George Lipkin, M.D.

Pseudoxanthoma elasticum
Gonzalez, Mercedes E; Votava, Henry J; Lipkin, George; Sanchez, Miguel
2009 ;15(8):17-17, Dermatology online journal
Pseudoxanthoma elasticum is an incurable, autosomal-recessive, genetic disorder that is caused by mutations in the ABCC6 gene. It is characterized by progressive mineralization and fragmentation of the elastic fibers in the skin, retina, and blood vessels. The characteristic cutaneous features bring the patient to medical attention, but morbidity is related to the degree of extracutaneous involvement. The disease is progressive with phenotypic variability and no definite genotype-phenotype correlation. Treatment is supportive and is directed at prevention and early detection of adverse ocular and cardiovascular sequelae. We present two siblings with pseudoxanthoma elasticum, who have considerable differences in disease related morbidity, which highlights intra-familiar phenotypic heterogeneity
— id: 107815, year: 2009, vol: 15, page: 17, stat: Journal Article,

Plasticity of the cancer cell: implications for epigenetic control of melanoma and other malignancies
Lipkin, George
2008 Sep;128(9):2152-2155, Journal of investigative dermatology
Current treatments of many advanced malignancies, including melanoma, have failed to significantly reduce mortality rates, necessitating newer approaches. There is now abundant evidence that cancer cells, given the appropriate environmental and molecular context, are capable of remarkable plasticity, including complete reversal of the malignant phenotype. Such reprogramming involves both extrinsic and intrinsic factors and can occur via three routes: perturbations of extracellular matrix-cell receptor interactions, modulation of intracellular signaling pathways, and exploitation of epigenetic inheritance. Studies demonstrate the potential for producing dramatic changes in structural, biochemical, immunological, and functional properties of a broad spectrum of tumor cell types, including melanoma, leading to growth arrest, differentiation, senescence, or self destruction. Translating the promise inherent in tumor cell plasticity to the clinical arena remains a major challenge, but it is likely that a variety of epigenetic methods will play an increasingly important and effective role in the future control of malignant melanoma and other cancers
— id: 83100, year: 2008, vol: 128, page: 2152, stat: Journal Article,

Acral dermatoses
Lipkin G
Current dermatologic diagnosis & treatment Philadelphia : Lippincott Williams & Wilkins, 2001,
— id: 3668, year: 2001, vol: , page: 6, stat: Chapter,

Making room for high-risk ideas
Lipkin G
2000 Jan;136(1):67-67, Archives of dermatology
— id: 11866, year: 2000, vol: 136, page: 67, stat: Journal Article,

A tribute to Bernie
Baer RL; Bystryn JC; Cohen D; Curwin J; Freedberg IM; Kopf AW; Lipkin G; Podwal M; Shupack J
1994 Feb;16(1):89-96, American journal of dermatopathology
— id: 16106, year: 1994, vol: 16, page: 89, stat: Journal Article,

MODULATION OF MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGENS ACCOMPANIES REVERSION OF MALIGNANT-MELANOMA PHENOTYPE BY CONTACT INHIBITORY FACTOR
LIPKIN, G; MERUELO, D
1992 APR ;40(2):A528-A528, Clinical research
— id: 52018, year: 1992, vol: 40, page: A528, stat: Journal Article,

MODULATION OF MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGENS ACCOMPANIES REVERSION OF MALIGNANT-MELANOMA PHENOTYPE BY CONTACT INHIBITORY FACTOR
LIPKIN, G; MERUELO, D
1992 APR ;98(4):643-643, Journal of investigative dermatology
— id: 52034, year: 1992, vol: 98, page: 643, stat: Journal Article,

Castleman's tumor and erosive lichen planus: coincidence or association?Report of a case
Ashinoff R; Cohen R; Lipkin G
1989 Nov;21(5 Pt 2):1076-1080, Journal of the American Academy of Dermatology
The rare association of severe erosive lichen planus and Castleman's tumor is presented. Castleman's tumor, or giant lymph node hyperplasia, is a benign neoplasm resembling thymic tumors and is associated with several immunologic abnormalities. Lichen planus also is associated with immunologic defects. One hypothesis linking these two diseases is that lymphocytes may become sensitized to tumor antigens on the Castleman's tumor and attack cross-reacting structures in the skin and other stratified squamous mucosae to produce the clinical picture of lichen planus
— id: 10433, year: 1989, vol: 21, page: 1076, stat: Journal Article,

