Review: Breast Cancer and Etiology
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Rare Presentation of Metastatic Lobular Breast Carcinoma Involving Clear Cell Renal Cell Carcinoma
Hindawi Case Reports in Oncological Medicine Volume 2020, Article ID 5315178, 5 pages https://doi.org/10.1155/2020/5315178 Case Report Rare Presentation of Metastatic Lobular Breast Carcinoma Involving Clear Cell Renal Cell Carcinoma Dayne Ashman,1 Gabriela Quiroga-Garza,1 and Daniel Lee 2 1Department of Pathology, University of Pittsburgh, 5230 Centre Avenue, Pittsburgh, PA 15232, USA 2Department of Medicine, University of Pittsburgh, 5150 Centre Avenue, Pittsburgh, PA 15232, USA Correspondence should be addressed to Daniel Lee; [email protected] Received 23 March 2020; Accepted 3 September 2020; Published 15 September 2020 Academic Editor: Raffaele Palmirotta Copyright © 2020 Dayne Ashman et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Although the first case of tumor-to-tumor metastasis was reported over a century ago, it remains a rare occurrence. We report a rare case of metastatic infiltrating lobular carcinoma involving clear cell renal cell carcinoma, as well as offer a brief literature review. 1. Introduction Microscopic examination of the biopsy specimen revealed two distinct neoplasms (Figure 3). The first neo- The phenomenon of one malignant tumor metastasizing to plasm identified demonstrated cells arranged in nests and another, unrelated, primary tumor, has been termed solid sheets with delicate vasculature. Cytologically, these “tumor-to-tumor” metastasis (TTM); it is a rare occurrence. neoplastic cells demonstrated clear cytoplasm with round To date, there have been fewer than 200 cases reported in nuclei and inconspicuous nucleoli, morphologically consis- the English literature. -
Activity of Larotrectinib, a Highly Selective Inhibitor of Tropomyosin
Activity of larotrectinib, a highly selective inhibitor of tropomyosin receptor kinase, in TRK fusion breast cancers Funda Meric-Bernstam,1 Neerav Shukla,2 Nir Peled,3,4 Yosef Landman,3 Adedayo A. Onitilo,5 Sandra Montez,1 Nora C Ku,6 David M. Hyman,2 Alexander Drilon,2 David S. Hong1 1The University of Texas MD Anderson Cancer Center, Houston, Texas, USA; 2Memorial Sloan Kettering Cancer Center, Weill Cornell Medical College, New York, New York, USA; 3Institute of Oncology, Davidoff Cancer Center, Rabin Medical Center, Petah Tikva, Israel; 4Soroka Cancer Institute, Ben Gurion University, Beer Sheva, Israel; 5Marshfield Clinic Weston Center, Weston, Wisconsin, USA;6 Loxo Oncology, Inc., South San Francisco, California, USA San Antonio Breast Cancer Symposium® - December 4-8, 2018 Introduction Table 1: Adverse events with larotrectinib seen in ≥15% of patients Patient case studies Patient 3: ETV6-NTRK3 secretory breast cancer Patient 5: ETV6-NTRK3 secretory breast cancer (n=207)4 ■■ The family of tropomyosin receptor kinases (TRK), TRKA, B, and C are encoded by three distinct genes, NTRK1, 2, and 31 Treatment-emergent AEs (%) Treatment-related AEs (%) Patient 1: TPM3-NTRK1 invasive ductal carcinoma of the breast Baseline Day 54 Baseline Cycle 17, day 27 ■■ After embryogenesis, TRK proteins are primarily restricted to the nervous system and function during Grade 1 Grade 2 Grade 3 Grade 4 Total Grade 3 Grade 4 Total normal neuronal development and maintenance2–5 ■■ 34-year-old female diagnosed with invasive ductal carcinoma with metastasis -
1 Effective January 1, 2018 ICD‐O‐3 Codes, Behaviors and Terms Are Site‐Specific Alpha Order Last Updat
