Mary Wigman, Szenenfoto

Signatur des Originals: S 36/F11926

Mary Wigman, Szenenfoto

Signatur des Originals: S 36/F11927

Alice Barbi, Brustbild

Signatur des Originals: S 36/G00345

Alice Barbi, Brustbild

Signatur des Originals: S 36/G00346

Alice Barbi, Brustbild

Signatur des Originals: S 36/G00347

Mary Ann Wilson, Hüftbild

Signatur des Originals: S 36/G02530

Mary Wurm, Brustbild

Signatur des Originals: S 36/G02543

Mary Wurm, Brustbild

Signatur des Originals: S 36/G02544

Robert il Diavolo, Act I., Scene 4 : Alice: Più non vie. Roberto: Che intendo! Ah madre! io gelo. ; Alice: She is no more. Robert: What! my mother? O torture.

Signatur des Originals: S 36/G03301

Na 1 Nachlass Max Horkheimer, 562 - Korrespondenzen u.a. mit Alice H. Maier und Leo Löwenthal (p. VI 26, 170-409)

Briefwechsel zwischen Alice H. Maier und Max Horkheimer; 3 Briefe zwischen Adolf Sturmthal und Alice H. Maier, 1951; 1 Brief von Alice H. Maier an Hattie Ross, 25.09.1951; 1 Brief an Franz Neumann von Alice H. Maier, 20.08.1951; 1 Brief von Alice H. Maier an Friede Fromm-Reichmann, 20.08.1951; 1 Brief an Leo Löwenthal von M. von Medelssohn, 13.08.1951; 1 Brief an The New York Academy of Science von Alice H. Maier, 20.03.1951; 1 Brief von dem Lee Travel Service (New York) an Max Horkheimer, 09.08.1948; 1 Brief an Max Horkheimer von Walter Hallstein, 02.07.1948; 1 Brief von E. Stein an Max Horkheimer, 26.06.1948; 2 Briefe zwischen Alice H. Maier und Gaby Onderwijzer, 1947; 1 Brief an Alfred Haas von Emmy Henne, 01.04.1955; 11 Briefe zwischen Emmy Henne und Alice H. Maier, 1954 - 1955; 2 Briefe zwischen Max Horkheimer und Morris L. Ernst, Oktober 1955; 1 Brief an Alfred Haas und Fritz Moses von Emmy Henne, 01.04.1955; 1 Brief an Alice H. Maier von Alfred Haas und Fritz Moses, 25.10.1954; 1 Brief an das Barbison Plaza Hotel (New York) von Alice H. Maier, 10.02.1955; 4 Briefe von dem Institut für Sozialforshung (Fankfurt am Main) an die Social Studies Association (New York), 1952 - 1954; 2 Briefe und 8 Briefentwürfe von Max Horkheimer an Nicholas Jory, September 1954; 1 Brief und 2 Briefentwürfe an Stroock von Alice H. Maier, [1954]; 1 Brief an Max Horkheimer von L. A. Chamberlin, 16.08.1954; 1 Brief von A. P. Bersohn an Max Horkheimer, 17.08.1954; 1 Brief von Max Horkheimer an Jacob K. Javits, 07.08.1954; 1 Brief an The Ideal Book Shop (New York) von Alice H. Maier, 07.08.1954; 1 Brief von Lothar Wendt (Internist) an Max Horkheimer, 30.07.1954; 1 Brief von Max Horkheimer an Young, 16.07.1954; 1 Brief an R. B. Shipley von Chauncy D. Harris, 16.07.1954; 1 Brief von Chauncy D. Harris an Max Horkheimer, 28.05.1954; 3 Briefe zwischen Max Horkheimer und John J. McCloy, 1954; 1 Brief von John J. McCloy an Ruth Shipley, 12.07.1954; 4 Briefe zwischen Alice H. Maier und Volker von Hagen, 1954; 1 Brief an York Lucci von Alice H. Maier, 13.04.1954; 3 Briefe von Alice H. Maier an H. P. Edelman, 1954; 3 Briefe zwischen Diedrich Osmer und Alice H. Maier, 1953; 1 Brief an die Indiana University (South Bend) von Diedrich Osmer, 26.02.1953; 3 Briefe zwischen Alice H. Maier und Elizabeth C. Krueger, 1953; 2 Briefe zwischen David Melvin Raul und Alice H. Maier, 1952; 1 Brief von Frederick Wild an The American Quaterly (Mineapolis), 25.06.1952; 1 Brief an Alice H. Maier von David Riesman, 19.05.1952; 1 Brief und 1 Briefentwurf an Felix Weil von Alice H. Maier, 23.04.1952;

