��ios��-(��315bet.net��)-��-��-��bet91.net��-��ios��-��ios��-��-(��315bet.net��)

Advanced

FindZebra Summary is loading...

Phyllodes Tumor Wikipedia

Some would extend the spectrum to include malignant phyllodes tumors and frank sarcoma . [ citation needed ] References [ edit ] ^ a b Tan BY, Acs G, Apple SK, Badve S, Bleiweiss IJ, Brogi E, Calvo JP, Dabbs DJ, Ellis IO, Eusebi V, Farshid G, Fox SB, Ichihara S, Lakhani SR, Rakha EA, Reis-Filho JS, Richardson AL, Sahin A, Schmitt FC, Schnitt SJ, Siziopikou KP, Soares FA, Tse GM, Vincent-Salomon A, Tan PH (2016). ... PMID 26768026 . ^ Moffat CJ, Pinder SE, Dixon AR, Elston CW, Blamey RW, Ellis IO (1995). "Phyllodes tumour of the breast: a clinicopathological review of the thirty-two cases".

MED12, KMT2D, RARA, FLNA, SETD2, TP53, EGFR, KIT, LOC110806263, TERT, ESR1, PDGFRA, RCAN2, PIK3CG, HIF1A, PIK3CA, CKAP4, MMP2, RASSF1, MDM2, RPE65, UVRAG, ESR2, DNAJC5, AR, TWIST1, CD34, MIR21, CDKN2A, RCAN1, PIK3CB, TP63, PIK3CD, GEMIN2, ZBED1, TNFRSF25, HMGA2, ZEB2, INPP4B, TOX, SLC9A3R2, SCAF11, ACTB, HOXB13, POSTN, SIK1B, MIR335, MIR155, SIK1, CD276, VTCN1, RBM15, IL21, ZNF410, IMPACT, FOXP3, IL22, OBP2A, PRAME, CXCR4, TRAM1, CXCL12, VIM, FASN, IGF1R, HTC2, NR3C1, MTOR, FOXC2, FHIT, FGFR1, ERBB2, TSC1, DPT, DCN, CTNNB1, CDK4, CA9, BRCA1, CCND1, IGF2, ILK, KIF22, MLH1, ZEB1, SSR1, SPARC, SDHB, SDHA, AKT1, CCL20, CCL19, CCL18, S100A4, NTRK1, NRAS, MYC, MMP14, MMP9, H3P10
- Phyllodes Tumor Of The Breast Orphanet
  
  Phyllode tumor of the breast is a rare fibroepithelial neoplasm accounting for less than 1% of all mammary tumors, usually presenting in adult females (most frequently between the ages of 35-55 years), ranging from benign to malignant and often presenting with well circumscribed mobile masses that grow rapidly and sometimes with additional non-specific symptoms such as dilated skin veins, nipple retraction, skin ulcers, palpable axillary lymphadenopathy or blue discoloration of the skin.
- Phyllodes Tumor Of The Breast GARD
  
  Phyllodes tumors of the breast are rare tumors that start in the connective (stromal) tissue of the breast. They get their name from the leaf-like pattern in which they grow (phyllodes means leaf-like in Greek). They are most common in women in their 30s and 40s, although women of any age can be affected. These tumors, which are usually painless, tend to grow quickly, but rarely spread outside of the breast. Most phyllodes tumors are benign. About 1 in 10 are cancerous. The underlying cause of these tumors in unknown.
Ocular Tilt Reaction Wikipedia

The initial head tilt to right will cause stimulation of the right utricle resulting in excitory signals to pass to the SR and SO (right eye), and IO and IR (left eye). Simultaneously, inhibitory signals pass to their antagonists.
Burnside-Butler Syndrome Wikipedia

"Further phenotypic expansion of 15q11.2 BP1-BP2 microdeletion (Burnside-Butler) syndrome - IOS Press" . Journal of Pediatric Genetics . 3 (1): 41–44. doi : 10.3233/pge-14082 .
- Chromosome 15q11.2 Deletion Syndrome OMIM
  
  A number sign (#) is used with this entry because it represents a contiguous gene deletion syndrome involving chromosome 15q11.2. The deleted region spans approximately 300 to 500 kb between breakpoints 1 (BP1) and 2 (BP2) of the Prader-Willi (PWS; 176270)/Angelman syndrome (AS; 105830) critical region. The deletion region between BP1 and BP2 contains 4 genes that are not imprinted: TUBGCP5 (608147), NIPA1 (608145), NIPA2 (608146), and CYFIP1 (606322). Description A heterozygous deletion of chromosome 15q11.2 may increase the susceptibility to neuropsychiatric or neurodevelopmental problems, including delayed psychomotor development, speech delay, autism spectrum disorder, attention deficit-hyperactivity disorder, obsessive-compulsive disorder, and possibly seizures (summary by Doornbos et al., 2009 and Burnside et al., 2011). See also chromosome 15q11.2 duplication syndrome (608636). Clinical Features Murthy et al. (2007) reported a 3.5-year-old boy with mental retardation who was found to carry a heterozygous 253-kb deletion of chromosome 15q11.2 between BP1 and BP2.
- 15q11.2 Microdeletion GARD
  
  15q11.2 microdeletion refers to a chromosome abnormality in which a tiny piece of genetic material on the long arm of chromosome 15 (at a location designated q11.2) is missing (deleted). The features of people with a 15q11.2 microdeletion vary widely. The most common features include developmental, motor, and language delays; behavior and emotional problems; attention deficit disorders ; and autism spectrum disorder . Other features may include birth defects and seizures. However, some people have no apparent physical, learning, or behavior problems. A 15q11.2 microdeletion may occur randomly for the first time in an affected person, or it may be inherited from a parent. Treatment depends on the signs and symptoms in each person.
- 15q11.2 Microdeletion Syndrome Orphanet
  
  15q11.2 microdeletion syndrome is a rare partial autosomal monosomy with a variable phenotypic expression and reduced penetrance associated with an increased susceptibility to neuropsychiatric or neurodevelopmental disorders including delayed psychomotor development, speech delay, autism spectrum disorder, attention deficit-hyperactivity disorder, obsessive-compulsive disorder, epilepsy or seizures. It may also include mild non-specific dysmorphic features (such as dysplastic ears, broad forehead, hypertelorism), cleft palate, neurological and neuroimaging abnormalities (such as ataxia and muscular hypotonia).
Boanthropy Wikipedia

See also [ edit ] Clinical lycanthropy (or zoanthropy) Hathor Io Therianthropy References [ edit ] ^ Onions, C.T. , ed. (1933).
Basal-Like Carcinoma Wikipedia

PMID 17438091 . ^ Rakha EA, Reis-Filho JS, Ellis IO (May 2008). "Basal-like breast cancer: a critical review". ... PMID 18487574 . ^ Rakha EA, El-Sayed ME, Green AR, Lee AH, Robertson JF, Ellis IO (January 2007). "Prognostic markers in triple-negative breast cancer" .

