Cansu Karakaş

University of Rochester Medical Center

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Khandan Keyomarsi

The University of Texas MD Anderson Cancer Center

164

Kelly K. Hunt

The University of Texas MD Anderson Cancer Center

162

Tuyen Bui

The University of Texas MD Anderson Cancer Center

Amriti R. Lulla

The University of Texas MD Anderson Cancer Center

Natalie W. Fowlkes

The University of Texas MD Anderson Cancer Center

Joseph A. Caruso

UCSF Helen Diller Family Comprehensive Cancer Center

Iman Doostan

The University of Texas Health Science Center at Houston

Saïd Akli

The University of Texas MD Anderson Cancer Center

Jing Wang

The University of Texas MD Anderson Cancer Center

Xiayu Rao

The University of Texas MD Anderson Cancer Center

Cooperative Institutions

The University of Texas MD Anderson Cancer Center

Harvard University

The University of Texas Health Science Center at Houston

University of Rochester Medical Center

Baylor College of Medicine

University of Rochester

Brigham and Women's Hospital

Heidelberg University

Cornell University

Massachusetts General Hospital

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Determination of apoptosis and cell cycle modulators (p16, p21, p27, p53, BCL-2,Bax, BCL-xL, and cyclin D1) in thyroid follicular carcinoma, follicular adenoma,and adenomatous nodules via a tissue microarray method

TURKISH JOURNAL OF MEDICAL SCIENCES (2015)

Peyker Temız Gizem Akkaş Nalan Neşe Fazilet UĞUR DUMAN Cansu Karakaş

Background/aim: To identify the role of gene products associated with apoptosis and cell cycle in the pathogenesis of thyroid follicular neoplasm. Materials and methods: Thirty follicular adenomas (FAs), 16 follicular carcinomas (FCs), and 20 adenomatous nodules (ANs) were investigated with immunohistochemical staining of p16, p21, p27, p53, Bcl-2, Bax, Bcl-xL, and cyclin D1 via a tissue microarray method. Results: Bcl-2 showed a significant difference between the benign groups (AN and FA) and the malignant group (FC). Bax was significantly higher in the FC group. p53 was lowest in the AN group and highest in the FC group with significant differences between the groups. p16 was significantly higher in the FC group than in the other groups. There was a significant difference between the AN group and neoplastic lesions in terms of p21 staining. The number of cases with positive p27 was lower in the AN group than the neoplastic groups. There was no significant difference in terms of Bcl-xL and cyclin D1. Conclusion: Cell cycle modulators, led by the Bcl-2 family, played an important role in the pathogenesis of thyroid follicular neoplasm, and p53, p16, and p21 in particular played a role in the carcinogenesis of FC.

Tissue microarray

Follicular carcinoma

Thyroid Nodules

Cyclin B

Cyclin B1

10.3906/sag-1406-48

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Supplemental Figure 1 and 2 from Cytoplasmic Cyclin E Mediates Resistance to Aromatase Inhibitors in Breast Cancer

Iman Doostan Cansu Karakaş Mehrnoosh Kohansal Kwang-Hui Low Matthew J. Ellis

Supplemental Figure 1: Nuclear and cytoplasmic scoring system for cyclin E. Supplemental Figure 2: Breast cancer recurrence-free interval in patients with estrogen receptor-positive comparing positive and negative staining for Ki67

Aromatase inhibitor

10.1158/1078-0432.22468964.v1

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Supplemental Figures 1-3 from Cytoplasmic Cyclin E Predicts Recurrence in Patients with Breast Cancer

Kelly K. Hunt Cansu Karakaş Min Jin Ha Anna Biernacka Min Yi

Supplementary Figure 1: Examples of staining and coring system for cyclin E; Supplementary Figure 2: Examples of LMW-E cyclin E staining; Supplementary Figure 3: REMARK diagram of biospecimen availability for the MDA Lab00-222, NCI TMA, MDA TMA, and UK TMA cohorts.