CONTACT INHIBITORY FACTOR (CIF) INDUCES MORPHOLOGIC REORGANIZATION IN MOUSE MALIGNANT-MELANOMA AND KIRSTEN SARCOMA VIRUS-TRANSFORMED RAT FIBROBLAST CELLS
HIGGINS, PJ; LIPKIN, G; ROSENBERG, M
1988 APR ;36(3):A655-A655, Clinical research
— id: 41796, year: 1988, vol: 36, page: A655, stat: Journal Article,

CONTACT INHIBITORY FACTOR (CIF) INDUCES MORPHOLOGIC REORGANIZATION IN MOUSE MALIGNANT-MELANOMA AND KIRSTEN SARCOMA VIRUS-TRANSFORMED RAT FIBROBLAST CELLS
HIGGINS, PJ; LIPKIN, G; ROSENBERG, M
1988 APR ;90(4):569-569, Journal of investigative dermatology
— id: 41804, year: 1988, vol: 90, page: 569, stat: Journal Article,

CAN MODULATION OF THE MALIGNANT PHENOTYPE BY AN ENDOGENOUS INHIBITOR LEAD TO TUMOR-REGRESSION INVIVO
LIPKIN, G; ROSENBERG, M; FASS, E
1988 APR ;65(4):462-&, Journal of the American Oil Chemists Society
— id: 41779, year: 1988, vol: 65, page: 462, stat: Journal Article,

Contact-inhibitory factor induces alterations in the distribution and content of specific cytoskeletal elements in an established line of rat hepatic tumor cells
Higgins PJ; Lipkin G; Rosenberg M; Ryan MP
1987 Dec 15;40(6):792-801, International journal of cancer
Established 72/22 rat hepatic epithelial tumor cells, which possess intracellular aggregates of intermediate-sized filaments resembling Mallory-body-like inclusions, were used to assess changes in tumor cell growth and morphology associated with exposure to contact-inhibitory factor (CIF). CIF reduced 72/22 proliferative rate, increased mean population doubling time by 42%, lowered culture saturation densities to 34-50% of control values and inhibited formation of dense foci. These proliferative changes were due to an apparent prolongation of the G1 phase of the cell cycle during the period of CIF exposure. CIF concomitantly induced a marked increase (by 70%) in cell spreading and loss of both the usual tight (epithelioid) cell juxtaposition and typical ordered colony structure characteristic of untreated populations. However, CIF exposure failed to achieve complete cytoarchitectural 'normalization' in 72/22 cells (i.e., dispersal of the Mallory-body-like aggregate of intermediate filaments and restoration of a more typical hepatocytic phenotype). Most obvious was a reduction in the integrity of the peripheral band of microfilaments (a structure involved in the maintenance of epithelial cell shape) and a decrease in the content of desmoplakin (a protein component of desmosomal plaques). Changes in these major structural elements appear to be critical events in development of the pleomorphic phenotype and reduced substratum adhesiveness observed during treatment. CIF-related fragmentation of peripheral band structures was not reflected in changes in either the total cellular or cytoskeletal-associated actin contents. The morphologic changes observed under conditions of CIF exposure closely paralleled induced decreases in the cellular content of the actin-associated membrane skeleton protein p35. These data collectively suggest that CIF may act to alter the composition of the cortical skeleton in cultured liver tumor cells
— id: 18494, year: 1987, vol: 40, page: 792, stat: Journal Article,

Liposome-entrapped contact inhibitory factor: transfer of capacity for density-dependent growth to melanoma cells
Fass, E; Lipkin, G; Rosenberg, M
1986 Sep;87(3):309-312, Journal of investigative dermatology
Contact inhibitory factor (CIF) is a growth inhibitor obtained from conditioned culture medium of a contact-inhibited line of hamster melanocytic cells, which reversibly restores density-, anchorage-, and serum-dependent growth to melanoma cells. The usefulness of liposomes as carriers for CIF was investigated in vitro. The stability of liposomes prepared both with and without CIF was demonstrated by measuring the rate of efflux of a K2CrO4 marker. Anionic multilamellar lipid vesicles (7 phosphatidylcholine:2 dicetyl phosphate:1 cholesterol) prepared with CIF-containing material and separated from unentrapped CIF by gel filtration on Sepharose 2B, showed retarded leakage of a K2CrO4 marker (half-efflux at 77 h) when compared with identical liposomes lacking CIF (half-efflux at 40 h). When added to subconfluent cultures of hamster melanoma cells, liposome-entrapped CIF restored contact-inhibited growth. Compared with aqueous solutions of CIF, liposome-CIF effects were characterized by longer latency and more sustained duration. The ability of CIF-bearing liposomes to effectively restore density-dependent growth in vitro should facilitate in vivo studies of the effects of this potent growth inhibitor on melanoma and other neoplasms
— id: 67448, year: 1986, vol: 87, page: 309, stat: Journal Article,