BRCA1, EGFR, ERBB2, TP53, ESR1, FOXC1, PIK3CA, CD44, PGR, FOXF2, PIK3CD, PIK3CB, PIK3CG, PTEN, YBX1, FOXC2, VIM, WWOX, SALL4, CD274, CDH1, SOX10, MET, HGF, FBP1, ETS1, EZH2, DUSP4, MYC, FOXQ1, EGF, MMP14, CLDN1, MBD2, MMP7, MIR100, PARP1, NES, CD24, ANXA1, SNAI2, KRT5, IL6, KRT14, BRCA2, MELK, KLF5, RPS6KA3, BRD4, THY1, CDKN2A, TWIST1, CLDN7, ACTB, ARHGAP11A, DCLK1, BCAR1, CD163, PDCD6IP, MAP4K4, MAP3K14, RAD50, ABCG2, ABAT, INPP4B, TNFRSF11A, SRC, TRIM21, STAT3, AURKA, SUV39H1, SYK, TAZ, TFRC, TGFB1, TGFBR2, UGT8, VEGFC, PDPN, VWF, WNT5A, MFAP5, USP9X, FZD7, CUL4A, MSLN, AGO2, POSTN, MIR205, CCDC8, HORMAD1, PPP1R9B, PRRT2, TWIST2, ROPN1B, MIR126, MIR143, MIR146A, MIR17, MIR200A, MIR21, KHDRBS3, MIR221, MIR29B1, MIR29C, MIR34C, MIR375, MIR424, LGALS7B, CCR2, MIR374B, MIR4274, FOXCUT, WNT5B, CSPP1, FTO, TRIB3, KDM5B, LYVE1, UBE2C, KLF12, SIRT2, KDM1A, WWTR1, PRPF31, USP21, DKK3, IL17B, TOX3, RACGAP1, PINX1, PHIP, IL17RB, INAVA, CLDND1, CAMK1D, NDRG2, ARRDC3, PREX1, CIP2A, SOX11, PLAU, FSCN1, GABRP, ESR2, ESRRB, FABP7, ACSL4, FAT2, FOXM1, FLNB, FLT4, FN1, FRA16D, GATA3, CTTN, GCNT2, GLI1, GLO1, GLS, GRB2, GRM1, HAS2, HDAC2, HMGA1, FOXA1, EPHB2, ELAVL2, HES1, CANX, ACTN1, AKT1, AKR1B1, ARF1, ARHGAP1, BCL2, BIK, BMI1, BSG, DDR1, CAV1, DUSP5, CBL, CD74, CD151, CDC42, CENPE, COL11A2, CRYAB, CTNNB1, DNMT1, DUSP1, FOXA2, TNC, SNAI1, PRKCD, NOS2, NRAS, NTRK1, ROR1, PDK1, PDPK1, PI3, PLA2G4A, PRKCA, PRKCB, MAPK1, MSH2, MAPK3, PTX3, S100A2, SALL1, CCL2, SKP2, SLC2A1, SLC22A3, SMN1, SMN2, MYBL2, MMP9, ID4, ITGAV, IGF1, IGF1R, IL1A, IL1B, IL1RN, CXCL8, IL13RA2, IDO1, ITGA6, ITGA5, ITK, MLH1, KIF5A, KIFC3, LEPR, LGALS7, LOXL2, LYN, EPCAM, MAZ, ME1, MGMT, H3P10
Malignant Infantile Osteopetrosis Wikipedia

The differential diagnosis of genetic osteosclerosing dysplasias including infantile osteopetrosis has been tabulated [1] and illustrated in literature citations. [3] Neuropathic infantile osteopetrosis Infantile osteopetrosis with renal tubular acidosis Infantile osteopetrosis with immunodeficiency IO with leukocyte adhesion deficiency syndrome (LAD-III) Intermediate osteopetrosis Autosomal dominant osteopetrosis (Albers-Schonberg) Pyknodysostosis (osteopetrosis acro-osteolytica) Osteopoikilosis (Buschke–Ollendorff syndrome) Osteopathia striata with cranial sclerosis Mixed sclerosing bone dysplasia Progressive diaphyseal dysplasia ( Camurati–Engelmann disease ) SOST-related sclerosing bone dysplasias Treatment [ edit ] The only effective line of treatment for malignant infantile osteopetrosis is hematopoietic stem cell transplantation . [2] [4] [5] It has been shown to provide long-term disease-free periods for a significant percentage of those treated;. [2] It can impact both hematologic and skeletal abnormalities; [2] [4] and has been used successfully to reverse the associated skeletal abnormalities. [4] [5] Radiographs of at least one case with malignant infantile osteopetrosis have demonstrated bone remodeling and recanalization of medullar canals following hematopoietic stem cell transplantation.

TCIRG1, CLCN7, SNX10, TNFSF11, ATP6V0A2, BCL2, CD34, NFKB1, RAC1, RAC2, RGS10, OSTM1, LRRK1
- Osteopetrosis, Autosomal Recessive 2 OMIM
  
  A number sign (#) is used with this entry because of evidence that an osteoclast-poor form of autosomal recessive osteopetrosis (OPTB2) is caused by homozygous mutation in the TNFSF11 gene (602642) on chromosome 13q14. For a general phenotypic description and a discussion of genetic heterogeneity of autosomal recessive osteopetrosis, see OPTB1 (259700). Clinical Features Burns et al. (1978) described a form of osteopetrosis resembling the autosomal dominant form (see OPTA2, 166600) in its benignity but displaying autosomal recessive inheritance. The clinical features were variable but included mandibular prognathism, genu valgum, anemia, hepatosplenomegaly, and tendency to fracture and mandibular osteomyelitis. Dental anomalies included retention of deciduous teeth, malformation of crowns, and strong tendency to caries.
- Osteopetrosis, Autosomal Recessive 8 OMIM
  
  A number sign (#) is used with this entry because of evidence that autosomal recessive osteopetrosis-8 (OPTB8) is caused by homozygous mutation in the SNX10 gene (614780) on chromosome 7p15. For a general phenotypic description and a discussion of genetic heterogeneity of autosomal recessive osteopetrosis, see OPTB1 (259700). Clinical Features Aker et al. (2012) studied 4 affected children from 2 consanguineous Palestinian families with osteopetrosis (OPT). All 4 patients had older relatives with OPT, and were suspected of having OPT at 1 to 4 months of age because of macrocephaly or failure to thrive due to feeding problems caused by upper airway issues. Examination revealed age-appropriate neurocognitive development, increased head circumference, broad open fontanel, frontal bossing, and hepatosplenomegaly.
- Autosomal Recessive Malignant Osteopetrosis Orphanet
  
