FDA APPROVED POMALIDOMIDE

Celgene Corporation is pleased to announce that POMALYST® (pomalidomide) capsules is now approved and available for patients with multiple myeloma who have received at least 2 prior therapies including lenalidomide and bortezomib and have demonstrated disease progression on or within 60 days of completion of the last therapy. Approval is based on response rate. Clinical benefit, such as improvement in survival or symptoms, has not been verified. CONTRAINDICATIONS: Pregnancy POMALYST can cause fetal harm and is contraindicated in females who are pregnant. If this drug is used during pregnancy or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to a fetus Pomalidomide is a thalidomide analogue and is teratogenic in both rats and rabbits when administered during the period of organogenesis ICD-9 Diagnostic Codes The ICD-9 diagnostic codes for the approved indication of POMALYST in multiple myeloma are 203.00 and 203.02 Pomalidomide is a thalidomide analogue and is teratogenic in both rats and rabbits when administered during the period of organogenesis Dosage and Administration The recommended starting dose of POMALYST is 4 mg once daily orally on Days 1‑21 of repeated 28-day cycles (21/28 days) until disease progression POMALYST may be given in combination with dexamethasone. In the study, dexamethasone was given on days 1, 8, 15, and 22, and dosed at 40 mg per day for patients 75 years or younger, or 20 mg per day for patients older than 75 years POMALYST may be taken with water Inform patients not to break, chew, or open the capsules POMALYST should be taken without food (at least 2 hours before or 2 hours after a meal) Dosage Forms and Strengths POMALYST is available in 1 mg, 2 mg, 3 mg, and 4 mg capsules Dose Modification Instructions for POMALYST for Hematologic Toxicities Toxicity Dose Modification Neutropenia ANC* < 500 per mcL or Febrile neutropenia (fever more than or equal to 38.5°C and ANC < 1,000 per mcL) Interrupt POMALYST treatment, follow CBC weekly ANC return to more than or equal to 500 per mcL Resume POMALYST at 3 mg daily For each subsequent drop < 500 per mcL Interrupt POMALYST treatment Return to more than or equal to 500 per mcL Resume POMALYST at 1 mg less than the previous dose Thrombocytopenia Platelets < 25,000 per mcL Interrupt POMALYST treatment, follow CBC weekly Platelets return to > 50,000 per mcL Resume POMALYST treatment at 3 mg daily For each subsequent drop < 25,000 per mcL Interrupt POMALYST treatment Return to more than or equal to 50,000 per mcL Resume POMALYST at 1 mg less than previous dose *ANC = Absolute Neutrophil Count For other Grade 3 or 4 toxicities hold treatment and restart treatment at 1 mg less than the previous dose when toxicity has resolved to less than or equal to Grade 2 at the physician's discretion To initiate a new cycle of POMALYST, the neutrophil count must be at least 500 per mcL, the platelet count must be at least 50,000 per mcL If toxicities occur after dose reductions to 1 mg, then discontinue POMALYST Important Dosing Information Pomalidomide may be given in combination with dexamethasone Pomalidomide may be taken with water Inform patients not to break, chew or open the capsules Pomalidomide should be taken without food (at least 2 hours before or 2 hours after a meal) Monitor CBCs every week for the first 8 weeks and monthly thereafter Patients may require dose interruption and/or modification No dosage adjustment is required for pomalidomide based on age Important Information about POMALYST and POMALYST REMS™ To avoid embryo-fetal exposure, POMALYST is only available under a restricted distribution program called "POMALYST REMS™" POMALYST is contraindicated in pregnant females and females capable of becoming pregnant. Females of reproductive potential may be treated with POMALYST provided adequate precautions are taken to avoid pregnancy Only prescribers and pharmacists certified by the POMALYST REMS™ program can prescribe and dispense POMALYST to patients who are enrolled and meet all the conditions of the POMALYST REMS™ program Information about POMALYST and the POMALYST REMS™ program can be obtained by visiting www.CelgeneRiskManagement.com, or by calling the Celgene Customer Care Center toll free at 1-888-423-5436 Effective contraception must be used by female patients of reproductive potential for at least 4 weeks before beginning POMALYST therapy, during therapy, during dose interruptions and for 4 weeks following discontinuation of POMALYST therapy Females of reproductive potential must have 2 negative pregnancy tests (sensitivity of at least 50 mIU/mL). The first test should be performed within 10-14 days, and the second test within 24 hours prior to writing an initial prescription Once treatment has started and during dose interruptions, pregnancy testing for females of reproductive potential should occur weekly during the first 4 weeks of use, then pregnancy testing should be repeated every 4 weeks in females with