Contact inhibitory factor also restores anchorage and serum dependence to hamster melanoma cells
Lipkin G; Rosenberg M; Klaus-Kovtun V
1986 Sep;87(3):305-308, Journal of investigative dermatology
Conditioned medium (CM) from confluent cultures of the contact-inhibited hamster melanocytic cell line, FF, contains a biologic activity, contact inhibitory factor (CIF), which reversibly restores density-dependent growth to melanoma cells. When a hydrophobic affinity-concentrated extract of CIF-containing CM was incorporated in agarose at a concentration of 1000 micrograms protein/ml, it restored anchorage-dependent growth to RPMI 1846 hamster melanoma cells. Colony-forming efficiency in CIF-treated wells decreased to 5% from levels of 51.5% in controls prepared with regular growth medium. In addition, CIF-containing CM restored serum-dependent growth to RPMI 1846 cells, markedly restricting proliferation in 1% calf serum-containing medium. Control cultures containing 1% calf serum and either complete growth medium or CM from the non-contact-inhibited hamster melanoma line itself, supported proliferation of RPMI 1846 cells to levels 3.9 X and 3.7 X that of CIF-treated cultures, respectively. CIF is the first factor derived from contact-inhibited mammalian cell cultures that has been shown to restore density-, anchorage-, and serum-dependent growth to malignant melanoma cells
— id: 16604, year: 1986, vol: 87, page: 305, stat: Journal Article,

Susceptibility to NK cell lysis is abolished in tumor cells by a factor which restores their contact inhibited growth
Nabi ZF; Zucker-Franklin D; Lipkin G; Rosenberg M
1986 Oct 1;58(7):1461-1465, Cancer
It is well recognized that physical contact between natural killer (NK) cells and tumor targets is necessary for cell lysis. Therefore, any modulation of the tumor cell surface that alters intercellular contact could affect NK cell cytotoxicity. To examine this hypothesis, a contact inhibitory factor (CIF), which had been shown to restore contact inhibition of growth to several malignant cell lines was tested for its ability to render such cells immune to recognition by NK cells. When three NK-sensitive melanoma and two NK-sensitive colon carcinoma targets were cultured with CIF, they did not only change morphologically, but also showed a 70% to 95% reduction in their sensitivity to lysis by NK cells. In addition, K562 cells, which grow in suspension and do not permit a morphologic evaluation of the CIF effect, also became resistant to lysis by NK cells after culture with CIF. CIF did not reduce the viability nor the cytotoxicity of NK cells. CIF did not contain interferon nor did the CIF-treated targets induce the production of interferon during the cytotoxicity assay. It is concluded that restoration of contact inhibition of growth and resistance to NK cell lysis are cell surface phenomena that may run in parallel
— id: 15723, year: 1986, vol: 58, page: 1461, stat: Journal Article,

CONTACT INHIBITED GROWTH RENDERS TUMOR-CELLS RESISTANT TO NATURAL-KILLER CELL-LYSIS
ZUCKERFRANKLIN, D; LIPKIN, G; NABI, ZF; ROSENBERG, M
1986 APR ;34(2):A728-A728, Clinical research
— id: 41414, year: 1986, vol: 34, page: A728, stat: Journal Article,