  Infantile malignant osteopetrosis is a rare congenital disorder of bone resorption characterised by generalised skeletal densification. Epidemiology Incidence is estimated at 1/200 000 live births. Osteopetrosis has been reported in most ethnic groups, although, as the disease is very rare, it is more frequently seen in ethnic groups where consanguinity is common. Clinical description Bone marrow failure, fractures and visual impairment are the classical features of the disease, which begins in early infancy or in foetal life. It results from the failure of osteoclasts to resorb immature bone. This leads to abnormal bone marrow cavity formation and to the clinical signs and symptoms of bone marrow failure. It is accompanied by hepatosplenomegaly due to compensatory extramedullary hematopoiesis.
- Osteopetrosis, Autosomal Recessive 4 OMIM
  
  A number sign (#) is used with this entry because of evidence that autosomal recessive osteopetrosis-4 (OPTB4) is caused by homozygous or compound heterozygous mutation in the CLCN7 gene (602727) on chromosome 16p13. An autosomal dominant form of osteopetrosis (OPTA2; 166600) is also caused by mutation in CLCN7. For a phenotypic description and a discussion of genetic heterogeneity of autosomal recessive osteopetrosis, see OPTB1 (259700). Clinical Features Cleiren et al. (2001) reported a girl, born to second-cousin parents of Chinese ancestry, who presented at 3 months of age with Bell palsy. Radiographic skeletal survey revealed severe osteopetrosis and several nondisplaced oblique fractures.
- Osteopetrosis, Autosomal Recessive 1 OMIM
  
  A number sign (#) is used with this entry because of evidence that autosomal recessive osteopetrosis-1 (OPTB1) is caused by homozygous or compound heterozygous mutation in the TCIRG1 subunit (604592) of the vacuolar proton pump on chromosome 11q13. Description Osteopetrosis (OPT) is a life-threatening disease caused by subnormal osteoclast function, with an incidence of 1 in 250,000 births. The disease usually manifests in the first few months of life with macrocephaly and frontal bossing, resulting in a characteristic facial appearance. Defective bone remodeling of the skull results in choanal stenosis with concomitant respiratory problems and feeding difficulties, which are the first clinical manifestation of disease. The expanding bone encroaches on neural foramina, leading to blindness, deafness, and facial palsy.
Breast Hematoma Wikipedia

Cance (1 January 2001). Breast Surgery . IOS Press. p. 96. ISBN 978-1-58603-159-6 .
Osteosclerosis Wikipedia

Osteosclerosis can be classified in accordance with the causative factor into acquired and hereditary. [2] [1] Contents 1 Types 1.1 Acquired osteosclerosis 1.2 Hereditary osteosclerosis 2 Diagnosis 3 Animals 4 See also 5 References 6 External links Types [ edit ] Acquired osteosclerosis [ edit ] Osteogenic bone metastasis caused by carcinoma of prostate and breast Paget's disease of bone Myelofibrosis (primary disorder or secondary to intoxication or malignancy) Osteosclerosing types of chronic osteomyelitis Hypervitaminosis D hypoparathyroidism Schnitzler syndrome [3] Skeletal fluorosis Monoclonal IgM Kappa cryoglobulinemia [4] Hepatitis C . [5] Hereditary osteosclerosis [ edit ] Malignant infantile osteopetrosis [6] Neuropathic infantile osteopetrosis Infantile osteopetrosis with renal tubular acidosis Infantile osteopetrosis with immunodeficiency IO with leukocyte adhesion deficiency syndrome (LAD-III) Intermediate osteopetrosis Autosomal dominant osteopetrosis (Albers-Schonberg) Pyknodysostosis (osteopetrosis acro-osteolytica) [2] Osteopoikilosis ( Buschke–Ollendorff syndrome ) [2] Osteopathia striata with cranial sclerosis [2] Mixed sclerosing bone dysplasia Progressive diaphyseal dysplasia ( Camurati–Engelmann disease ) [2] SOST -related sclerosing bone dysplasias Sclerosis of the bones of the thoracic spine due to prostate cancer metastases (CT image) Sclerosis of the bones of the thoracic spine due to prostate cancer metastases (CT image) Diagnosis [ edit ] Osteosclerosis can be detected with a simple radiography.

LTBP3, TBCE, TNFRSF11B, SOST, CLCN7, FAM20C, DLX3, LRP5, RUNX2, LRP4, CTSK, MC4R, GBA, RNF113A, LIMK1, LPIN2, HSPG2, ENPP1, TBL2, GTF2IRD1, WRN, GTF2E2, GNAS, GTF2I, FLNA, SCARB2, GTF2H5, TBXAS1, AGXT, MPLKIP, RFC2, PTH1R, CLIP2, ERCC3, FAM111A, DMP1, SLC26A2, SLC29A3, BAZ1B, ERCC2, ELN, TGFB1, FGF23, BMP2, BGLAP, PLEKHM1, TCIRG1, ATP6V0A2, LEMD3, VDR, NOD2, BEST1, VEGFA, ADO, ANO5, ABL1, SMAD3, TPO, GZMB, ADRB2, ADRB3, ALPL, AIRE, COL1A1, DMD, DVL1, EDN1, GH1, GZMH, IL4, PTH, IL11, JAK2, LEPR, LRP6, ADRB1, MPL, PCNA, PLCL1, MAPK1, MAPK3, LINC01152
Sexual Headache Wikipedia

Uterga, JM; De Garay, MA; De Luna, IO; Uribarri, JB (2009). "Recurrent coital headache associated with an unruptured carotid saccular aneurysm".