regular menstrual cycles. If menstrual cycles are irregular, the pregnancy testing should occur every 2 weeks If pregnancy does occur during treatment, POMALYST must be discontinued immediately Access Assistance Celgene Patient Support® can offer assistance with access to POMALYST for both insured and uninsured patients. This includes benefits investigations, co-pay assistance or free drug to those patients who qualify, as well as appeals support For assistance or more information, contact your dedicated Celgene Patient Support® Specialist at 1-800-931-8691 or visit www.CelgenePatientSupport.com For a list of pharmacies registered in the POMALYST REMS™ program, visit www.Celgene.com/PharmacyNetwork. POMALYST® (pomalidomide) is indicated for patients with multiple myeloma who have received at least two prior therapies including lenalidomide and bortezomib and have demonstrated disease progression on or within 60 days of completion of the last therapy. Approval is based on response rate. Clinical benefit, such as improvement in survival or symptoms, has not been verified. Important Safety Information WARNING: EMBRYO-FETAL TOXICITY and VENOUS THROMBOEMBOLISM Embryo-Fetal Toxicity POMALYST is contraindicated in pregnancy. POMALYST is a thalidomide analogue. Thalidomide is a known human teratogen that causes severe birth defects or embryo-fetal death. In females of reproductive potential, obtain 2 negative pregnancy tests before starting POMALYST treatment Females of reproductive potential must use 2 forms of contraception or continuously abstain from heterosexual sex during and for 4 weeks after stopping POMALYST treatment POMALYST is only available through a restricted distribution program called POMALYST REMS™. Venous Thromboembolism Deep Venous Thrombosis (DVT) and Pulmonary Embolism (PE) occur in patients with multiple myeloma treated with POMALYST. Prophylactic anti-thrombotic measures were employed in the clinical trial. Consider prophylactic measures after assessing an individual patient’s underlying risk factors CONTRAINDICATIONS: Pregnancy POMALYST can cause fetal harm and is contraindicated in females who are pregnant. If this drug is used during pregnancy or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to a fetus Pomalidomide is a thalidomide analogue and is teratogenic in both rats and rabbits when administered during the period of organogenesis WARNINGS AND PRECAUTIONS Embryo-Fetal Toxicity Females of Reproductive Potential: Must avoid pregnancy while taking POMALYST and for at least 4 weeks after completing therapy. Must commit either to abstain continuously from heterosexual sexual intercourse or to use 2 methods of reliable birth control, beginning 4 weeks prior to initiating treatment with POMALYST, during therapy, during dose interruptions and continuing for 4 weeks following discontinuation of POMALYST therapy. Must obtain 2 negative pregnancy tests prior to initiating therapy Males: Pomalidomide is present in the semen of patients receiving the drug. Males must always use a latex or synthetic condom during any sexual contact with females of reproductive potential while taking POMALYST and for up to 28 days after discontinuing POMALYST, even if they have undergone a successful vasectomy. Males must not donate sperm Blood Donation: Patients must not donate blood during treatment with POMALYST and for 1 month following discontinuation of the drug because the blood might be given to a pregnant female patient whose fetus must not be exposed to POMALYST POMALYST REMS Program Because of the embryo-fetal risk, POMALYST is available only through a restricted program under a Risk Evaluation and Mitigation Strategy (REMS) called "POMALYST REMS." Prescribers and pharmacists must be certified with the program; patients must sign an agreement form and comply with the requirements. Further information about the POMALYST REMS program is available at [celgeneriskmanagement.com] or by telephone at 1‑888‑423‑5436. Venous Thromboembolism: Patients receiving POMALYST have developed venous thromboembolic events reported as serious adverse reactions. In the trial, all patients were required to receive prophylaxis or antithrombotic treatment. The rate of DVT or PE was 3%. Consider anticoagulation prophylaxis after an assessment of each patient’s underlying risk factors. Hematologic Toxicity: Neutropenia of any grade was reported in 50% of patients and was the most frequently reported Grade 3/4 adverse event, followed by anemia and thrombocytopenia. Monitor patients for hematologic toxicities, especially neutropenia, with complete blood counts weekly for the first 8 weeks and monthly thereafter. Treatment is continued or modified for Grade 3 or 4 hematologic toxicities based upon clinical and laboratory findings. Dosing interruptions and/or modifications are recommended to manage neutropenia and thrombocytopenia. Hypersensitivity Reactions: Patients with a prior history of serious hypersensitivity associated with thalidomide or