Vitiligo-related pigment cell differentiation antigens are expressed on malignant melanoma cells following phenotypic reversion induced by contact inhibitory factor
Lipkin G; Naughton GK; Rosenberg M; Bystryn JC
1985 ;30(1):35-39, Differentiation
Most vitiligo sera contain antibodies to surface antigens on pigmented human melanocytes but not to human or mouse amelanotic melanoma cells. A density-dependent line of hamster amelanotic melanocytic cells (FF) produces a diffusible factor (CIF) which restores contact inhibition of growth as well as several other normal phenotypic characteristics to hamster, murine, and human melanoma cells. The ability of CIF to induce the expression of a phenotypic characteristic of pigmented human melanocytic cells, i.e., the vitiligo-related surface antigens, on hamster and mouse amelanotic melanoma cells was investigated. Vitiligo and normal sera were reacted with CIF-treated and untreated hamster and mouse amelanotic melanoma cells for both indirect-immunofluorescence assays and ELISA. Immunofluorescence testing showed that about 80% of hamster and mouse melanoma cells had pigment-cell antigens (in the absence of pigmentation) in a granular surface pattern after, but not prior to, CIF-induced morphologic reversion and confluent growth. Less than 5% of the control hamster and mouse melanoma cells expressed such antigens at confluence. These results were confirmed by ELISA. Metabolic-labeling studies with 35S-methionine showed that the vitiligo antigens were synthesized by the CIF-treated melanoma cells. The slowing of melanoma cell proliferation in isoleucine-deficient medium failed to elicit the expression of vitiligo antigens. Since antigen appearance following phenotypic reversion occurred without pigment induction, it is concluded that vitiligo-related surface antigens and pigmentation are distinct aspects of a differentiated function which may be non-coordinately expressed. The expression of pigment-cell differentiation antigens on amelanotic melanoma cells is an additional feature of the pleiotypic trans-species response to CIF
— id: 57429, year: 1985, vol: 30, page: 35, stat: Journal Article,

EXPRESSION OF VITILIGO-RELATED PIGMENT CELL-DIFFERENTIATION ANTIGENS ON MELANOMA-CELLS AFTER PHENOTYPIC REVERSION BY CONTACT INHIBITORY FACTOR
Lipkin, G; Naughton, GK; Rosenberg, M; Bystryn, JC
1985 ;33(2):A662-A662, Clinical research
— id: 30756, year: 1985, vol: 33, page: A662, stat: Journal Article,

EXPRESSION OF VITILIGO-RELATED PIGMENT CELL-DIFFERENTIATION ANTIGENS ON MELANOMA-CELLS AFTER PHENOTYPIC REVERSION BY CONTACT INHIBITORY FACTOR
Lipkin, G; Naughton, GK; Rosenberg, M; Bystryn, JC
1985 ;84(4):295-295, Journal of investigative dermatology
— id: 30765, year: 1985, vol: 84, page: 295, stat: Journal Article,

Alpha 1-antitrypsin deficiency genes: contributory defect in a subset of psoriatics?
Lipkin G; Galdston M; Kueppers F
1984 Oct;11(4 Pt 1):615-619, Journal of the American Academy of Dermatology
Since proteolytic processes are prominent in psoriasis, sera of forty-five psoriatics were examined for alpha 1-antitrypsin (alpha 1-AT) phenotype and eighteen sera, for alpha 1-AT content and function. Five sera (11.1%) had heterozygous phenotypes (2 MZ and 3 MS), a prevalence of Z and S variants similar to that reported in nonpsoriatic populations. Two of three variants examined for content and function exhibited marked reductions. Since MZ heterozygotes are almost always, and MS phenotypes sometimes, associated with decreased serum alpha 1-AT levels, and since Z and MZ phenotypes are associated with increased hepatic fibrosis or cirrhosis, these variants may be relevant to problems of spontaneous fibrosis or methotrexate-induced hepatotoxicity in psoriasis. alpha 1-AT deficiency may also contribute to guttate flares with infection and to increased O-2 . production by psoriatic sera-stimulated polymorphonuclear leukocytes (PMNs). Although no evidence exists that psoriasis is more prevalent among persons with hypomorphic alpha 1-AT phenotypes, such defects may contribute to severity of inflammation and hyperplasia
— id: 16605, year: 1984, vol: 11, page: 615, stat: Journal Article,

ALPHA-1-ANTITRYPSIN DEFICIENCY GENES IN A SUBSET OF PSORIATICS
LIPKIN, G; GALDSTON, M; KUEPPERS, F
1984 ;32(3):A713-A713, Clinical research
— id: 40780, year: 1984, vol: 32, page: A713, stat: Journal Article,