ALB, OXA1L, DEFB4A, S1PR1, IL6, KIT, PGF, PIK3CA, PIK3CB, PIK3CD, PIK3CG, TGFB1, JPH3, DEFB4B
- Headache Associated With Sexual Activity OMIM
  
  Description The International Headache Society (1988) classifies headache associated with sexual activity (HSA) as an idiopathic headache under 'miscellaneous headaches unassociated with structural lesions.' Based on initial descriptions, 3 subtypes are differentiated: type 1 is a dull ache in the head and neck that slowly intensifies as sexual excitement increases, and is believed to be caused by muscle contraction similar to tension-type headache; type 2, also called 'vascular-type,' is a sudden severe, explosive headache occurring at orgasm, which may be due to increased intracranial pressure; type 3, the most uncommon type, is a postural headache resembling that caused by decreased CSF pressure, perhaps due to a meningeal tear during coitus (summary by Frese et al., 2003). Clinical Features Johns (1986) reported 4 sisters with the vascular type of benign sexual headache (type 2 HSA). The most severely affected patient was successfully treated with beta-blocker prophylaxis. In a review of the literature, the author found that 28% of those affected had either personal history or family history of migraine (see 157300), suggesting that type 2 HSA is a migraine variant.
Phantom Vibration Syndrome Wikipedia

Retrieved September 4, 2011 . v t e Mobile phones mobile networks , protocols Channel capacity Frequencies Multi-band Network operator list Roaming Signal SIM card dual SIM SIM lock Standards comparison Tethering VoIP WAP XHTML-MP generations analogue : 0G 1G digital : 2G 3G adoption 3.5G 4G 4.5G 5G 6G general operation Features GSM services History Operating system Security phone cloning Telephony airplane mode Text messaging SMS MMS RCS Spam Tracking Web browsing mobile devices Manufacturers 3D phone Camera phone Car phone Feature phone Projector phone Satellite phone Smartphone form factors Bar Flip Phablet Slider Smartwatch smartphones Android devices rooting BlackBerry 10 iPhone iOS jailbreaking Open-source mobile phones Symbian devices Windows Phone devices mobile specific software apps Development Distribution Management Cloud computing commerce Banking Marketing advertising campaigns Payments contactless donating Ticketing content Blogging Email Gambling Gaming Health Instant messaging Learning Music News Search local Social address book Television culture Box breaking Charms Comics Dating Japanese culture Novels Ringtones silent mode Selfie Txt-spk Wallpaper environment and health BlackBerry thumb Driving safety Electronic waste External power supply Mental health from overuse Phantom vibration syndrome Radiation and health Recycling law Carrier IQ Legality of recording by civilians Mobile phones in prison Photography and the law Telephone tapping Texting while driving USA use restrictions while driving Category Portal
Lymphocytic Esophagitis Wikipedia

. ^ a b c d e f g h i j k l m n o p q r Rouphael C, Gordon IO, Thota PN (February 2017). "Lymphocytic esophagitis: Still an enigma a decade later" .
Lateral Periodontal Cyst Wikipedia

. ^ a b Ramalingam S, Alrayyes YF, Almutairi KB, Bello IO (2019-07-08). "Lateral Periodontal Cyst Treated with Enucleation and Guided Bone Regeneration: A Report of a Case and a Review of Pertinent Literature" .

CASP3
Problematic Smartphone Use Wikipedia

For 3-4 year-old children: 180 minutes physical activity, 1 hour screen time, 10–13 hours of sleep time per day. [81] Phone settings [ edit ] Many smartphone addiction activists (such as Tristan Harris) recommend turning one's phone screen to grayscale mode, which helps reduce time spent on mobile phones by making them boring to look at. [82] Other phone settings alterations for mobile phone non-use included turning on airplane mode, turning off cellular data and/or Wi-Fi, turning off the phone, removing specific apps, and factory resetting. [83] Phone apps [ edit ] German psychotherapist and online addiction expert Bert te Wildt recommends using apps such as Offtime and Menthal to help prevent mobile phone overuse. [84] In fact, there are many apps available on Android and iOS stores which help track mobile usage. For example, in iOS 12 Apple added a function called "Screen Time" that allows users to see how much time they have spent on the phone. ... PMID 27736736 . ^ Young, Kimberly (27 February 1998). Caught in the net : how to recognize the signs of Internet addiction--and a winning strategy for recovery .
Congenital Disorder Of Glycosylation Wikipedia

Mutations in DPM2 (DPM2-CDG) and DPM3 (DPM3-CDG (CDG-Io)) [19] cause syndromes with a muscle phenotype resembling an a-dystroglycanopathy, possibly due to lack of Dol-P-Man required for O-mannosylation. ... Types include: Type OMIM Gene Locus Ia ( PMM2-CDG ) 212065 PMM2 16p13.3-p13.2 Ib ( MPI-CDG ) 602579 MPI 15q22-qter Ic (ALG6-CDG) 603147 ALG6 1p22.3 Id (ALG3-CDG) 601110 ALG3 3q27 Ie (DPM1-CDG) 608799 DPM1 20q13.13 If (MPDU1-CDG) 609180 MPDU1 17p13.1-p12 Ig (ALG12-CDG) 607143 ALG12 22q13.33 Ih (ALG8-CDG) 608104 ALG8 11pter-p15.5 Ii (ALG2-CDG) 607906 ALG2 9q22 Ij (DPAGT1-CDG) 608093 DPAGT1 11q23.3 Ik ( ALG1-CDG ) 608540 ALG1 16p13.3 1 L (ALG9-CDG) 608776 ALG9 11q23 Im (DOLK-CDG) 610768 DOLK 9q34.11 In (RFT1-CDG) 612015 RFT1 3p21.1 Io (DPM3-CDG) 612937 DPM3 1q12-q21 Ip (ALG11-CDG) 613661 ALG11 13q14.3 Iq (SRD5A3-CDG) 612379 SRD5A3 4q12 Ir (DDOST-CDG) 614507 DDOST 1p36.12 DPM2-CDG n/a DPM2 9q34.13 TUSC3-CDG 611093 TUSC3 8p22 MAGT1-CDG 300716 MAGT1 X21.1 DHDDS-CDG 613861 DHDDS 1p36.11 I/IIx 212067 n/a n/a Type II [ edit ] Type II disorders involve malfunctioning trimming/processing of the protein-bound oligosaccharide chain.

PMM2, SRD5A3, MPI, SLC35A2, MOGS, DPM1, DOLK, MPDU1, SLC35A1, FCSK, ALG1, MAGT1, SRD5A3-AS1, TMEM165, PGM1, COG8, ALG6, COG6, ALG3, ALG9, PGM3, ALG8, DPAGT1, MAN1B1, COG7, COG5, APOC3, MGAT2, ALG12, DPM3, SLC35C1, SERPINA1, LEMD3, ALPI, ALPP, ATP6V0A2, ALG11, SLC39A8, STT3B, MAN1A1, GOLPH3, CD47, STT3A, IAPP, DHDDS, RFT1, ALG2, PGAP3, NUS1P3, COG2, GFM1, SLC35A3, POFUT2, CCDC115, NUS1, PGAP1, ALG13, CSGALNACT1, TRAPPC11, GRIN3A, AGA, RXYLT1, IGF1, GPI, B4GALT1, FUT8, FXN, F11, SLC26A3, DLD, DDOST, DCN, DAG1, SERPINA6, BGN, BCHE, ATP6AP1, SERPINC1, APRT, APOB, HP, IGFBP5, MGAM, ITGB2, ST3GAL5, DPM2, TUSC3, AKR1B1, TF, SSR4, SSR3, ST3GAL3, SI, RNASE4, RAB1A, PYCR1, ATXN3, MFAP1, LAMP2, LAMP1, LAD1, PGR-AS1
- Congenital Disorders Of N-Linked Glycosylation And Multiple Pathway Overview GeneReviews
  