Na 1 Nachlass Max Horkheimer, 563 - Korrespondenzen u.a. mit Alice H. Maier und Leo Löwenthal (p. VI 27, 1-253)

Briefwechsel zwischen Max Horkheimer und Alice H. Maier; 5 Briefe an Maurice und Carolyn Tumarkin von Max Horkheimer, 1957/1964; 1 Brief von Max Horkheimer an Charles Gorman, 27.04.1957; 1 Brief von Alice H. Maier an die Marquis Company (Chicago), 06.05.1957; 2 Briefe an H. P. Edelman von Max Horkheimer, 1964; 3 Briefe zwischen Alice H. Maier und H. P. Edelman, 1957/1963; 1 Brief von Margot von Mendelssohn an Alice H. Maier, 01.04.1957; 1 Brief an Richard Corwine Stevenson von Max Horkheimer, 16.03.1957; 1 Brief von Max Horkheimer an Inge Aicher-Scholl, 26.02.1957; 1 Brief an Herman Strasburger von Max Horkheimer, 21.01.1957; 1 Brief von Elisabeth Richter an Alice H. Maier, [1957]; 1 Brief an den Director of International Operations (Washington) von Chauncy D. Harris, 05.02.1957; 1 Brief von Alice H. Maier an Comptroller of Customs (New York), 11.01.1957; 1 Brief an Herbert Marcuse von Alice H. Maier, 14.01.1957; 2 Briefe zwischen Alice H. Maier und The Saturday Evening Post (Philadelphia), Oktober 1956; 1 Brief an die Staats-Herold Corporation (Woodside) von Alice H. Maier, 24.09.1956; 2 Briefe zwischen Alice H. Maier und Werner Thönnessen, 1956; 2 Briefe zwischen dem National Better Business Bureau (New York) und Alice H. Maier, 1956; 2 Briefe zwischen Alice H. Maier und Herman L. Filene, Januar 1956; 5 Briefe zwischen Max Horkheimer und Edwin J. Lukas, 1962 - 1963; 7 Briefe zwischen Monroe Karasik und Max Horkheimer, 1963; 1 Brief von Max Horkheimer an James Conant, 30.05.1963; 1 Brief an John J. McCloy von Max Horkheimer, 30.05.1963; 3 Briefe an Herman S. Klein von Alice H. Maier, 1960/1963; 1 Brief von Max Horkheimer an Hartley Chemists (New York), 06.02.1962; 1 Brief an Columbia Chemists (New York) von Max Horkheimer, 06.02.1962; 1 Brief von Max Horkheimer an A. P. Bersohn, 06.06.1962; 1 Brief an A. P. Bersohn von Alice H. Maier, 20.04.1962; 1 Brief an Alice H. Maier von Paul Kind, 22.05.1962; 1 Brief an Cyrus C. Hoffman von Alice H. Maier, 23.03.1961; 2 Briefe von Alice H. Maier an Friedrich Pollock, 1960/1966;

Na 1 Nachlass Max Horkheimer, 564 - Korrespondenzen u.a. mit Alice H. Maier und Leo Löwenthal (p. VI 27, 254-402)