ALPHA-1-ANTITRYPSIN DEFICIENCY GENES IN A SUBSET OF PSORIATICS
LIPKIN, G; KUEPPERS, F
1984 ;32(2):A599-A599, Clinical research
— id: 40840, year: 1984, vol: 32, page: A599, stat: Journal Article,

EXPRESSION OF VITILIGO-RELATED PIGMENT CELL-DIFFERENTIATION ANTIGENS ON MELANOMA-CELLS AFTER PHENOTYPIC REVERSION BY CONTACT INHIBITORY FACTOR
LIPKIN, G; NAUGHTON, GK; ROSENBERG, M; BYSTRYN, JC
1984 ;32(3):A713-A713, Clinical research
— id: 40781, year: 1984, vol: 32, page: A713, stat: Journal Article,

Expression of vitiligo antigen on a revertant line of hamster melanoma cells
Naughton GK; Lipkin G; Bystryn JC
1984 Nov;83(5):317-319, Journal of investigative dermatology
Our laboratory has recently reported that over 80% of patients with common vitiligo have circulating antibodies to cell-surface antigens on normal human melanocytes. The slow growth rate of these cells limits the assays that can be performed for antibody detection. We now have found that the antigens defined by vitiligo sera on melanocytes are also expressed on FF cells, a revertant line of hamster melanoma cells. These antigens can be detected both by indirect immunofluorescence and specific immunoprecipitation assays. The presence of 'vitiligo' antigens on hamster FF cells will aid further study of the abnormal immune response in vitiligo
— id: 16261, year: 1984, vol: 83, page: 317, stat: Journal Article,

INDUCTION OF PHENOTYPIC CHANGE BY CONTACT INHIBITORY FACTOR
Lipkin, G; Rosenberg, M
1981 ;60(4):341-342, Bollettino della'Instituto Sieroterapico Milanese
— id: 30509, year: 1981, vol: 60, page: 341, stat: Journal Article,

Malignancy in controlled regression. A new aspect of pathology
Lipkin G
1980 Spring;2(1):75-77, American journal of dermatopathology
— id: 16606, year: 1980, vol: 2, page: 75, stat: Journal Article,

A potent inhibitor of normal and transformed cell growth derived from contact-inhibited cells
Lipkin G; Knecht ME; Rosenberg M
1978 Mar;38(3):635-643, Cancer research
— id: 16608, year: 1978, vol: 38, page: 635, stat: Journal Article,

Glycoprotein-containing factor that mediates contact inhibition of growth
Lipkin G; Knecht ME; Rosenberg M
1978 Jun 20;312(1):382-391, Annals of the New York Academy of Sciences
— id: 16607, year: 1978, vol: 312, page: 382, stat: Journal Article,

Biochemical studies of a protein which restores contact inhibition of growth to malignant melanocytes
Knecht ME; Lipkin G
1977 Aug;108(1):15-22, Experimental cell research
— id: 16610, year: 1977, vol: 108, page: 15, stat: Journal Article,

BIOCHEMICAL STUDIES OF A PROTEIN WHICH RESTORES CONTACT INHIBITION OF GROWTH TO MALIGNANT MELANOCYTES
Knecht, ME; Lipkin, G
1977 ;18(MAR):142-142, Proceedings (American Association for Cancer Research)
— id: 29587, year: 1977, vol: 18, page: 142, stat: Journal Article,

Restoration of in vitro growth control to malignant cells
Lipkin G; Knecht ME; Rosenberg M
1977 Nov;40(5 Suppl):2699-2705, Cancer
A glycoprotein (molecular weight, ca. 160,000) from culture medium of contact-inhibited hamster melanocytes restores contact inhibition of growth to malignant melanocytes of man, mouse, and hamsters, and also effectively inhibits growth in vitro of a broad spectrum of malignant and normal cell types of ectodermal, mesodermal and endodermal origins, including human colon carcinomas. The melanocyte contact inhibitory factor (MCIF) produces G1 growth arrest in malignant melanocytes; inhibition of all cell types is reversible, does related, and nontoxic at concentrations below 200 microgram/ml, but selectively lethal to malignant cells at higher concentrations. An electrophoretically identical protein is present in culture media of contact-inhibited melanocytes, fibroblasts, and epidermal cells, but absent from those of colon carcinomas, HeLa cells and malignant melanomas. Nevertheless, an MCIF-like band is present in whole cell homogenates of human colon carcinomas and hamster melanomas. MCIF may permit normal surface interactions required for feedback inhibition of growth
— id: 16609, year: 1977, vol: 40, page: 2699, stat: Journal Article,