  Summary Purpose. Many human disorders of glycosylation pathways have now been identified; they include defects in synthetic pathways for N-linked oligosaccharides, O-linked oligosaccharides, shared substrates, glycophosphatidylinositol (GPI) anchors, and dolichols. This overview will focus on disorders of the N-linked glycan synthetic pathway and some disorders that overlap this metabolic network (multiple-pathway disorders). The goals of this overview on congenital disorders of glycosylation are the following: Goal 1. To describe the clinical characteristics of congenital disorders of N-linked glycosylation Goal 2. To review the causes of congenital disorders of N-linked glycosylation Goal 3.
- Congenital Disorders Of Glycosylation GARD
  
  Congenital disorders of glycosylation (CDG) are a group of inherited metabolic disorders that affect a process called glycosylation. Glycosylation is the complex process by which all human cells build long sugar chains that are attached to proteins, which are called glycoproteins. There are many steps involved in this process, and each step is triggered by a type of protein called an enzyme. Individuals with a CDG are missing one of the enzymes that is required for glycosylation. The type of CDG that a person has depends on which enzyme is missing.
- Congenital Disorder Of Glycosylation Orphanet
  
  A fast growing group of inborn errors of metabolism characterized by defective activity of enzymes that participate in glycosylation (modification of proteins and other macromolecules by adding and processing of oligosaccharide side chains). This group is comprised of phenotypically diverse disorders affecting multiple systems including the central nervous system, muscle function, immunity, endocrine system, and coagulation. The numerous entities in this group are subdivided, based on the synthetic pathway affected, into disorder of protein N-glycosylation, disorder of protein O-glycosylation, disorder of multiple glycosylation, and disorder of glycosphingolipid and glycosylphosphatidylinositol anchor glycosylation.
Unilateral Hearing Loss Wikipedia

. ^ OS X Mavericks: Audio pane of Accessibility preferences ^ Apple - Accessibility - iOS External links [ edit ] Classification D ICD - 10 : H90.1 , H90.4 , H90.7 MeSH : D046088 Profound Unilateral Hearing Loss FAQ's and Flash Animation BoysTownHospital.org Unilateral Hearing Loss - Notes v t e Diseases of the outer and middle ear Outer ear Otitis externa Otomycosis Middle ear and mastoid Otitis media Mastoiditis Bezold's abscess Gradenigo's syndrome Tympanosclerosis Cholesteatoma Perforated eardrum Symptoms Ear pain Hearing loss Tests Otoscope pneumatic tympanometry

H3-3A, FOXI1, KCNJ10
- Deafness, Unilateral OMIM
  
  Clinical Features Smith (1939) described a sibship of 8 children, 4 of whom had total deafness in one or the other ear. The tympanic membranes were normal. Labyrinthine testing was normal. There was no history of consanguinity, mumps, or syphilis. The mother, her father, and her sister also had unilateral deafness while another sister became deaf and lost speech after measles. This latter sister married a deaf and dumb man. One of their 3 children, a girl, had unilateral deafness. She had 2 children, one of whom has unilateral deafness. Thus there were 9 persons with total unilateral deafness in 4 generations.
Cerebral Infarction Wikipedia

It is also possible to calculate the risk of stroke in the next decade based on information gathered through the Framingham Heart Study . [8] Pathophysiology [ edit ] Cerebral infarction Hemodynamic changes seen using an IOS camera specific for hemoglobin volume changes where we see the occlusion of a Middle Cerebral Artery (MCA) and how Spreading Depolarizations appear and spread over the cortex. [9] Whether a cerebral infarction is thrombotic or embolic based, its pathophysiology , or the observed conditions and underlying mechanisms of the disease.