Effective January 1, 2018 ICD‐O‐3 codes, behaviors and terms are site‐specific Alpha Order Last updated 8/22/18 Status ICD‐O‐3 Term Reportable Comments Morphology Y/N Code New Term 8551/3 Acinar adenocarcinoma (C34. _) Y Lung primaries diagnosed prior to 1/1/2018 use code 8550/3 For prostate (all years) see 8140/3 New Term 8140/3 Acinar adenocarcinoma (C61.9 ONLY) Y For prostate only, do not use 8550/3 New Term 8572/3 Acinar adenocarcinoma, sarcomatoid (C61.9) Y New Term 8550/3 Acinar cell carcinoma Y Excludes C61.9‐ see 8140/3 New Term 8316/3 Acquired cystic disease‐associated renal cell carcinoma (RCC) Y (C64.9) New 8158/1 ACTH‐producing tumor N code/term New Term 8574/3 Adenocarcinoma admixed with neuroendocrine carcinoma (C53. _) Y Behavior 8253/2 Adenocarcinoma in situ, mucinous (C34. _) Y Important note: lung Code/term primaries ONLY: For cases diagnosed 1/1/2018 forward do not use code 8480 (mucinous adenocarcinoma) for in‐ situ adenocarcinoma, mucinous or invasive mucinous adenocarcinoma. 1 Status ICD‐O‐3 Term Reportable Comments Morphology Y/N Code Behavior 8250/2 Adenocarcinoma in situ, non‐mucinous (C34. _) Y code/term New Term 9110/3 Adenocarcinoma of rete ovarii (C56.9) Y New 8163/3 Adenocarcinoma, pancreatobiliary‐type (C24.1) Y Cases diagnosed prior to code/term 1/1/2018 use code 8255/3 Behavior 8983/3 Adenomyoepithelioma with carcinoma (C50. _) Y Code/term New Term 8620/3 Adult granulosa cell tumor (C56.9 ONLY) N Not reportable for 2018 cases New Term 9401/3 Anaplastic astrocytoma, IDH‐mutant (C71. -
Post-Translational Control of Retinoblastoma Protein Phosphorylation
Western University Scholarship@Western Electronic Thesis and Dissertation Repository 9-25-2014 12:00 AM Post-Translational Control of Retinoblastoma Protein Phosphorylation Paul M. Stafford The University of Western Ontario Supervisor Dr. Fred Dick The University of Western Ontario Graduate Program in Biochemistry A thesis submitted in partial fulfillment of the equirr ements for the degree in Master of Science © Paul M. Stafford 2014 Follow this and additional works at: https://ir.lib.uwo.ca/etd Part of the Biochemistry Commons, and the Molecular Biology Commons Recommended Citation Stafford, Paul M., "Post-Translational Control of Retinoblastoma Protein Phosphorylation" (2014). Electronic Thesis and Dissertation Repository. 2449. https://ir.lib.uwo.ca/etd/2449 This Dissertation/Thesis is brought to you for free and open access by Scholarship@Western. It has been accepted for inclusion in Electronic Thesis and Dissertation Repository by an authorized administrator of Scholarship@Western. For more information, please contact [email protected]. POST-TRANSLATIONAL CONTROL OF RETINOBLASTOMA PROTEIN PHOSPHORYLATION (Thesis format: Integrated Article) by Paul Stafford Graduate Program in Biochemistry A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science The School of Graduate and Postdoctoral Studies The University of Western Ontario London, Ontario, Canada © Paul Stafford 2015 i Abstract The retinoblastoma tumor suppressor protein (pRB) functions through multiple mechanisms to serve as a tumor suppressor. pRB has been well characterized to be inactivated through phosphorylation by CDKs. pRB dephosphorylation and activation is a much less characterized aspect of pRB function. In this thesis, I detail work to study the post translational control of pRB phosphorylation. -
Nipple-Areolar Complex:Diagnostic Challenges
Nipple-areolar complex:diagnostic challenges. Poster No.: C-1547 Congress: ECR 2014 Type: Educational Exhibit Authors: S. Manso Garcia1, S. Plaza Loma2, Y. Rodríguez de Diego1, V. Zurdo de Pedro1, R. Pintado Garrido1, E. Villacastin Ruiz1, M. Moya de la Calle1, M. J. Velasco Marcos1, H. Calero1; 1Valladolid/ ES, 2Valladolid, VA/ES Keywords: Inflammation, Hyperplasia / Hypertrophy, Biopsy, Ultrasound, Mammography, Breast DOI: 10.1594/ecr2014/C-1547 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to third- party sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. www.myESR.org Page 1 of 12 Learning objectives We describe normal anatomy and clinical and radiological findings of nipple-aerolar complex (NAC) disorders. -
2018 SEER Solid Tumor Manual
