal carcinoma (TC) is an uncommon cutaneous neoplasm that develops from the external root sheath of the hair follicle.
  • We report here on a case of metastatic TC in the skin over the thigh, and this tumor was treated with cisplatin and cyclophosphamide combination chemotherapy.

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  • (PMID = 20948924.001).
  • [ISSN] 2005-9256
  • [Journal-full-title] Cancer research and treatment : official journal of Korean Cancer Association
  • [ISO-abbreviation] Cancer Res Treat
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2953782
  • [Keywords] NOTNLM ; Lymphatic metastasis / Palliative care / Skin neoplasms
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19. Luistro L, He W, Smith M, Packman K, Vilenchik M, Carvajal D, Roberts J, Cai J, Berkofsky-Fessler W, Hilton H, Linn M, Flohr A, Jakob-Røtne R, Jacobsen H, Glenn K, Heimbrook D, Boylan JF: Preclinical profile of a potent gamma-secretase inhibitor targeting notch signaling with in vivo efficacy and pharmacodynamic properties. Cancer Res; 2009 Oct 01;69(19):7672-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RO4929097 is a potent and selective inhibitor of gamma-secretase, producing inhibitory activity of Notch signaling in tumor cells.
  • The RO4929097 IC50 in cell-free and cellular assays is in the low nanomolar range with >100-fold selectivity with respect to 75 other proteins of various types (receptors, ion channels, and enzymes).
  • RO4929097 inhibits Notch processing in tumor cells as measured by the reduction of intracellular Notch expression by Western blot.
  • RO4929097 does not block tumor cell proliferation or induce apoptosis but instead produces a less transformed, flattened, slower-growing phenotype.
  • In addition, comparative microarray analysis suggests tumor cell differentiation as an additional mode of action.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Benzazepines / pharmacology. Neoplasms / drug therapy. Protease Inhibitors / pharmacology. Receptors, Notch / metabolism
  • [MeSH-minor] Animals. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / enzymology. Carcinoma, Non-Small-Cell Lung / metabolism. Cell Line, Tumor. Hair Follicle / drug effects. Hair Follicle / metabolism. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / enzymology. Lung Neoplasms / metabolism. Mice. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Signal Transduction / drug effects. Transcription, Genetic / drug effects. Xenograft Model Antitumor Assays


20. Amoh Y, Katsuoka K, Hoffman RM: Color-coded fluorescent protein imaging of angiogenesis: the AngioMouse models. Curr Pharm Des; 2008;14(36):3810-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have utilized multicolored fluorescent proteins to develop three imaging models of tumor angiogenesis.
  • In one model, the nonluminous induced capillaries are clearly visible by contrast against the very bright tumor green fluorescent protein (GFP) fluorescence examined either intravitally or by whole-body imaging in real time.
  • Intravital images of an orthotopic model of human pancreatic tumors expressing GFP visualized angiogenic capillaries at both primary and metastatic sites.
  • Opening a reversible skin-flap in the light path markedly reduces signal attenuation, increasing detection sensitivity many-fold and enables vessels to be externally visualized in GFP-expressing tumors growing on internal organs.
  • In another model, dual-color fluorescence imaging was effected by using red fluorescent protein (RFP)-expressing tumors growing in GFP-expressing transgenic mice that express GFP in all cells.
  • This dual-color model visualizes with great clarity the details of the tumor-stroma interaction, especially tumor-induced angiogenesis.
  • The GFP-expressing tumor vasculature, both nascent and mature, are readily distinguished interacting with the RFP-expressing tumor cells.
  • RFP-expressing tumors transplanted to nestin-GFP mice enable specific visualization of nascent vessels.
  • We also observed, using ND-GFP mice, that the hair follicle is angiogenic and that the hair-follicle vascular network is a prime target for chemotherapy drugs which cause hair loss (chemotherapy-induced alopecia).
  • [MeSH-minor] Animals. Hair. Intermediate Filament Proteins / genetics. Mice. Mice, Nude. Mice, Transgenic. Neoplasms, Experimental / blood supply. Nerve Tissue Proteins / genetics. Nestin. Stem Cells

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  • (PMID = 19128234.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 099258; United States / NCI NIH HHS / CA / CA 101600; United States / NCI NIH HHS / CA / CA 103563
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 147336-22-9 / Green Fluorescent Proteins
  • [Number-of-references] 58
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21. Gupta P, Freyschmidt-Paul P, Vitacolonna M, Kiessling S, Hummel S, Hildebrand D, Marhaba R, Zöller M: A chronic contact eczema impedes migration of antigen-presenting cells in alopecia areata. J Invest Dermatol; 2006 Jul;126(7):1559-73

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Long-lasting allergen treatment is the most efficient therapy in alopecia areata (AA).
  • We here asked whether treatment with a contact sensitizer influences leukocyte migration such that dendritic cell (DC) migration or the recruitment of activated T-cells towards the skin become hampered.
  • Allergen treatment of AA mice was not accompanied by a decrease in skin-infiltrating leukocytes or draining lymph node cells (LNC).
  • However, FITC labelling of the skin and subcutaneous transfer of dye-labelled DC revealed that allergen treatment created a chemokine milieu severely hampering DC migration from the skin towards the draining node.
  • An allergic eczema-induced reduction in DC migration and antigen transfer could well contribute to insufficient T-cell activation and the recovery of hair follicle in AA and possibly be of relevance for other skin-related autoimmune diseases.
  • [MeSH-minor] Animals. Cell Adhesion Molecules / physiology. Chemokines / metabolism. Chronic Disease. Cyclobutanes / pharmacology. Dendritic Cells, Follicular / immunology. Dendritic Cells, Follicular / pathology. Dendritic Cells, Follicular / physiology. Female. Gene Expression Regulation / drug effects. Hair Follicle / immunology. Leukocytes / immunology. Lymph Nodes / cytology. Lymph Nodes / immunology. Mice. Mice, Inbred C3H. Receptors, Chemokine / physiology. Skin / cytology. Skin / immunology. T-Lymphocytes / immunology

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  • (PMID = 16675965.001).
  • [ISSN] 0022-202X
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Chemokines; 0 / Cyclobutanes; 0 / Receptors, Chemokine; 4RTO57VG65 / squaric acid dibutyl ester
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22. Michard Q, Jaouen G, Vessieres A, Bernard BA: Evaluation of cytotoxic properties of organometallic ferrocifens on melanocytes, primary and metastatic melanoma cell lines. J Inorg Biochem; 2008 Nov;102(11):1980-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • After a long incubation time the latter is highly toxic for malignant cells but not for normal cells while the former was very highly toxic for primary malignant cells and significantly less toxic for normal cells.
  • Finally, investigation on hair follicle growth revealed that the two organometallic derivatives induced an irreversible ejection of the hair shaft, thus predicting a potential hair loss side effect if used as a chemotherapeutic treatment.
  • [MeSH-major] Antineoplastic Agents / toxicity. Ferrous Compounds / toxicity. Melanocytes / drug effects. Melanoma / drug therapy
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Cell Survival. Drug Evaluation, Preclinical. Hair Follicle / drug effects. Humans. Neoplasm Metastasis / pathology. Organometallic Compounds / toxicity. Oxidative Stress

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  • (PMID = 18783831.001).
  • [ISSN] 1873-3344
  • [Journal-full-title] Journal of inorganic biochemistry
  • [ISO-abbreviation] J. Inorg. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ferrous Compounds; 0 / Organometallic Compounds; 0 / ferrocifen; 0 / ferrociphenol
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