Contact inhibition of growth is restored to malignant melanocytes of man and mouse by a hamster protein
Lipkin G; Knecht ME
1976 Oct 15;102(2):341-348, Experimental cell research
— id: 16611, year: 1976, vol: 102, page: 341, stat: Journal Article,

Factors affecting growth of normal and malignant cells in vitro
Lipkin G; Rosenberg M; Knecht ME
1976 Jun 15;25(12):1333-1337, Biochemical pharmacology
— id: 16612, year: 1976, vol: 25, page: 1333, stat: Journal Article,

POTENT INHIBITOR OF NORMAL AND TRANSFORMED-CELL GROWTH DERIVED FROM CONTACT INHIBITED MELANOCYTES
Lipkin, G; Knecht, ME
1976 ;24(3):A494-A494, Clinical research
— id: 28761, year: 1976, vol: 24, page: A494, stat: Journal Article,

POTENT INHIBITOR OF NORMAL AND TRANSFORMED-CELL GROWTH DERIVED FROM CONTACT-INHIBITED MELANOCYTES
Lipkin, G; Knecht, ME
1976 ;66(4):280-280, Journal of investigative dermatology
— id: 28772, year: 1976, vol: 66, page: 280, stat: Journal Article,

BIOCHEMICAL ASPECTS OF A PROTEIN WHICH RESTORES CONTACT INHIBITION OF GROWTH TO MALIGNANT MELANOCYTES
Knecht, ME; Lipkin, G
1975 ;23(3):A452-A452, Clinical research
— id: 28545, year: 1975, vol: 23, page: A452, stat: Journal Article,

BIOCHEMICAL ASPECTS OF A PROTEIN WHICH RESTORES CONTACT INHIBITION OF GROWTH TO MALIGNANT MELANOCYTES
Knecht, ME; Lipkin, G
1975 ;64(3):211-211, Journal of investigative dermatology
— id: 28572, year: 1975, vol: 64, page: 211, stat: Journal Article,

[Restoration of growth contact inhibition in malignant melanocytes from man, mice, and hamsters]
Lipkin G; Knecht ME
1975 Oct 18;105(42):1360-1364, Schweizerische medizinische wochenschrift = Journal suisse de medecine
Contact inhibition of growth is the in vitro property whose loss is most closely correlated with in vivo tumorigenicity. A contact inhibited line of hamster melanocytes produces a diffusible high molecular weight protein (melanocyte contact inhibitory factor, MCIF) which restores contact inhibition of growth to hamster malignant melanocytes. MCIF, extracted from culture medium of confluent contact-inhibited cultures, is now shown to restore the same capacity for in vitro growth regulation to malignant melanocytes of human and murine origins. In all 3 species MCIF produces characteristic changes in growth and morphology of cultures, with significant reductions of saturation densities. MCIF, the first protein identified which restores contact inhibition of growth to malignant cells, may be the prototype for a closely related class of surface-associated proteins concerned with regulation of normal cell-cell interactions leading to feedback inhibition of growth
— id: 16613, year: 1975, vol: 105, page: 1360, stat: Journal Article,

CONTACT INHIBITION OF GROWTH - RESTORATION IN MALIGNANT MELANOCYTES OF MAN, MOUSE, AND HAMSTER
Lipkin, G; Knecht, ME
1975 ;23(3):A453-A453, Clinical research
— id: 28546, year: 1975, vol: 23, page: A453, stat: Journal Article,

CONTACT INHIBITION OF GROWTH - RESTORATION IN MALIGNANT MELANOCYTES OF MAN, MOUSE, AND HAMSTER
Lipkin, G; Knecht, ME
1975 ;64(3):211-212, Journal of investigative dermatology
— id: 28573, year: 1975, vol: 64, page: 211, stat: Journal Article,

HAMSTER MELANOCYTE CONTACT-INHIBITORY FACTOR (MCIF) - EFFECTS TRANSCEND TISSUE AND SPECIES BARRIERS
Lipkin, G; Knecht, ME
1975 ;16(MAR):140-140, Proceedings (American Association for Cancer Research)
— id: 28667, year: 1975, vol: 16, page: 140, stat: Journal Article,