lenalidomide were excluded from studies and may be at higher risk of hypersensitivity. Dizziness and Confusional State: 18% of patients experienced dizziness and 12% of patients experienced a confusional state; 1% of patients experienced grade 3/4 dizziness, and 3% of patients experienced grade 3/4 confusional state. Instruct patients to avoid situations where dizziness or confusion may be a problem and not to take other medications that may cause dizziness or confusion without adequate medical advice. Neuropathy: 18% of patients experienced neuropathy (approximately 9% peripheral neuropathy). There were no cases of grade 3 or higher neuropathy adverse reactions reported. Risk of Second Primary Malignancies: Cases of acute myelogenous leukemia have been reported in patients receiving POMALYST as an investigational therapy outside of multiple myeloma. ADVERSE REACTIONS In the clinical trial of 219 patients who received POMALYST alone (n=107) or POMALYST + low-dose dexamethasone (low-dose dex) (n=112), all patients had at least one treatment-emergent adverse reaction. In the POMALYST alone versus POMALYST + low dose dexamethasone arms, respectively, most common adverse reactions (≥30%) included fatigue and asthenia (55%, 63%), neutropenia (52%, 47%), anemia (38%, 39%), constipation (36%, 35%), nausea (36%, 22%), diarrhea (34%, 33%), dyspnea (34%, 45%), upper respiratory tract infection (32%, 25%), back pain (32%, 30%), and pyrexia (19%, 30%) 90% of patients treated with POMALYST alone and 88% of patients treated with POMALYST + low-dose dex had at least one treatment-emergent NCI CTC Grade 3 or 4 adverse reaction In the POMALYST alone versus POMALYST + low dose dexamethasone arms, respectively, most common Grade 3/4 adverse reactions (≥15%) included neutropenia (47%, 38%), anemia (22%, 21%), thrombocytopenia (22%, 19%), and pneumonia (16%, 23%). For other Grade 3 or 4 toxicities besides neutropenia and thrombocytopenia, hold treatment and restart treatment at 1 mg less than the previous dose when toxicity has resolved to less than or equal to Grade 2 at the physician’s discretion 67% of patients treated with POMALYST and 62% of patients treated with POMALYST + low-dose dex had at least one treatment-emergent serious adverse reaction In the POMALYST alone versus POMALYST + low dose dexamethasone arms, respectively, most common serious adverse reactions (≥5%) were pneumonia (14%, 19%), renal failure (8%, 6%), dyspnea (5%, 6%), sepsis (6%, 3%), pyrexia (3%, 5%) dehydration (5%, 3%), hypercalcemia (5%, 2%), urinary tract infection (0%, 5%), and febrile neutropenia (5%, 1%) DRUG INTERACTIONSNo formal drug interaction studies have been conducted with POMALYST. Pomalidomide is primarily metabolized by CYP1A2 and CYP3A. Pomalidomide is also a substrate for P‑glycoprotein (P‑gp). Coadministration of POMALYST with drugs that are strong inhibitors or inducers of CYP1A2, CYP3A, or P‑gp should be avoided. Cigarette smoking may reduce pomalidomide exposure due to CYP1A2 induction. Patients should be advised that smoking may reduce the efficacy of pomalidomide. USE IN SPECIFIC POPULATIONS Pregnancy: If pregnancy does occur during treatment, immediately discontinue the drug and refer patient to an obstetrician/gynecologist experienced in reproductive toxicity for further evaluation and counseling. Report any suspected fetal exposure to POMALYST to the FDA via the MedWatch program at 1‑800‑332‑1088 and also to Celgene Corporation at 1‑888‑423‑5436. Nursing Mothers: It is not known if pomalidomide is excreted in human milk. Pomalidomide was excreted in the milk of lactating rats. Because many drugs are excreted in human milk and because of the potential for adverse reactions in nursing infants from POMALYST, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother. Pediatric Use: Safety and effectiveness of POMALYST in patients under the age of 18 have not been established. Geriatric Use: No dosage adjustment is required for POMALYST based on age. Patients greater than or equal to 65 years of age were more likely than patients less than or equal to 65 years of age to experience pneumonia. Renal and Hepatic Impairment: Pomalidomide is metabolized in the liver. Pomalidomide and its metabolites are primarily excreted by the kidneys. The influence of renal and hepatic impairment on the safety, efficacy, and pharmacokinetics of pomalidomide has not been evaluated. Avoid POMALYST in patients with a serum creatinine >3.0 mg/dL. Avoid POMALYST in patients with serum bilirubin >2.0 mg/dL and AST/ALT >3.0 x ULN. Please see full Prescribing Information, including Boxed WARNINGS, CONTRAINDICATIONS, WARNINGS AND PRECAUTIONS, and ADVERSE REACTIONS. POMALYST is only available under a restricted distribution program, POMALYST REMS™. Sent on behalf of Celgene Corporation. POMALYST® and Celgene Patient Support® are registered trademarks of Celgene Corporation. POMALYST REMS™ is a trademark of Celgene Corporation. ©2013 Celgene Corporation. 02/13 US-POM120061a