10.1158/1078-0432.22462569

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Supplemental Figure Legends from Cytoplasmic Cyclin E Predicts Recurrence in Patients with Breast Cancer

Kelly K. Hunt Cansu Karakaş Min Jin Ha Anna Biernacka Min Yi

Figure legends pertaining to supplemental figures 1-3

10.1158/1078-0432.22462572

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Supplementary Figure 2 from Cyclin E Associates with the Lipogenic Enzyme ATP-Citrate Lyase to Enable Malignant Growth of Breast Cancer Cells

Kimberly S. Lucenay Iman Doostan Cansu Karakaş Tuyen Bui Zhiyong Ding

ACLY downregulation in LMW-E TDCs does not affect the cell cycle.

ATP citrate lyase

Cyclin D

Lyase

10.1158/0008-5472.22412267.v1

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Supplemental R File 1-Lab222 from Cytoplasmic Cyclin E Predicts Recurrence in Patients with Breast Cancer

Kelly K. Hunt Cansu Karakaş Min Jin Ha Anna Biernacka Min Yi

R File codes pertaining to the Lab222 cohort

10.1158/1078-0432.22462566.v1

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Liver Cyst Hydatid Fistulated Into Duodenum

Electronic Journal of General Medicine (2012)

Serden Ay Ahmet Okuş Cansu Karakaş Mustafa Çarpraz Mehmet Ali Eryılmaz

Hydatid cyst of liver is a disease usually seen in endemic regions. While it is very small at the beginning, cyst diameter increases approximately 1-3 cm per year. Among known complications of hydatid disease, pressure to the adjacent organs due to the cyst growth, perforation into peritoneal cavity or bile truct are most noteable. However, its fistulization into gastrointestinal tract is very rare. A 80-year-old male patient presented with the complaints of abdominal pain, fever and deterioration in general physical condition. It was determined that the patient was diagnosed with hydatid cyst of liver about 15 years ago but refused treatment. Imaging revealed a 20x15 cm multiseptal cystic lesion filled with air in the right lobe of liver. Patient was admitted to OR and exploration revealed that cyst had fistulized into the duodenum. The fistulization of liver hydatid cyst into the duodenum is very rare. We believe that the size of cyst and the delay in treatment caused the cystoduodenal fistula.

Perforation

Hydatid cyst

Duodenal Diseases

10.29333/ejgm/82543

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Liver Cyst Hydatid Fistulated Into Duodenum: A Case Report

Deleted Journal (2012)

Ahmet Okuş Serden Ay Cansu Karakaş Mustafa Çarpraz Mehmet Ali Eryılmaz

Hydatid cyst

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Supplementary Materials and Methods 1 from Neutrophil Elastase Remodels Mammary Tumors to Facilitate Lung Metastasis

Amriti R. Lulla Saïd Akli Cansu Karakaş Joseph A. Caruso Lucas D. Warma

Supplementary Materials and Methods, clean copy version

Neutrophil elastase

10.1158/1535-7163.25523424

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Figure S9 from Neutrophil Elastase Remodels Mammary Tumors to Facilitate Lung Metastasis

Amriti R. Lulla Saïd Akli Cansu Karakaş Joseph A. Caruso Lucas D. Warma

Supplementary Figure S9: Human TNBC cell lines MDA-MB-231 and MDA-MB-468 were injected in the T4 mammary fat pad of 12 week old nude mice. When tumors reached size of 100mm3, mice were randomized in Vehicle and AZD9668 100mg/kg groups. Mice were then treated daily B.I.D until the endpoint of Vehicle tumors reaching 2000mm3. (A, B) Tumor growth curves of mice treated with either Vehicle or AZD9668 100mg/kg in the MDA-MB-231 and MDA- MB-468 models respectively. Endpoint tumors harvested were subject to BrdU staining. (C, D) Representative images BrdU staining and (E, F) their corresponding quantitation in the MDA- MB-231 and MDA-MB-468 models respectively. (G) Spontaneous tumors isolated from PyMT NE+/+ were implanted in FVB NE+/+ mice. When tumors reached a measurable size of 30- 50mm3, mice were randomized into Vehicle and AZD9668 100mg/kg group and treated B.I.D until 400-500mm3. Tumor growth curves, as a function of time are shown.

Neutrophil elastase

10.1158/1535-7163.25523430

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