[Proceeding a protein factor re-establishing the contact-inhibition of hamster melanoma cells in vitro]
Knecht M; Lipkin G
1974 ;148(5):275-275, Dermatologica
— id: 16615, year: 1974, vol: 148, page: 275, stat: Journal Article,

A diffusible factor restoring contact inhibition of growth to malignant melanocytes
Lipkin G; Knecht ME
1974 Mar;71(3):849-853, Proceedings of the National Academy of Sciences of the United States of America
— id: 16614, year: 1974, vol: 71, page: 849, stat: Journal Article,

MELANOCYTE CONTACT-INHIBITORY FACTOR (MCIF) - TRANSFER OF NORMAL IN-VITRO GROWTH-CONTROL TO HAMSTER MALIGNANT MELANOCYTES
Lipkin, G; Knecht, ME
1974 ;15(MAR):61-61, Proceedings (American Association for Cancer Research)
— id: 28452, year: 1974, vol: 15, page: 61, stat: Journal Article,

Pigment transformation and induction
Lipkin G
1973 Jun;60(6):381-398, Journal of investigative dermatology
— id: 16616, year: 1973, vol: 60, page: 381, stat: Journal Article,

PIGMENT INDUCTION IN SYNCHRONIZED AMELANOTIC MELANOCYTES BY SYNTHETIC RNA, A HALOGENATED THYMIDINE ANALOG, AND DMSO
Lipkin, G; Hodgins, LT
1973 ;46(5):710-711, Yale journal of biology & medicine
— id: 28465, year: 1973, vol: 46, page: 710, stat: Journal Article,

Pigment transformation and induction in hamster malignant amelanotic melanocytes. An effect of nucleic acids from hamster benign blue nevus
Lipkin, G
1971 Jul;57(1):49-65, Journal of investigative dermatology
— id: 16617, year: 1971, vol: 57, page: 49, stat: Journal Article,

Studies of the lipids of dog skin. IV. The in vivo incorporation of blood lipids into the lipids of isolated perfused dog skin
Lipkin G; Wheatley VR; Woo TH; March C
1968 Jun;50(6):456-458, Journal of investigative dermatology
— id: 16619, year: 1968, vol: 50, page: 456, stat: Journal Article,

Influence of anti-lymphocyte serum on malignant melanoma
Wolf-Jurgensen P; Kopf AW; Lipkin G; Bart RS
1968 Dec;51(6):441-444, Journal of investigative dermatology
— id: 16618, year: 1968, vol: 51, page: 441, stat: Journal Article,

Lipogenesis from amino acids in perfused isolated dog skin
Wheatley VR; Lipkin G; Woo TH
1967 Mar;8(2):84-89, Journal of lipid research
Lipogenesis from amino acids has been studied in isolated perfused dog skin. Uniformly labeled alanine-(14)C, glycine-(14)C, isoleucine-(14)C, leucine-(14)C, phenylalanine-(14)C, and valine-(14)C are all incorporated into the cutaneous lipids, with significant incorporation into most of the isolated lipid fractions. Efficiency of lipogenesis has been expressed relative to the extent of incorporation of acetate under the same experimental conditions. This efficiency was highest for the three branched-chain amino acids. The accuracy, uses, and limitations of the perfusion technique for the study of cutaneous lipogenesis have been evaluated
— id: 39028, year: 1967, vol: 8, page: 84, stat: Journal Article,

Studies of the lipids of dog skin. 3. The in vivo incorporation of acetate, pyruvate, and certain amino acids into the lipids of isolated perfused dog skin
Lipkin G; Wheatley VR; March C
1965 Nov;45(5):356-361, Journal of investigative dermatology
— id: 16620, year: 1965, vol: 45, page: 356, stat: Journal Article,

CHANGING PATTERNS OF SENSITIVITY TO COMMON CONTACT ALLERGENS
BAER RL; LIPKIN G; KANOF NB; BIONDI E
1964 Jan;89:3-8, Archives of dermatology
— id: 60073, year: 1964, vol: 89, page: 3, stat: Journal Article,

SKIN COPPER LEVELS IN PSORIASIS
LIPKIN, G; GOWDEY, J; WHEATLEY, V R
1964 Feb;42:205-207, Journal of investigative dermatology
— id: 124569, year: 1964, vol: 42, page: 205, stat: Journal Article,