Please see Important Safety Information and full Prescribing Information, including Boxed WARNINGS, CONTRAINDICATIONS, WARNINGS AND PRECAUTIONS and ADVERSE REACTIONS. WARNING: EMBRYO-FETAL TOXICITY and VENOUS THROMBOEMBOLISM Embryo-Fetal Toxicity POMALYST is contraindicated in pregnancy. POMALYST is a thalidomide analogue. Thalidomide is a known human teratogen that causes severe birth defects or embryo-fetal death. In females of reproductive potential, obtain 2 negative pregnancy tests before starting POMALYST treatment Females of reproductive potential must use 2 forms of contraception or continuously abstain from heterosexual sex during and for 4 weeks after stopping POMALYST treatment POMALYST is only available through a restricted distribution program called POMALYST REMS™. Venous Thromboembolism Deep Venous Thrombosis (DVT) and Pulmonary Embolism (PE) occur in patients with multiple myeloma treated with POMALYST. Prophylactic anti-thrombotic measures were employed in the clinical trial. Consider prophylactic measures after assessing an individual patient's underlying risk factors

MUTATION IN "p" IN A CHROMOSOME IS GOOD FOR YOU!

To further confirm that "p" is better that "q", I went back to see what is the mutation in a curable cancer and germ cell tumors or testicular cancer. And guess what? It is not 12q that is abnormal in testicular cancer, IT IS INDEED 12p that is involved in the Malignant transformation.

CCND2 is at 12p13, but also SOX5, JAW1, and KRAS is at 12p11.2-12.1
You know angry corresponding family members are located on other chromosomes, but not amplified in Testicular cancer and would confer resistance to therapy.  In fact it would be interesting to see if they are amplified in refractory cases for proof of concept!
The association with endoreduplication (Multiple ploidies) is another good thing to look into further as it relates (or not) to 12p Mutation!

Certainly the response to chemotherapy alone is an intriguing phenomena by itself and should open up cues to look for in other cancers!  I believe it is in the "p" and in the "ploidy" thing or tendency to multiply that is where the cancer vulnerability is squarely located!  

Cellular Variations/language *New German study finds Kras stimulation in Pancreatic cancer is not the same as Kras stimulation in the lung and therefore PI3K expression will not have same implications

Selective Requirement of PI3K/PDK1 Signaling for Kras Oncogene-Driven Pancreatic Cell Plasticity and Cancer
Stefan Eser, Nina Reiff, et al.

Read it.  It tells you that not only the implications of a stimulation of one molecule change with the tissue because of tissue specific genetic silencing ,  but also changes can occur on different RAS family member (NRas or Hras) leading to different meaning in terms of consequence for the cell.
Another discrimination level is that many types of stimulation can induce the same pathway.  C-JUN can be induced by radiation, chemical, hypoxia or infection.  Any thing that is considered stressful, including lack of extracellular stimulation.  This last point is very important in the Central nervous system where pre-synaptic stimulation is critical for post synaptic neurons.  Lack of stimulation induces an inflammatory process in both the neuron and the glial cell.  In the glial cell, the myelin sheath is scarily attacked or no longer formed.
The duplicity phenomena occurs particularly at the cellular membrane where many receptors would be stimulated by several stimulants and vice versa (many stimulants for same receptor).  Only the cell and its tissue type know what to give out!

*New study concurs that mammogram should be done every 2 years and after 50 years of age.   That only those women with dense breasts should start at 40 years of age and annually.  The controversy dance is fueled once again and I don't blame anyone!  We have seen cases of course which did not fit these prescription.  Why change things that work.

PANCREATIC CANCER GENE (CONTINUED)

1' KRT20: keratin related gene, most likely of an early expression in neoplastic transformation
more predictive and diagnostic than of less therapeutic potential.