Briefwechsel zwischen Max Horkheimer und Alice H. Maier; 5 Briefe an Maurice und Carolyn Tumarkin von Max Horkheimer, 1957/1964; 3 Briefe zwischen Alice H. Maier und H. P. Edelman, 1957/1963; 2 Briefe von Alice H. Maier an Friedrich Pollock, 1960/1966; 2 Briefe von Max Horkheimer an The Diners Club (New York), 1965; 1 Brief an Patricia und Edward R. Wilbur von Alice H. Maier, 17.05.1965; 2 Briefe von Max Horkheimer an Patricia und Edward R. Wilbur, 1964; 2 Briefe zwischen Alice H. Maier und Alfred L. Copley, 1965; 5 Briefe zwischen William C. Kirkwood und Max Horkheimer, 1964; 2 Briefe von Max Horkheimer an Ulla Posnansky, 1964; 1 Brief an Leo Löwenthal von Max Horkheimer, 23.06.1964; 1 Brief von Max Horkheimer an Amerino Lionetti, 03.06.1964; 10 Briefe zwischen Herbert Marcuse und Max Horkheimer, 1935 - 1936; 1 Brief von R. Piper an Herbert Marcuse, 26.03.1936;

Modifier genes and susceptibility to colorectal cancer in individuals with Lynch syndrome

Lynch syndrome, is caused by inherited germ-line mutations in the DNA mismatch repair genes resulting in cancers at an early age, predominantly colorectal (CRC) and endometrial cancers. Though the median age at onset for CRC is about 45 years, disease penetrance varies suggesting that cancer susceptibility may be modified by environmental or other low-penetrance genes. Genetic variation due to polymorphisms in genes encoding metabolic enzymes can influence carcinogenesis by alterations in the expression and activity level of the enzymes. Variation in MTHFR, an important folate metabolizing enzyme can affect DNA methylation and DNA synthesis and variation in xenobiotic-metabolizing enzymes can affect the metabolism and clearance of carcinogens, thus modifying cancer risk. ^ This study examined a retrospective cohort of 257 individuals with Lynch syndrome, for polymorphisms in genes encoding xenobiotic-metabolizing enzymes-- CYP1A1 (I462V and MspI), EPHX1 (H139R and Y113H), GSTP1 (I105V and A114V), GSTM1 and GSTT1 (deletions) and folate metabolizing enzyme--MTHFR (C677T and A1298C). In addition, a series of 786 cases of sporadic CRC were genotyped for CYP1A1 I462V and EPHX1 Y113H to assess gene-gene interaction and gene-environment interaction with smoking in a case-only analysis. ^ Prominent findings of this study were that the presence of an MTHFR C677T variant allele was associated with a 4 year later age at onset for CRC on average and a reduced age-associated risk for developing CRC (Hazard ratio: 0.55; 95% confidence interval: 0.36–0.85) compared to the absence of any variant allele in individuals with Lynch syndrome. Similarly, Lynch syndrome individuals heterozygous for CYP1A1 I462V A>G polymorphism developed CRC an average of 4 years earlier and were at a 78% increased age-associated risk (Hazard ratio for AG relative to AA: 1.78; 95% confidence interval: 1.16-2.74) than those with the homozygous wild-type genotype. Therefore these two polymorphisms may be additional susceptibility factors for CRC in Lynch syndrome. In the case-only analysis, evidence of gene-gene interaction was seen between CYP1A1 I462V and EPHX1 Y113H and between EPHX1 Y113H and smoking suggesting that genetic and environmental factors may interact to increase sporadic CRC risk. Implications of these findings are the ability to identify subsets of high-risk individuals for targeted prevention and intervention. ^

Carcinoma of the lower uterine segment: A newly described association with Lynch Syndrome