4/6/2018 Eight Groups are Revised for 2018 Head & Neck Colon (includes rectosigmoid and rectum for cases diagnosed 1/1/2018 forward) 2018 SEER Lung (2018 Draft not yet available) Breast Solid Tumor Manual Kidney Urinary Sites (2018 Draft not yet available) 2018 KCR SPRING TRAINING Non‐malignant CNS (2018 Draft not yet available) Malignant CNS and Peripheral Nerves (2018 Draft not yet available) 2019 Changes for other two Groups Solid Tumor Rules What we will cover: ◦ Overview of General rules Cutaneous melanoma (minor revisions and draft available now) • Cutaneous melanoma site rules will be revised for 2019 implementation to incorporate ◦ New Head and Neck rules information from the new WHO 4th Ed Tumors of Skin scheduled to be released in 2018. ◦ New Colorectal rules ◦ New Breast rules Other sites (minor revisions and draft available now) ◦ New Kidney rules • Primary sites excluded are: •Rectosigmoid and rectum which are included in 2018 Colon rules. •Peripheral nerves which are included in 2018 Malignant Brain rules. •Other sites rules will be revised for 2019 implementation. The Solid Tumor Task Force has identified Remember: These are currently in draft form and may change slightly in the final version! the need to expand the rules to include GYN, soft tissue, thyroid and other site‐specific solid tumors. NEW! Code subtypes/variants when definitively described (with no modifiers) General Instructions Example: Well ‐differentiated neuroendocrine tumor 8240. Do not code a histology (*including subtypes or variants) when described as below: The 2018 solid tumor rules replace all previous MP/H rules, but they are effective for diagnoses on or after 1/1/2018. -
The Pathology of Breast Cancer - Ali Fouad El Hindawi
MEDICAL SCIENCES – Vol.I -The Pathology of Breast Cancer - Ali Fouad El Hindawi THE PATHOLOGY OF BREAST CANCER Ali Fouad El Hindawi Cairo University. Kasr El Ainy Hospital. Egypt. Keywords: breast cancer, breast lumps, mammary carcinoma, immunohistochemistry Contents 1. Introduction 2. Types of breast lumps 3. Breast carcinoma 3.1 In Situ Carcinoma of the Mammary Gland 3.1.1 Lobular Neoplasia (LN) 3.1.2 Duct Carcinoma in Situ (DCIS) 3.2 Invasive Carcinoma of the Mammary Gland 3.2.1 Microinvasive Carcinoma of the Mammary Gland 3.2.2 Invasive Lobular Carcinoma (ILC) 3.2.3 Invasive Duct Carcinoma 3.3 Paget’s disease of the Nipple 3.4 Bilateral Breast Carcinoma 4. Conclusions Glossary Bibliography Summary Breast cancer is the most common cancer in females. It may have strong family history (genetically related). It most commonly arises from breast ducts and less frequently from lobules. Since mammary carcinoma is the most common form of breast malignancy and one of the most common human cancers, most of this chapter is concentrated on the differential diagnosis of breast carcinoma 1. Introduction In clinicalUNESCO practice, a breast lump is very common.– EOLSS It may be accompanied in some cases by other patient’s complaints such as pain and/ or nipple discharge, which may be bloody. Sometimes more than one lump is detected in the same breast, or in both breasts. Cutaneous manifestations asSAMPLE nipple retraction, nipple and/ orCHAPTERS skin erosion, skin dimpling, erythema and peau d’ orange may also be noted; both by the patient and her physician. A lump may not be palpable in spite of breast symptoms such as pain and or nipple discharge. -
Renal Mass in a Patient with Invasive Lobular Adenocarcinoma
132 Renal mass in a patient with invasive lobular adenocarcinoma X. Mortiers, MD1, H. Vandeursen, MD, PhD2, T. Adams, MD2, T. Van den Mooter, MD3 SUMMARY Breast cancer often metastasises to bone, lymph nodes, liver and lung. In this case report, we present a 75-year-old woman with a suspicious mammography and ultrasound of the breast who had a synchronous painless renal lesion. On computed tomography, the renal mass was suspected of being a primary lesion of the renal pelvis, but anatomopathological examination of the nephro-ureterectomy specimen revealed that it was a metastatic deposit of invasive lobular adenocarcinoma of the breast. (BELG J MED ONCOL 2019;13(4):132-134) INTRODUCTION breast. A mammography and ultrasound were performed Breast cancer is the most frequent cancer in women, with and showed a retroareolar lobulated