2-TEM 7: The blood vessels of Tumors seems to have an exclusive marker called Tumor Endothelial Marker or TEM.   Target therapy directed at this stuff may lead tumor to anoxic death by closing these vessels, at least that the wish of researchers, will follow their efforts!
Certainly this used as serologic marker or radiologically, can locate metastatic lesions.

3-MAP2K4" direct activator of the MAPK/c-JUNK through MAP8& 14. (Not the standard MAPK1)
but it also interact with an anchor called Filamin Though FLNC, filamin is actin binding protein, raising the issue of whether or not it is using this tract to quickly influence the Nucleus or whether it allows it to phosphorylate things right there!  we know its expression is, like the MTOR stimulated path, preserving survival!  Does this open the door to MTOR Inhibitor in Pancreatic cancer? Does expression of this pathway, an opportunity to introduce MTOR inhibitors?

4-BAT-26

please read this:
"BAT-26, an indicator of the replication error phenotype in colorectal cancers and cell lines" by

Hoang JM, Cottu PH, Thuille B, Salmon RJ, Thomas G, Hamelin R.

BAT 26 IS THEREFORE AN INDICATOR OF MICRO-SATELLITE INSTABILITY STATUS IN CANCER.

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5-ALOX12

6-TP53

7-BIRC5

8-NME1
9-ERBB2
10-GAS
11-TM4SF5

An interesting set of Circumstances
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We seem to live an interesting time, unusual things happening, the government is late doing stuff.  Although it claims it is pro-business, licenses are delayed and the emphasis seems to crack down, and pay less.  Shrinking everything seems to be the impetus!
The most interesting scenario is what is happening with the IRS.  Because I need to meet some money demands, I filed my taxes early in February or as soon as I got my W-2 and related 1099.  4 weeks after I filed, I got a text on my phone that the IRS has rejected my filing.  I thought it was a joke but sure enough I got confirmation through my e-mail and from the IRS office.  We must live an interesting revolution!  When the IRS is now evading tax-filing.  It used to be that if you do something incorrect, the IRS corrects it.  I had come to expect that and normally sent my best evaluation for their smart correction. NOW if they are rejecting Tax submission where the hell should I go?  The interesting thing is, according to their not, a rejected Tax file is not a "Filing, and the can still charge me for late filing and evasion if not refiled".  Can you possibly evade Taxes when you are repeatedly trying to file?  The IRS is getting it both ways I believe.  They refuse to do the work, and still threaten to punish me!  What in the world is going on?  If you figure it out, help me!

NOMENCLATURE OF GENE (III ), PANCREATIC CANCER!

BETA 4 INTEGRIN: a gene that does more than being an adhesion molecules
it is the road to a poorly described and not well recognized pathway

The LysRS-Ap₄A-MITF signaling pathway

The LysRS-Ap₄A-MITF signaling pathway was first discovered in mast cells, in which , the MAPK pathway is activated upon allergen stimulation. Lysyl-tRNA synthetase (LysRS), which normally resides in the multisynthetase complex with other tRNA synthetases, is phosphorylated on Serine 207 in a MAPK-dependent manner.^[30] This phosphorylation causes LysRS to change its conformation, detach from the complex and translocate into the nucleus, where it associates with the MITF-HINT1 inhibitory complex. The conformational change switches LysRS activity from aminoacylation of Lysine tRNA to diadenosine tetraphosphate (Ap₄A) production. Ap₄A binds to HINT1, which releases MITF from the inhibitory complex, allowing it to transcribe its target genes.^[31] Activation of the LysRS-Ap₄A-MITF signaling pathway by isoproterenol has been confirmed in cardiomyocytes, where MITF is a major regulator of cardiac growth and hypertrophy.<sup>[32][33](wikipedia)

Not only it gives Hypertrophy but epidermolysis goes through this intergrin, it participates in the ERBB pathways.  Mark my word these are critical pathways in pancreatic cancers.