Purpose. We performed a case-comparison study to describe the characteristics of LUS tumors and their association with risk factors for endometrial cancer. ^ Patients and Methods. From January 1996 through October 2007, 3,892 women were identified with a diagnosis of primary endometrial carcinoma or primary cervical adenocarcinoma. Pathology records from the 1,009 women who had a hysterectomy were reviewed. Subjects were included in the LUS group only if the tumor was clearly originating from the area between the lower corpus and upper cervix in the hysterectomy specimen. The LUS group was compared to all patients with endometrial corpus carcinoma who underwent hysterectomy at our institution in a 12-month period randomly selected from the study period. Risk factors for endometrial carcinoma such as body mass index (BMI) and Lynch Syndrome were assessed. Expression of estrogen receptor (ER), vimentin, carcinoembryonic antigen (CEA), p16, and human papilloma virus DNA (HPV DNA) was assessed; this panel is known to be effective in distinguishing adenocarcinomas of endometrial versus endocervical origin. Fisher's Exact, Chi-square, Mann-Whitney, and Student's t-tests were utilized for statistical analysis. ^ Results. Thirty-five of 1,009 women had endometrial carcinoma of the LUS (3.5%; 95% CI: 2–4%). Compared to patients with corpus tumors, LUS patients were younger (54.2 vs. 62.9 years, P = .001), had higher stage (P < .001), and more invasive tumors (P = .001). Preoperative diagnosis of the LUS tumors more frequently included the possibility of endocervical adenocarcinoma ( P < .001), leading to preoperative radiation therapy in 4 patients. Median BMI was similar in the LUS and corpus groups. Seventy-three percent of the available LUS tumors had a similar immunohistochemical expression pattern to conventional endometrioid adenocarcinoma. Because of the young median age for the LUS group, we performed immunohistochemistry for Lynch syndrome-associated DNA mismatch repair proteins MLH1, MSH2, MSH6, and PMS2. Microsatellite instability testing (MSI) and MLH1 promoter hypermethylation were performed when indicated. Thirty-six percent of the LUS tumors were MSI-high. Ten of thirty-five (29%) women with LUS tumors were either confirmed to have Lynch Syndrome or were strongly suspected to have Lynch Syndrome based on tissue-based molecular assays (95% CI, 16 to 45%). ^ Conclusions. Endometrial carcinoma arising in the LUS is a clinical and pathologic entity which can be diagnostically confused with cervical adenocarcinoma. In general, LUS tumors can be correctly identified as being endometrial carcinoma using the immunohistochemical panel noted above. The prevalence of Lynch Syndrome in patients with LUS tumors is much greater than that of the general endometrial cancer population (1.8%) or in endometrial cancer patients younger than 50 years of age (8–9%). Based on our results, the possibility of Lynch Syndrome should be considered in women with LUS tumors. ^

Mismatch Repair Deficient Tumors Lacking Known Sporadic Causes: Are They All Due to Lynch Syndrome?

BACKGROUND: Mismatch repair deficient (MMRD) colorectal (CRC) or endometrial (EC) cancers in the absence of MLH1 promoter hypermethylation and BRAF mutations are suggestive of Lynch syndrome (LS). Positive germline genetic test results confirm LS. It is unclear if individuals with MMRD tumors but no identified germline mutation or sporadic cause (MMRD+/germline-) have LS. HYPOTHESIS: Since LS is hereditary, individuals with LS should have a stronger family history of LS-related cancers than individuals with sporadic tumors. We hypothesized that MMRD+/germline- CRC and/or EC patients would have less suggestive family histories than LS CRC and/or EC patients. METHODS: 253 individuals with an MMRD CRC or EC who underwent genetic counseling at one institution were included in analysis in 1 of 4 groups: LS, MMRD+/germline-, MMRD+/VUS, sporadic MSI-H (MMRD tumor with MLH1 promoter hypermethylation or BRAF mutation). Family histories were analyzed utilizing MMRpro and PREMM1,2,6. Kruskal-Wallis tests were used to compare family history scores. Logistic regression was used to determine what factors were predictive of LS. RESULTS: MMRD+/germline- individuals had significantly lower median family history scores (PREMM1,2,6=7.3, MMRpro=8.1) than LS individuals (PREMM1,2,6=26.1, MMRpro=89.8, p CONCLUSION: MMRD+/germline- individuals have less suggestive family histories of LS than individuals with LS, but more suggestive family histories than sporadic MSI-H individuals. CRC and/or EC patients with abnormal tumor studies are more likely to have a germline LS mutation if they have a family history suggestive of hereditary cancer. These results imply that the MMRD+/germline- group may not all have LS. This finding highlights the need to determine other somatic, epigenetic or germline causes of MMRD tumors so that these patients and their families can be accurately counseled regarding screening and management.