and dense, though not worldwide an estimated two million new cases each year, well delineated, structure with a spicular appearance, mul- and is currently the second most frequent cause of cancer tiple pathological vessels and enlarged axillary lymph nodes. death.1,2 This type of cancer has a five-year overall relative A biopsy of the lesion in the right breast showed the presence survival rate of 90.4%.3 The Belgian screening program of an invasive lobular adenocarcinoma, moderately differen- with mammography has increased the number of patients tiated (E-Cadherin negative, oestrogen receptor [ER]-posi- with breast cancers being diagnosed in an early setting. A tive, progesterone receptor [PR]-negative, human epidermal minority of patients with breast cancer is diagnosed with growth factor receptor 2 [HER2 negative]). -
Formation of PGE2 in the Tumor Microenvironment and Its Impact on Tumorigenesis” Im Institut Für Biochemie I – Pathobiochemie Unter Betreuung Und Anleitung Von Prof
Formation of PGE2 in the tumor microenvironment and its impact on tumorigenesis Dissertation for attaining the PhD degree of Natural Sciences submitted to the Faculty of Biochemistry, Chemistry and Pharmacy of the Johann Wolfgang Goethe-University in Frankfurt am Main by Weixiao Sha from Beijing – PR China Frankfurt am Main 2014 Accepted by the Faculty of Biochemistry, Chemistry and Pharmacy Johann Wolfgang Goethe-University Dean: Prof. Dr. Thomas Prisner Referees: Prof. Dr. Dieter Steinhilber Prof. Dr. Bernhard Brüne Date of the disputation: “...There are known knowns; there are things we know that we know. There are known unknowns: that is to say, there are things that we now know we don't know. But there are also unknown unknowns – there are things we do not know we don't know.” —Donald Rumsfeld, United States Secretary of Defense Index 1 Index Index .......................................................................................................................... 1 List of figures ............................................................................................................ 5 Abbrevations ............................................................................................................. 7 1 Summary .............................................................................................. 11 2 Zusammenfassung .............................................................................. 13 3 Introduction .......................................................................................... 18 -
New Jersey State Cancer Registry List of Reportable Diseases and Conditions Effective Date March 10, 2011; Revised March 2019
New Jersey State Cancer Registry List of reportable diseases and conditions Effective date March 10, 2011; Revised March 2019 General Rules for Reportability (a) If a diagnosis includes any of the following words, every New Jersey health care facility, physician, dentist, other health care provider or independent clinical laboratory shall report the case to the Department in accordance with the provisions of N.J.A.C. 8:57A. Cancer; Carcinoma; Adenocarcinoma; Carcinoid tumor; Leukemia; Lymphoma; Malignant; and/or Sarcoma (b) Every New Jersey health care facility, physician, dentist, other health care provider or independent clinical laboratory shall report any case having a diagnosis listed at (g) below and which contains any of the following terms in the final diagnosis to the Department in accordance with the provisions of N.J.A.C. 8:57A. Apparent(ly); Appears; Compatible/Compatible with; Consistent with; Favors; Malignant appearing; Most likely; Presumed; Probable; Suspect(ed); Suspicious (for); and/or Typical (of) (c) Basal cell carcinomas and squamous cell carcinomas of the skin are NOT reportable, except when they are diagnosed in the labia, clitoris, vulva, prepuce, penis or scrotum. (d) Carcinoma in situ of the cervix and/or cervical squamous intraepithelial neoplasia III (CIN III) are NOT reportable. (e) Insofar as soft tissue tumors can arise in almost any body site, the primary site of the soft tissue tumor shall also be examined for any questionable neoplasm. NJSCR REPORTABILITY LIST – 2019 1 (f) If any uncertainty regarding the reporting of a particular case exists, the health care facility, physician, dentist, other health care provider or independent clinical laboratory shall contact the Department for guidance at (609) 633‐0500 or view information on the following website http://www.nj.gov/health/ces/njscr.shtml. -