NPY, PLAT, ALOX5AP, NOS3, F2, F5, PRKCH, PLAU, VDR, ADH1B, HBA1, SERPINE1, MAP3K5, ICAM1, ANXA1, MAP2, IL18, PTGDR, ADORA1, SLC6A1, VIM, EPHX2, TNF, IL1B, GABPA, TSPAN33, APOE, NFE2L2, SIRT1, C20orf181, MMP9, PIK3CA, PIK3CB, PIK3CD, PIK3CG, VEGFA, TLR4, BDNF, HMGB1, BCL2, CASP3, IL6, HIF1A, PPARG, NLRP3, ACE, IL1A, IL1RN, MTHFR, ACSM3, MIR210, MAPK3, STAT3, HSPB3, AQP4, MAPK1, TGFB1, HSPA4, HSPB1, HSPB2, IL10, PTEN, HGF, SOD1, MIR155, ADIPOQ, ANGPT1, NGB, CSF3, FGB, CRP, FGF2, LPL, FGFR1, MAPK14, ABCA1, AGT, EPHB2, APOH, AKT1, ALB, NGF, REST, MMP2, PINK1, KCNK2, ALDH2, PLG, SPP1, TNFSF4, TBXA2R, PLA2G7, CXCL12, CAV1, CBS, TRPM2, TXN, BSG, MIR126, S100B, F2R, NTF3, EPO, ABCC8, SOD3, ROS1, GDNF, LDLR, LCN2, DNM1L, GFAP, ATM, JAK2, NOX4, TRPC6, THBD, IGF1, TLR2, MIR21, HP, MANF, NTN1, RAC1, PON1, PROZ, CCL5, PTGS2, ROCK2, CCL2, KDR, TFRC, KLK1, SPHK1, APLN, SLC1A2, CKLF, POLDIP2, MAP2K7, CDKN2B-AS1, PTGIS, AGTR1, TNFRSF12A, LEP, IL4, RIPK1, ANXA6, TRPM7, REN, HSPG2, TRAF2, MTCO2P12, MEG3, ACKR3, TP53, CLDN5, PPIG, SLC2A1, LGALS3, DAPK2, PHB, XBP1, NAMPT, PDE4D, PDE4A, AIF1, PAEP, OLR1, PLA2G4A, AGER, CBSL, NUCB2, NR4A1, NOTCH3, SP1, NFKB1, LILRB1, STC1, COX2, ADM, SYP, MAP3K7, UTRN, SLC5A1, MAP3K11, SIRT2, MBL2, MAPK8, TRPV1, DENR, SETD2, HMOX1, GPR17, CD40, GLP1R, MIR195, GAS5, CIRBP, GCG, BIRC5, MIR130A, MTOR, CPB2, CREB1, MALAT1, CRMP1, CSF2, FOXO3, CST3, RTN4R, CTNNB1, CTSS, CX3CR1, FABP2, CYBB, FABP1, F7, RAB7B, ESR1, DECR1, DLG4, UBASH3B, MIR223, G6PD, GPER1, SERPINC1, MIR451A, GRN, GRIK2, XIAP, SEMA6A, GRIN2A, MRS2, BRINP3, MIR431, BDNF-AS, S1PR2, SLC33A1, USP14, MIR497, ARHGEF7, ANGPTL1, HAP1, TMEM119, MIR146B, KL, PERCC1, SELENBP1, RGMB, BTBD8, MIR424, NPAS4, PGR-AS1, OSBPL9, OLIG1, LRG1, SLCO6A1, SRXN1, OR2AG1, MIR490, CXCL14, VPS4B, PDIK1L, GAL3ST1, MAPK8IP1, TNFRSF1B, ADAMTS18, MIR376B, GRAP2, SNHG14, ZBTB7C, OPN5, HSP90B1, GSTK1, MIR323A, NRP1, TFPI2, MIR145, MIR146A, MIR29B1, MIR149, MIR15A, RAB7A, MIR183, SCG2, YWHAZ, MIR29A, VWF, MIR204, MIR24-1, CERNA3, VEGFC, MIR224, MIR212, MIR217, RN7SL263P, AIMP2, AXIN2, CST12P, MIR29B2, MIR133B, AOC3, CDNF, MIAT, UCHL1, TP63, PSMG1, KHSRP, UGCG, CYP4F2, MIR106B, MIR128-2, PIK3R3, CARTPT, MIR93, PPM1D, MIR140, MIR320A, BRAP, OCLN, GDF11, KLK4, SIGLEC7, ASCC1, TAS2R13, IL22, TRIB3, DUOX2, KCNIP3, UBQLN1, IL21, HTRA2, ACE2, HPGDS, TRPV4, OPN4, FGF21, PTPN22, NEUROG2, RNF19A, NOD2, XYLT2, PART1, TXN2, SNHG1, BACE1, RPL13A, ANGPTL4, RNF213, GP6, DCDC2, MIR634, TIGAR, DENND11, RETN, CLDND1, MCOLN1, TUG1, NDRG3, NDRG2, ADPRS, POTEF, SLC12A5, CASZ1, NLN, KIDINS220, ERCC6L, TREM2, TNFRSF1A, DUOX1, SHC3, BCL11A, STK26, ISYNA1, CBX5, TARDBP, NMNAT1, SPAG11A, AHSA1, SLC35A1, ATG7, COASY, SEMA4D, SLC9A6, RNF146, SPAG11B, SEMA3A, IMMP2L, KLF2, AKT1S1, AKR1A1, RAMP1, RAMP2, RTN4, SNHG12, CEBPZ, OTULIN, EDIL3, MUC16, BMS1, ATG13, P3H4, MIR544A, NCS1, TXNIP, MIR940, P2RY12, SIRT3, SMG1, MIR365A, DKK1, NDRG4, LMTK2, MGLL, LINC01672, KLK8, MAP4K1, PSIP1, RIPK3, NOX5, ADIPOR2, PPP1R13L, PLK2, NES, EBP, NLRX1, ZC3H12A, POSTN, MIR491, MAP2K1, TNFAIP6, CYP4A11, FOSB, FOS, FLT1, FOXF2, FGA, FCN1, PTK2B, F12, F10, ESR2, EPHA4, ENO2, ENO1, EMP1, EMD, ELANE, EGFR, EFNB2, EEF1A1, EDNRB, EDN1, DUSP2, HBEGF, DSCAM, DPYSL2, DPP4, DIO2, DDC, DCR, GCY, GDF1, MSTN, HFE, CXCL8, IL4R, IL2RB, RBPJ, IGF1R, TNC, HSPA5, HSPA1B, HSPA1A, HES1, HRG, HPX, HOXC13, HCLS1, GH1, H2AX, GZMB, GSTM1, GSK3B, CXCL1, NR3C1, GRIN2C, GPI, GOT1, GLUL, GCLC, GJA1, CBLIF, CYP11B2, CYP3A5, TMSB4X, CYP3A4, VPS51, TSPO, BMP7, CEACAM1, BAX, ADGRB2, ALDH7A1, ATP2B1, ATF4, ARNTL, APP, APOBEC1, APOB, APEX1, APEH, ANGPT2, ANG, ALOX15, ALOX5, ABCD2, AHSG, AGTR2, ADRA2A, PARP1, ADORA2B, ADCYAP1R1, ADAM10, ACTB, ACACA, CACNA1B, CAD, CALB1, CDK9, CYP2C19, CYP1A1, CUX1, CTSG, CRK, CP, KLF6, COL11A2, COL4A2, COL3A1, CNR1, CCR5, CFTR, CDK5, CAPN1, CDK4, CDC42, CD68, ENTPD1, SCARB1, CD36, CD14, CCK, CAV2, CAT, CASP6, CASP4, CASP1, IL11, IL13, IL15, IL16, RNH1, RBP4, RAF1, MOK, PTMAP4, PTMA, PTGS1, PTGIR, PTGER2, PTGER1, PSEN1, HTRA1, PROS1, PSPN, PRNP, MAP2K3, ABCA4, MAPK10, PRKCB, PREP, PPIA, PON3, PON2, PLSCR1, SERPINF2, SERPINE2, SERPINB6, PFKFB3, PER1, RPS6KB1, RYR1, S100A11, SUMO3, TM7SF2, TLR5, THPO, TGFBR2, TGFA, TEK, TEAD1, TCF3, TBXAS1, TAT, TRIM21, SRY, SUMO2, SMARCA4, SAA1, SLC19A1, SLC12A2, SLC9A1, SLC8A3, SLC8A1, SLC8A2, SMTN, ST3GAL4, SFTPD, SELP, SELE, CX3CL1, CCL3, SERPINF1, PDPK1, ENPP2, KCNK3, MAG, SMAD3, LTA, LPA, LIMK1, LIG4, LIF, LGALS2, LCAT, LBP, LAMC2, LAMP1, KCNN4, KCND2, MAS1, JUND, JUNB, JUN, JAK3, ITPR3, ITGB1, ITGAM, IRAK1, PDX1, CXCL10, IMPA1, IL17A, TNFRSF9, MAPT, MC4R, PDK1, NOTCH1, PCYT1A, PCSK1, PRKN, SERPINB2, PRDX1, P2RY2, OPRM1, ODC1, NR4A2, NRDC, NPR2, NPPB, NPPA, NOS2, MDK, NUBP1, GADD45B, MYD88, MYCN, RNR2, COX1, CD200, MMP14, MMP12, NR3C2, KMT2A, MIF, MFGE8, H3P40
Congenital Muscular Dystrophy Wikipedia

PMID 22675738 . update 2012 ^ "OMIM Entry - # 612937 - CONGENITAL DISORDER OF GLYCOSYLATION, TYPE Io; CDG1O" . www.omim.org . Retrieved 2016-04-26 . ^ "OMIM Entry - # 615042 - CONGENITAL DISORDER OF GLYCOSYLATION, TYPE Iu; CDG1U" . www.omim.org .