MTIF GIVES YOU MOTIVES TO AFTER IT!
MAKING THE ERBIN A PLAUSIBLE TARGET.
MAKING ALSO A STRONGER CASE THAT MEMBRANE CYTOSKELETON SHOULD BE A GOOD TARGET BECAUSE OF THE WAY IT DRIVES ITS PATHWAY NOT THROUGH THE CYTOSOL( ALTHOUGH THERE IS A SECONDARY RAS/MAPK STIMULATION,) BUT THE PATHWAY HERE IS THROUGH THE RETICULUM ENDOTHELIUM DIRECTLY TO THE NUCLEUS!  CONCEPTUALLY, AN ANTIBODY TO LAMININ ATTACHED TO A SUBUNIT OF A LIPOLYTIC COMPOUND SHOULD HAVE A THERAPEUTIC OR CHEMICAL EFFECT AT THIS LEVEL.  AN INTERESTING APPROACH.  CHANCES ARE IT MAY ALSO HAVE A STRONG IMPACT ON THE WNT-PATHWAY WHICH TRAVELS CLOSE BY AND IS IMPORTANT IN BREAST CANCER!</sup>

MTA-1: THIS IS A REAL OPPORTUNITY
Here the cell stopped fooling around trying to lie to you.  Here the cell says to you this is one of my ways to metastasize.  yes this is my gene to metastasize and I will work like any CBF like molecule by attaching to DNA and make me protein that will have me spread like wild fire!   And by the way, I will use a growth hormone like Estrogen. No kidding around.
 "MTA1 has been shown to interact with HDAC1,^[4][5] Histone deacetylase 2,^[4][6][5] MTA2,^[4] Estrogen receptor alpha^[7][5] and MNAT1.^[8] MTA1 has also been shown to inhibit SMAD7 at the transcriptional level[9]<sup>"  

IT DOES NEED TGF TO WORK, TGF IS FOR LOCAL GROWTH ANYWAY, THAT IS WHY IT BLOCKS THE SMAD.</sup>

SPINT2
Mutation at SPINT2 leads to significant Malignant Ascites and peritoneal invasion, SPINT 2 is a suppressor of this phenomena. On the Intestinal membrane deficiency of SPINT2 leads to sodium induced/containing diarrhea.  This is also true in Ovarian cancer or peritoneal based tumors.  Targeting this is better than trying Avastin, a blind approach when it comes to effusion management.

MMP11

A metalloproteinase, aimed at breaking down extracellular matrix and be on the move.  Targeting MMP for cancer has proven futile.  The cell is not stupid, it does not put out things that are going to hunt it!  It builds first a strong inhibitor to metalloproteinases.  In fact, the lack of inhibitors has been recognized as the main pathogenesis of TTP.   With the ADAMs being the integrins involved!  and next is that Inhibitor which is, of course, expressed in pancreatic cancer.

TIMP1

TIMP1

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TIMP metallopeptidase inhibitor 1
PDB rendering based on 1d2b.
Available structures PDB Ortholog search: PDBe, RCSB [show]List of PDB id codes
Identifiers
Symbols	TIMP1; CLGI; EPA; EPO; HCI; TIMP
External IDs	OMIM: 305370 MGI: 98752 HomoloGene: 36321 GeneCards: TIMP1 Gene
[show]Gene Ontology
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	7076	21857
Ensembl	ENSG00000102265	ENSMUSG00000001131
UniProt	P01033	P12032
RefSeq (mRNA)	NM_003254	NM_001044384
RefSeq (protein)	NP_003245	NP_001037849
Location (UCSC)	Chr X: 47.44 – 47.45 Mb	Chr X: 20.87 – 20.87 Mb
PubMed search	[1]	[2]

TIMP metallopeptidase inhibitor 1, also known as TIMP1, a tissue inhibitor of metalloproteinases, is a glycoprotein that is expressed from the several tissues of organisms.
This protein a member of the TIMP family. The glycoprotein is a natural inhibitor of the matrix metalloproteinases (MMPs), a group of peptidases involved in degradation of the extracellular matrix. In addition to its inhibitory role against most of the known MMPs, the encoded protein is able to promote cell proliferation in a wide range of cell types, and may also have an anti-apoptotic function.
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PRKCA  see PRKCG
Here Phorbol esters, diacylglycerol, and calcium become important for the cell performance of various functions.  Did I mention few targets, I truly believe I did!

CDH1  The Cadherin by excellence, not only important as adhesion molecule and role in metastasis.  Its role is amplified by what else anchors here such as Vinculin, and others molecules such as Plakoglobins, amplifying the role.  Remember even Cytochrome C is anchored at the mitochondrial membrane and its release leads to apoptosis!
The anchors are legitimate targets therefore, and brings to mind NACA1 in the anchoring to Histone deacetyl transferase (SEE OUR LEUKEMIA SECTION)  CDH13 THAT'S ANOTHER BALL GAME ALL TOGETHER.  THE CELL TWEACKS SOMETHING AND IT IS ANOTHER BALL GAME ALL TOGETHER!
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