Estrogens, BRCA1, and Breast Cancer1
[CANCER RESEARCH 60, 4993–5001, September 15, 2000] Review Estrogens, BRCA1, and Breast Cancer1 Leena Hilakivi-Clarke2 Lombardi Cancer Center, Georgetown University, Washington, D.C. 20007 Abstract breast tumor development (6). However, it is not clear that there is a correlation between high estrogen exposure and high breast cancer Findings obtained in in vitro assays and animal studies indicate that risk during the years when women have functional ovaries. In fact, an estrogens might influence the activity of the tumor suppressor gene increase in breast cancer risk may be seen after a modest reduction in BRCA1, and BRCA1 in turn may suppress the activity of the estrogen receptor. This review will discuss the possibility that interactions between circulating estrogens, such as that produced by unilateral ovariectomy estrogens and BRCA1 partly explain why elevated circulating estrogen (4, 5), oral contraceptive (7, 8) or contraceptive depot use [both of levels appear to increase breast cancer risk among postmenopausal which inhibit ovulation and ovarian estrogen production (9, 10)], or women but not among young women. A hypothesis is proposed that low body weight and low fat intake (11–14). In contrast, an increase estrogens have a dual role in affecting breast cancer risk. In young women in exposure to circulating estrogens during premenopausal years whose breasts have not yet accumulated critical mutations required for caused by several pregnancies (15), short menstrual cycle length (16, cancer initiation and promotion, activation of BRCA1 by estrogens helps 17), high BMI (18), or a high fat intake (11) may reduce the risk of to maintain genetic stability and induce differentiation, and therefore developing breast cancer. -
Performance Characteristics of Adenoid Cystic Carcinoma of The
Letters to the Editor Many salivary gland neoplasms con- Medical City, Abu Dhabi, United Arab Performance tain both stroma and epithelial and Emirates Characteristics of myoepithelial cells, which have differ- ent and variable characteristics with 1. Tabatabai ZL, Auger M, Kurtycz DF, et al. Adenoid Cystic Performance characteristics of adenoid cystic carci- different stains. In addition, the spatial noma of the salivary glands in fine-needle aspirates: Carcinoma of the Salivary relationship between the stroma and results from the College of American Pathologists the cells is of importance in different Nongynecologic Cytology Program. Arch Pathol Glands in Fine-Needle Lab Med. 2015;139(12):1525–1530. doi:10.5858/ salivary gland tumors. Therefore, we arpa.2013-0173-CP. Aspirates strongly believe that these issues play 2. Kopec´ T, Mikaszewski B, Jackowska J, Was´- aroleininflatingthedegreeof niewska-Okupniak E, Szyfter W, Wierzbicka M. Treatment of parotid malignancies—10 years of misinterpretation at both ends of the experience. J Oral Maxillofac Surg. 2015;73(7): spectrum (both false negatives and 1397–1402. doi:10.1016/j.joms.2014.12.036. To the Editor.—We read with depth false positives). We are quite sure that 3. Bruzgielewicz A, Osuch-Wojcikiewicz´ E, and interest the article by Tabatabai et the authors are aware of these limita- Majszyk D, et al. Adenoid cystic carcinoma of the 1 head and neck—a 10 years experience [in Polish]. al addressing the performance char- tions but we were compelled to raise Otolaryngol Pol. 2011;65(5 suppl):6–11. acteristics of adenoid cystic carcinoma these important points in this letter to 4.