COL6A3
Dravet Syndrome Wikipedia

PMID 21463289 . S2CID 573375 . ^ a b c d Miller IO, de Menezes MA (April 2019). "SCN1A seizure disorders.".

SCN1A, SCN9A, STXBP1, SCN2A, SCN1B, PCDH19, GABRG2, GABRA1, TNRC6A, POMC, PMP22, RAPGEF2, SAMD12, KCNQ2, SCN8A, ADRA1D, PVALB, POLG, SCN2B, KCNQ3, SST, GABRB3, GPR55, PRRT2, TLR1, VIP, LINC01672, CPLX1, EPM2A, B3GNT2, OPN1MW2, SLC12A5, LOH19CR1, GPHN, ARX, EJM2, B3GNTL1, CACNA1G, TSPYL4, ACHE, CDKL5, FOXM1, ALDH7A1, CACNA1A, CACNB4, CHD2, CSTB, CYP2C19, E2F1, EPHA5, FOXG1, MTOR, SLC12A2, GABRA2, GABRD, GAPDH, OPN1MW, IGF1, MECP2, RPS19, SCN7A, SLC2A1, OPN1MW3
- Epileptic Encephalopathy, Early Infantile, 4 OMIM
  
  A number sign (#) is used with this entry because early infantile epileptic encephalopathy-4 (EIEE4) is caused by heterozygous mutation in the STXBP1 gene (602926) on chromosome 9q34.1. For a general phenotypic description and a discussion of genetic heterogeneity of EIEE, see EIEE1 (308350). Clinical Features Tohyama et al. (2008) reported a Japanese infant girl who developed tonic seizures, tremulous arm movements, and oral automatisms at 45 days of age. Her dizygotic twin was unaffected; the pregnancy resulted from in vivo fertilization. The proband continued to have seizures with increased frequency, spastic quadriplegia, and poor visual attention.
- Epileptic Encephalopathy, Early Infantile, 6 OMIM
  
  A number sign (#) is used with this entry because early infantile epileptic encephalopathy-6 (EIEE6) is caused by heterozygous mutation in the SCN1A gene (182389) on chromosome 2q24. About 95% of the mutations are de novo (Claes et al., 2001; Vadlamudi et al., 2010). Mutations in the SCN1A gene are also responsible for autosomal dominant generalized epilepsy with febrile seizures plus (GEFS+) (GEFSP2; 604403). Description Dravet syndrome, first described by Dravet (1978), is a clinical term for early-onset epileptic encephalopathy (EIEE) characterized by generalized tonic, clonic, and tonic-clonic seizures that are initially induced by fever and begin during the first year of life. Seizures are usually refractory to treatment. Later, patients also manifest other seizure types, including absence, myoclonic, and partial seizures.
- Epileptic Encephalopathy, Early Infantile, 19 OMIM
  
  A number sign (#) is used with this entry because early infantile epileptic encephalopathy-19 (EIEE19) is caused by heterozygous mutation in the GABRA1 gene (137160) on chromosome 5q34. For a general phenotypic description and a discussion of genetic heterogeneity of EIEE, see 308350. Clinical Features Carvill et al. (2014) reported 4 unrelated patients with onset of seizures between ages 8 and 11 months. Seizure types included hemiclonic, tonic-clonic, focal dyscognitive, myoclonic, absence, and atonic. Three patients had status epilepticus. Febrile sensitivity to seizures was present in all patients.
- Dravet Syndrome Orphanet
  
  Dravet syndrome (DS) is a genetic epilepsy of childhood characterized by a variety of drug-resistant seizures often induced by fever, presenting in previously healthy children, and which frequently leads to cognitive and motor impairment. Epidemiology Worldwide birth prevalence is thought to be <1/40,000. In the UK it is estimated at 1/28,000. Clinical description Onset of the first seizure is mainly in the 1st year of life (usually at 5-8 months of age) in previously healthy infants and most often consists of a unilateral or generalized, clonic seizure. Fever often triggers the seizures that include generalized tonic-clonic, alternating unilateral clonic and generalized tonic-clonic seizures. Afebrile complex partial and focal seizures are also reported during the course of the disease.
- Dravet Syndrome GARD
  
  Dravet syndrome is the most severe of a group of conditions known as SCN1A- related seizure disorders . Symptoms include seizures which first occur in infancy that are often triggered by high temperatures ( febrile seizures ). In childhood, many types of seizures may occur and they may increase in frequency. Seizures may be difficult to treat. Other symptoms include loss of motor skills, intellectual disability, speech impairment, and difficulty with movement. Most cases of Dravet syndrome occur when the SCN1A gene is not working correctly.
Triple-Negative Breast Cancer Wikipedia

PMID 27185638 . Further reading [ edit ] Alanazi IO, Khan Z (2016). "Understanding EGFR Signaling in Breast Cancer and Breast Cancer Stem Cells: Overexpression and Therapeutic Implications" .

BARD1
Ductal Carcinoma In Situ Wikipedia

. ^ J, Cuzick; I, Sestak; Se, Pinder; Io, Ellis; S, Forsyth; Nj, Bundred; Jf, Forbes; H, Bishop; Is, Fentiman (January 2011).

SLC2A1, HIF1A, CA9, LDHB, STAT5A, BRCA2, ATM, SEC23B, BRCA1, CCND1, ESR1, PGR, TP53, ERBB2, C11orf65, LMNA, PALB2, BRIP1, PTGS2, EGFR, PIK3CA, CYP19A1, PTEN, BCL2, VEGFA, CDKN2A, RASSF1, S100A7, UVRAG, TP63, RPE65, CKAP4, AR, TRIM27, LMLN, COX2, MSMB, MUC1, PLAU, MTCO2P12, SERPINE1, MMP9, RET, AVP, RUNX3, TMPRSS13, MST1, MKI67, ZNF469, MMP11, NEURL1, ACTB, NEU1, NME1, ESR2, EZH2, CD274, HGF, PIK3CG, GATA3, ERG, CD44, AKT1, BCS1L, SNAI1, NCOA4, PIK3CD, TBPL1, PDGFRA, PDCD4, KLK3, FOXP3, PIK3CB, MSH6, RBM39, MIR21, PLG, SFN, BNIP3, PPARG, MAPK1, GSTP1, NOTCH3, IRF5, AURKA, H3P10, MME, TERF2, MET, TBX3, TGFB1, HOTAIR, LOX, TRPS1, LGALS3, ATP6AP2, KRT19, KRT14, ALDH1A1, ANXA8, NOTCH1, SAGE1, TERT, MAP2K4, SULF2, RAP1A, CCND2, SDC1, CTNNB1, SIM2, CAV1, COL11A1, MIR183, FGFR1, CST6, FHIT, COX8A, CDKN1A, CXCR4, VWF, TIAM1, VIM, THOC1, MRC2, AKR1C3, HDAC6, PDZK1IP1, WNT1, MTA1, RABEPK, LANCL1, THBS1, TUBA1B, SPAG11B, INPP4B, TGFBI, ALDH5A1, NCOA3, FST, USO1, SEMA7A, NXF1, IRS2, CELSR1, TLK1, TIMP2, ARHGEF2, XPR1, CD163, CLDN1, SLIT2, SLC9A3R1, MAP3K14, HSPB3, TWIST1, CUL3, TOP2A, TNFAIP3, ADIPOQ, TMPRSS2, COX5A, GAB2, UGCG, P4HA2, GRAP2, LPXN, EIF2AK3, CCN5, CXCL14, APOBEC3B, NRP1, TIE1, NCOR1, NCOR2, DIRAS3, KIAA0100, NRIP1, AAMP, NCOA2, CD276, GADL1, ARMH1, CCDC112, GATA5, MUC17, CKS1BP7, SPATA18, ACVR1C, ANIB1, AZIN2, SCGB3A1, PPP1R2C, CIB1, LPCAT1, VTCN1, ADIPOR2, WDR77, CDK15, NOD2, HEATR6, MUC3B, MIB1, INTS2, PCBP4, TNFAIP8L3, MIR106B, MIR10B, MIR126, H3P28, SCHLAP1, LY75-CD302, MIR671, POTEF, MIR557, SPAG11A, MIR455, MIR409, MIR151A, MIR93, MIR29C, MIR223, MIR205, MIR195, MIR181A2, MIR17, MIR155, MIR150, MIR146A, MIR140, MIR139, MIR132, SLC12A9, PBK, PAG1, AMACR, SEC14L2, POFUT1, CBX7, SULF1, TFAP2B, KDM2A, CILK1, VASH1, GALNT6, PTP4A3, DNAJB4, COPS5, KCNQ1OT1, EBNA1BP2, SMR3B, PGRMC1, PLAC1, CTCF, SCGB1D2, POSTN, TXNIP, OLFM4, IFI44, SMUG1, TMEFF2, DOK4, CADM1, DEPDC1, TRIM62, TET2, OTUD4, KRT20, SPA17, WWOX, GDE1, SIRT6, HSD17B7, UBR5, ADIPOR1, MEMO1, PRLH, ADGRE2, PYCARD, HPGDS, FOXP1, PELP1, TES, PART1, BRMS1, QPCT, PEG10, RB1, TFAP2A, NR5A2, FLT1, FLOT2, FLNB, FOXO3, FOXC1, FHL2, FGF3, FAT1, FASN, ETV6, FBL, EREG, ERBB4, ERBB3, ELF3, EIF4EBP1, EIF4E, DUSP6, NQO1, ECI1, DBT, FPR2, FYB1, DAP, GAS6, IGF1R, IDH2, IDH1, ICAM1, TNC, HSPB2, HSPB1, HSPA8, HOXA5, FOXA1, HHEX, NRG1, HDLBP, H3-3B, H3-3A, GTF2H2, GSTM2, GSN, GPT, GJB2, GATA4, DAPK3, CYC1, IGFBP3, CD19, DDR1, BNIP3L, BMP2, BCR, BCL9, BCL6, BAG1, STS, NUDT2, ANXA2, AMCN, AIC, AGTR1, AGT, JAG1, AP2B1, PARP1, ADH5, ADH4, ADH1C, ADH1B, RUNX1, MS4A1, CTSV, CD86, CTSB, CTLA4, CSTA, CSK, CREBBP, CPOX, CLDN7, CPD, COL10A1, COL5A2, COL1A1, CLU, CISH, CHEK1, CDKN1B, CDH13, CDH11, CDH1, CD59, CD34, CD33, IGF2, IGFBP7, SYK, S100A6, OPN1LW, RBP1, RASA1, RARB, RAP1GAP, RAC1, PTHLH, PTGER2, PTCH1, PSMD10, PSMD7, KLK10, MAPK3, PRKD1, PRKACG, PPP2R2B, PON1, PMS2, SERPINB5, PI3, PECAM1, S100A1, S100A8, PDGFRB, S100A9, SULT1E1, STAT5B, STAT1, SREBF1, SPARC, SPAM1, SOX11, SOX9, SOX2, FSCN1, SNCG, SMARCE1, SMARCA4, SLN, SKP2, SIX1, SIAH2, SFRP1, CXCL12, S100B, S100A10, ENPP3, CDK16, IL2RA, MDM2, EPCAM, LY75, LGALS1, LEPR, LBR, RPSA, KRT81, KRT18, KRT17, KRT15, KRT5, KPNA2, KIT, CD82, ITGA4, ISG20, IRS1, IRF1, INHBA, IL9, IL6, SMAD4, MIP, PCOS1, MMP1, PAX6, PAX5, P2RX5, OSM, OPRD1, DDR2, NRDC, NOTCH4, NOTCH2, NEK2, NEFL, MYLK, MYC, MYB, MUC4, MUC3A, MUC2, MRC1, MMP13, MMP8, MMP2, H3P33
- Ductal Carcinoma In Situ (Dcis) Mayo Clinic
  
  Overview Ductal carcinoma in situ (DCIS) is the presence of abnormal cells inside a milk duct in the breast. DCIS is considered the earliest form of breast cancer. DCIS is noninvasive, meaning it hasn't spread out of the milk duct and has a low risk of becoming invasive. DCIS is usually found during a mammogram done as part of breast cancer screening or to investigate a breast lump. While DCIS isn't an emergency, it does require an evaluation and a consideration of treatment options. Treatment may include breast-conserving surgery combined with radiation or surgery to remove all of the breast tissue.